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Abstract Background There is limited evidence of the relationship between cognitive changes and all-cause mortality. And it has no report of population-attributable fraction (PAF) of mortality due to cognitive impairment in Chinese elderly. In light of this, we comprehensively examined the relationship between cognitive impairment and all-cause mortality after 20-year follow-up among the elderly Chinese. Methods This is an epidemiological survey with a 20-year prospective cohort study design. A total of 9093 participants came from the Chinese Longitudinal Healthy Longevity Survey 1998–2018 waves. Cox proportional hazards regressions were performed to analyze the relationship between baseline cognitive impairment status, the rate of change in the MMSE scores over two years and subsequent all-cause mortality. Results We observed a dose–response relationship between cognition and mortality. Compared to those with no impairment, elderly with mild (AHR = 1.11, 95% CI 1.05–1.18), moderate (AHR = 1.22, 95% CI 1.13–1.33) and severe (AHR = 1.30, 95% CI 1.19–1.42) cognitive impairment showed increased mortality risk. Elderly with rapid cognitive decline had 24% higher mortality risk than those with stable cognitive (AHR = 1.24, 95%CI 1.10–1.39). The PAF of mortality due to severe cognitive impairment was 3.69% (95%CI:2.36–5.25%). Impairment in the subdomain of naming foods (AHR = 1.12, 95% CI 1.04–1.21), registration (AHR = 1.18, 95% CI 1.11–1.26), attention and calculation (AHR = 1.13, 95% CI 1.07–1.21), copy figure (AHR = 1.13, 95% CI 1.06–1.20), delayed recall (AHR = 1.14, 95% CI 1.07–1.20) and language (AHR = 1.14, 95% CI 1.05–1.24) were independently associated with increased mortality risk among participants. Conclusion Baseline cognitive impairment was inversely associated with longevity among the elderly Chinese. The rapid cognitive decline increased all-cause mortality, and this risk would continue for 20 years. These findings underscore the crucial role of early detection and management of cognitive impairment in the elderly.

Abstract Introduction Numerous studies have demonstrated the effects of transcranial direct current stimulation (tDCS) on cognitive function in the older people. This study further explores the impact of tDCS and its dosage parameters on cognitive enhancement in older people with cognitive impairments. Methods Randomized controlled trials (RCTs) published through November 2023 were retrieved from databases including PubMed, Scopus, EMBASE, EBSCO, and the Cochrane Library. Participants were older adults with cognitive impairments, including Alzheimer’s disease (AD), mild cognitive impairment (MCI), and dementia. AD was diagnosed based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), or the National Institute of Neurological and Communicative Disorders and Stroke – Alzheimer’ Disease and Related Disorders Association (NINCDS-ADRDA) criteria. Dementia was diagnosed using the DSM-V or NINCDS-ADRDA criteria, while MCI was diagnosed using the DSM-V, the Petersen criteria, or assessments such as Montreal Cognitive Assessment (MoCA) and Clinical Dementia Rating (CDR). Standardized mean difference (SMD) values were analyzed to assess the effects. Results A total of 19 RCTs were included. tDCS significantly improved the Mini-Mental State Examination score both immediately post-intervention (SMD = 0.51, p = 0.005) and at follow-up (SMD = 2.29, p = 0.0003). Significant effects were observed when tDCS was used alone (SMD = 0.39, p = 0.04), at current densities $$\le$$ ≤ 0.06 mA/cm2 (SMD = 0.25, p = 0.04), session durations exceeding 20 min (SMD = 0.89, p = 0.01), up to 15 sessions (SMD = 0.28, p = 0.009), and when an active electrode was placed over the temporal area (SMD = 0.33, p = 0.02). People with AD showed greater improvements compared to those with MCI or dementia (SMD = 0.91, p = 0.02). However, tDCS did not significantly improve memory or executive function. Conclusion tDCS demonstrated efficacy in enhancing global cognition in older people with cognitive impairments, providing insight into optimal parameters for clinical application. However, no improvement were observed in memory or executive function.

Cognitive impairment has become one of the major public health problems due to population aging and the increased morbidity associated with stroke. In this study, we aimed to analyze the correlations of vascular cognitive impairment (VCI) with brain-derived neurotrophic factor (BDNF) and trace elements.

Xiaoqi Chu,1,2,* Yusong Ge,3,* Chao Geng,1,2 Peipei Cao,1,2 Penghu Wei,2 Bin Fu,2 Zihao Deng,4 Yuhao Li,5,6 Guoguang Zhao2,7 1Optometry Institute, School of Medicine Nankai University, Tianjin, People’s Republic of China; 2Department of Neurosurgery, Xuanwu Hospital Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, People’s Republic of China; 3Department of Neurology, The Second Hospital of Dalian Medical University, Dalian, People’s Republic of China; 4Cancer Center, Capital Medical University, Beijing, People’s Republic of China; 5Central Laboratory, Xuanwu Hospital Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, People’s Republic of China; 6Department of Pathology, School of Medicine Nankai University, Tianjin, People’s Republic of China; 7National Medical Center for Neurological Diseases, Beijing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Guoguang Zhao, Department of Neurosurgery, Xuanwu Hospital Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, People’s Republic of China, Email ggzhao@vip.sina.com Yuhao Li, Central Laboratory, Xuanwu Hospital Capital Medical University, Beijing Municipal Geriatric Medical Research Center, Beijing, People’s Republic of China, Email liyuhao@xwhosp.orgPurpose: Lactate, previously considered a metabolic waste product, has been shown to have neuroprotective potential. This study aims to investigate the impact of lactate intervention and its underlying mechanisms on epilepsy.Methods: HT22 cells were stimulated with glutamate to construct an excitotoxicity cell model. An acute epilepsy model was established in mice by kainic acid induction. The neuronal damage, microglial activation, inflammatory responses, and functional changes were determined by TUNEL assays, immunohistochemistry, quantitative real-time polymerase chain reaction and behavioral tests. The differentially gene expression and functional enrichment were analyzed with RNA sequencing.Results: The in vitro lactate intervention reduced the number of apoptotic cells, the release of inflammatory factors, and the expression of vesicular glutamate transporter 1. In mice with acute epilepsy, lactate treatment mitigated neuronal damage, microglial activation, and inflammatory responses in the hippocampus and ameliorated anxiety-like behavior and cognitive impairment.Conclusion: Lactate exerts therapeutic effects on epilepsy through the chemokine signaling pathway. The neuroinflammation is an important contributor to cognitive impairment. Targeting inflammatory pathways is a promising strategy for improving the prognosis of epilepsy. Keywords: lactate, neuroinflammation, cognitive impairment, neuronal damage, chemokine, epilepsy

Abstract Background Psychiatric signs may be induced by the cytokine storm that is implicated in the immune response to coronavirus through neuro-inflammation. Survivors disclosed symptoms of obsessive–compulsive disorder, melancholy, anxiety, panic disorder, and post-traumatic stress disorder. For the first year following the SARS disease, they generally suffer from suicide and psychosis. Aim To evaluate the presence of cognitive impairment, anxiety disorders, and depression in adult survivors of COVID-19, 1 month and 3 months post-recovery. Method It is an observational longitudinal study. Forty-four COVID-19 survivor patients, with no past psychiatric history were evaluated at 3 months and 1 month after recovery. The Montreal Cognitive Impairment Basic (MoCA-B) was employed to evaluate cognitive impairment. However, anxiety and depressive disorders were identified via structured clinical interview for DSM IV, axis I (SCID-I) and their severity was examined by the Beck Depression Inventory (BDI) and Beck Anxiety Inventory (BAI) consecutively. Results Regarding cognitive impairment, MoCA-B results showed a mean score of 25.95 ± 1.98 in the 1st interview and 27.7 ± 1.05 in the 2nd interview, with a marked change, P-value = 0.001. SCID-I showed that 43.2% of our sample was diagnosed with both anxiety and depression at 1 month post-recovery, with the improvement of some cases at 3 months to affect only 18.2%, showing a statistically significant difference, P-value = 0.036. The percentage of patients who suffered from sleep difficulties was 59.1% at 1st interview and 27.3% at 2nd interview. While 61.4% of patients suffered from fatigue and low concentration at 1st interview and went down to 31.8% at 2nd interview, showing a statistically significant difference, P-value

Abstract Background Cerebral creatine deficiency disorders (CCDD) are rare diseases caused by defects in the enzymes L-arginine: glycine amidinotransferase (AGAT) or guanidinoacetate-N-methyltransferase (GAMT), which are involved in synthesis of creatine; or by a defect in the creatine transporter (CRTR), which is essential for uptake of creatine as important energy source into the target cells. Patients with CCDD can present with a variety of unspecific symptoms: global developmental delay, speech-language disorder, behavioral abnormalities and seizures. Early treatment initiation is essential in AGAT and GAMT deficiencies to achieve a favorable outcome. This study describes the CCDD patient cohort in a single center, and an analysis of the referrals to two Swiss laboratories in Lausanne and Zurich between 2015 and 2023 for the two marker metabolites guanidinoacetate and creatine. Results The patient cohort comprised 6 patients (defects: 2 GAMT, 4 CRTR), who were initially seen by different subspecialties depending on first symptoms. There was a diagnostic and therapeutic delay between 3 and 32 months (mean 13.8). Numbers of biomarker requests showed a constant increase during the study period, with a majority of tests performed in urine, the preferred sample for CCDD detection. Almost all samples (93.3%) were sent in by large hospitals (mainly from neurology, developmental pediatrics and metabolism) and only few (5.2%) by pediatricians in private practice, although those usually see the patients first. Conclusions The data from this study demonstrate a relevant delay in identifying patients with these rare conditions, and a predominance of biomarker analysis requested from pediatric subspecialties that are involved in patient management often long after occurrence of symptoms. To reduce the diagnostic delay and the outcome of patients, the current practice of sample referral should be reflected and first-contact healthcare providers should be encouraged to initiate selective screening.

Ziwei Yang,1,2,&ast; Xiao Liang,1,2,&ast; Yuqi Ji,1,2 Wei Zeng,1,2 Yao Wang,1,2 Yong Zhang,3 Fuqing Zhou1,2 1Jiangxi Provincial Key Laboratory for Precision Pathology and Intelligent Diagnosis, Department of Radiology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, People’s Republic of China; 2Neuroradiology Laboratory, Jiangxi Province Medical Imaging Research Institute, Nanchang, 330006, People’s Republic of China; 3Department of Pain Clinic, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, 330006, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Yong Zhang, Department of Pain Clinic, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, Jiangxi, 330006, People’s Republic of China, Tel +86 791 8869 5036, Email zy830226@163.com Fuqing Zhou, Jiangxi Provincial Key Laboratory for Precision Pathology and Intelligent Diagnosis, Department of Radiology, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Nanchang, Jiangxi, 330006, People’s Republic of China, Tel +86 791 8869 5132, Email ndyfy02301@ncu.edu.cnPurpose: To investigate whether functional radiomic features in bilateral hippocampi can identify the cognitively impaired patients from low-back-related leg pain (LBLP).Patients and Methods: For this retrospective study, a total of 95 clinically definite LBLP patients (40 cognitively impaired patients and 45 cognitively preserved patients) were included, and all patients underwent functional MRI and clinical assessments. After calculating the amplitude of low-frequency fluctuations (ALFF), regional homogeneity (ReHo), voxel-mirrored homotopic connectivity (VMHC) and degree centrality (DC) imaging, the radiomic features (n = 819) of bilateral hippocampi were extracted from these images, respectively. After feature selection, machine learning models were trained. Finally, we further analyzed the relationship between the hippocampal functional radiomic features and clinical measures, to explore the clinical significance of these features.Results: The combined radiomic features model logistic regression algorithm superior performance in distinguishing cognitively impaired patients from LBLP (AUC = 0.970, accuracy = 92.3%, sensitivity = 92.3%, specificity = 92.3%) compared to the other models. Additionally, radiomic wavelet features were correlated with Montreal Cognitive Assessment (MoCA) and Hamilton Anxiety Scale, present pain intensity scores in cognitively impaired LBLP patients (P < 0.05, with Bonferroni correction).Conclusion: Hippocampal functional radiomic features are valuable for diagnosing cognitively impaired patients from LBLP.Keywords: cognitive impairment, resting-state functional MRI, low-back-related leg pain, radiomic, logistic regression algorithm

Abstract Background Early diagnosis is crucial to the optimal management of patients with cognitive impairment due to Alzheimer’s disease (AD) or AD-related dementias. For some patients, early detection of cognitive impairment enables access to disease-modifying therapies. For all patients, it allows access to psychosocial supports. Patients typically first present their concerns about their cognition to a primary care provider, but in this setting, cognitive impairment is commonly underdiagnosed. There is also high variability in how cognitive evaluations are performed. We sought to understand barriers to and facilitators of cognitive evaluations in primary care, map barriers to implementation strategies, and gain consensus from stakeholders on possible strategies to improve dementia diagnosis in primary care. Methods Semi-structured interviews conducted with primary care providers (PCPs). We used the Consolidated Framework for Implementation Research to inform our question guide and analysis, and incorporated chart-stimulated recall – using actual patients who had cognitive complaints who had presented to these providers – to understand clinicians’ medical decision-making processes. These data were used to map identified barriers and facilitators to targeted implementation strategies. Then, this candidate list of strategies was presented to an expert stakeholder panel including clinicians and clinical operations specialists. Through a modified Delphi process, the list was narrowed to select the most promising strategies to incorporate in an intervention to improve cognitive evaluations in primary care. Results Twenty PCPs were interviewed and mentioned barriers included lack of expertise to perform or interpret an assessment, time pressures, lack of incentives, competing priorities, lack of decision-making supports, and limited access to dementia specialists. Facilitators included the presence of an informant or caregiver and having additional staff to conduct cognitive testing. Implementation mapping resulted in a list of 15 candidate strategies. Using the modified Delphi process, these were narrowed to six. Conclusions We used a rigorous process to identify barriers to and facilitators of cognitive assessments in primary care, identify promising implementation strategies to address these barriers, and obtain the feedback of front-line users on these strategies. This holds substantial promise for improving cognitive assessments in primary care in future implementation trials.

Abstract Iron overload has been associated with cerebrovascular disease and cognitive impairment in β-thalassaemia patients, typically appearing earlier than in the general population. However, the mechanisms of iron overload on cerebrovascular pathology remain unclear. This study investigated the effects of heavy iron overload on the blood-brain barrier and neurohistology, particularly in the CA3 region of hippocampus and its contribution to cognitive impairment in β-thalassaemia mice. Three-month-old female β-thalassaemia and wild-type mice received iron dextran via intraperitoneal injection to induce heavy iron overload. While β-thalassaemia mice with low baseline iron show cognitive impairment at 22 months, equivalent to 70–80 human years, heavy iron overload accelerated cognitive decline, leading to impaired spatial learning and memory by 12 months, equivalent to 35–40 human years, in both β-thalassaemia and wild-type mice. Iron-loaded mice have reduced hippocampal CA3 pyramidal neurons and significant iron accumulation in blood vessels, with no increase in neuronal iron levels. A significant decrease in ZO-1, a tight junction protein, indicated decreased blood-brain barrier integrity and potential iron leakage into the brain. While iron-loading had no effect on astrocytes, elevated Iba1 expression in microglia suggests microglia activation as a protective response. However, persistent iron overload may lead to chronic neuroinflammation, neurodegeneration, and cognitive decline. These results underscore the critical role of iron overload in accelerating cognitive decline in β-thalassaemia and suggest that regular monitoring of iron levels and chelation therapy may help prevent early cognitive impairment, ultimately improving the quality of life for β-thalassaemia patients.

Abstract Genetics plays a significant role in Multiple Sclerosis (MS), with approximately 12.6% of cases occurring in familial form. While previous studies have demonstrated differences in disease progression and MRI findings between familial and sporadic MS, there has been no comparison of cognitive impairment between them. In this study, we evaluated cognitive performance among patients with sporadic and familial MS, along with a healthy control group. A total of 130 individuals, matched for age, sex, and education, were recruited for each group. The mean age of participants was 37.8 ± 9.8 years, and 77.6% of them were female. Cognitive performance was assessed using the Brief International Cognitive Assessment for MS (BICAMS) across the three groups. Both familial and sporadic MS patients showed poorer cognitive performance in the Symbol Digit Modalities Test (SDMT) (Familial: 46.96 ± 12.59, Sporadic: 45.88 ± 14.13, Normal: 56.48 ± 11.89), California Verbal Learning Test (CVLT) (Familial: 66.90 ± 14.01, Sporadic: 68.19 ± 16.49, Normal: 75.18 ± 13.02), and the Brief Visuospatial Memory Test-Revised (BVMT-R) (Familial: 24 (12), Sporadic: 24 (12), Normal: 35 (4)) compared to healthy controls. Meanwhile, no significant differences in cognitive impairment were observed between the familial and sporadic MS groups in the SDMT (p = 1.000), CVLT (p = 0.775), and BVMT-R (p = 0.733). Furthermore, this study found significant relationships between education, depression, age, and sex with different aspects of cognitive performance in MS. Overall, both familial and sporadic MS patients demonstrated similar levels of cognitive impairment.

Abstract Background Over the past decades, self-directed models of care have been implemented throughout the world to support older people, including those with dementia, to live at home. However, there is limited information about how self-directed home care is experienced by older people with cognitive impairment and dementia, and how their thinking informs their care choices and quality of life. Methods We used the ASCOT-Easy Read, a staggered reveal method, talk aloud techniques, probing questions, and physical assistance to support users of self-directed home care in Australia with cognitive impairment and dementia to discuss their Social Care Related Quality of Life (SCRQoL). Interviews were recorded, transcribed and analysed thematically in NVivo. Demographic, functional, cognitive and SCRQoL scores were analysed in Excel and SPSS. Analysis of both the quantitative and qualitative data for each participant allowed us to examine consistency or discordance between ratings and participants’ comments about their experiences within each domain. Results Twenty six older people with cognitive impairment and/or dementia completed an interview. Ratings of SCRQoL were more favourable in lower order domains (e.g. food and drink, personal cleanliness, accommodation comfort and cleanliness and safety) than in the higher order domains (e.g. occupation and social participation). Overall SCRQOL also varied significantly from 0.40 to 0.97. Despite variable ratings, all participants described unmet needs associated with limitations in personal function and mobility, transport and the amount and flexibility of home care services they received. Qualitative comments suggest many experienced more significant limitations than some of their ratings may imply. This was attributed to adaptation and acceptance of limitations as a normal part of aging. The choice to remain living in one’s own home was perceived as the most important outcome. Conclusions Some older people living at home with cognitive impairment and/or dementia adapt and accept their limitations as a normal part of the aging process. This affects expectations about their lives at home and their support. Rather than relying on self-direction, supports to live well at home could be enhanced by a greater emphasis on comprehensive needs assessment and more supports to promote reablement and enhance personal and community level participation.

Abstract Background Cognitive impairment is a common health problem among older adults. Previous studies have proven the association between sleep quality and cognitive impairment, but the specific underlying mechanisms need to be further explored. This study aimed to examine the relationship between sleep quality and cognitive impairment and the mediating effect of frailty in this relationship among the rural older adults. Methods Data from a cross-sectional study conducted in rural areas of Shandong Province from September to December in 2023. A total of 695 rural older adults were included. The Pittsburgh Sleep Quality Index (PSQI) was used to measure sleep quality. Frailty was defined using the FRAIL scale. We assessed cognitive impairment using the Dementia Screening Interview (AD8). Logistic regression analyse was used to assess the relationship between sleep quality and cognitive impairment. And the Karlson-Holm-Breen (KHB) method was performed to test the mediating role of frailty in this relationship. Results After adjusting for all covariates, sleep quality was significantly associated with cognitive impairment (OR = 1.047, 95% CI: 1.005—1.090). Frailty mediated the relationship between sleep quality and cognitive impairment, with a mediation effect value of 0.010 (95% CI: 0.001—0.020), accounting for 17.86% of the total effect. Conclusions We found there was an association between sleep quality and cognitive impairment, and frailty mediated the above relationship. Comprehensive intervention measures should be taken to reduce the incidence of frailty in the older adults and to improve their sleep quality, thereby preventing and delaying the occurrence and development of cognitive impairment.

Background: Dementia is the leading cause of disability and imposes a significant burden on society. Previous studies have suggested an association between metabolites and cognitive decline. Although the metabolite composition differs between Western and Asian populations, studies targeting Asian populations remain scarce. Methods: This cross-sectional study used data from a cohort survey of community-dwelling older adults aged ≥60 years living in Miyagi, Japan, conducted by Tohoku Medical Megabank Organization between 2013 and 2016. Forty-three metabolite variables quantified using nuclear magnetic resonance spectroscopy were used as explanatory variables. Dependent variable was the presence of cognitive decline (≤23 points), assessed by the Mini-Mental State Examination. Principal component (PC) analysis was performed to reduce the dimensionality of metabolite variables, followed by logistic regression analysis to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for cognitive decline. Results: A total of 2,940 participants were included (men: 49.0%, mean age: 67.6 years). Among them, 1.9% showed cognitive decline. The first 12 PC components (PC1–PC12) accounted for 71.7% of the total variance. Multivariate analysis showed that PC1, which mainly represented essential amino acids, was associated with lower odds of cognitive decline (OR 0.89; 95% CI, 0.80–0.98). PC2, which mainly included ketone bodies, was associated with cognitive decline (OR 1.29; 95% CI, 1.11–1.51). PC3, which included amino acids, was associated with lower odds of cognitive decline (OR 0.81; 95% CI, 0.66–0.99). Conclusion: Amino acids are protectively associated with cognitive decline, whereas ketone metabolites are associated with higher odds of cognitive decline.

Novel coronavirus infection (COVID-19) is a highly contagious respiratory disease caused by the SARS-CoV-2 coronavirus. COVID-19 is known to affect both the respiratory, digestive, excretory, and nervous systems. The incidence of chronic effects of the novel coronavirus infection is now on the rise. This paper is aimed to review the epidemiology, pathogenesis and components of post-COVID asthenia. Material and methods. Sixty-three references published between 2005 and 2023 and indexed in the PubMed, CyberLeninka, Russian Citation Index, Semantic Scholar, and Google Scholar databases were included in this review. Results. The study revealed the most common symptoms of post-COVID asthenia are fatigue, muscle weakness, shortness of breath, sleep disturbances, anxiety or depression, impaired memory and cognitive functions (“foggy brain”), hyposmia, and reduced work performance. One of the specific symptom complexes for post-COVID is asthenovegetative syndrome, the incidence of which according to the meta-analysis ranged from 13.1 to 72.8 %, with a cumulative percentage of 45 ± 0.05 % (95 % confidence interval 0.31–0.54). Conclusions. Nowadays, post-COVID asthenia is becoming extremely severe. It is necessary to review in detail the available data on the epidemiology and components of post-COVID asthenia in order to develop an adequate strategy for post-COVID management.

Abstract Background Quantitative susceptibility mapping (QSM) can study the susceptibility values of brain tissue which allows for noninvasive examination of local brain iron levels in both normal and pathological conditions. Purpose Our study compares brain iron deposition in gray matter (GM) nuclei between cerebral small vessel disease (CSVD) patients and healthy controls (HCs), exploring factors that affect iron deposition and cognitive function. Materials and methods A total of 321 subjects were enrolled in this study. All subjects had cognitive examination including the Stroop color word test (SCWT) and MRI including multiecho gradient echo (mGRE) sequence. The patients with CSVD were divided into mild to moderate group (CSVD-M, total CSVD score ≤ 1) and severe group (CSVD-S, total CSVD score > 1). Morphology-enabled dipole inversion with an automated uniform cerebrospinal fluid zero reference algorithm (MEDI + 0) was used to generate brain QSM maps from mGRE data. Deep gray regional susceptibility values and cognitive function were compared among three groups (CSVD-S, CSVD-M, and HC) using multiple linear regression analysis and mediation effect analysis. Results There were significant differences in the SCWT scores and mean susceptibility values of the globus pallidus (GP), putamen (Put), and caudate nucleus (CN) among the three groups (P

Abstract Cognitive impairment (CI) frequently occurs in patients with systemic lupus erythematosus (SLE) and may result from neuroinflammation processes and neurovascular changes in the brain. The cerebral hemodynamics underlying SLE with CI (SLE-CI) remain unclear. 97 patients with SLE and 51 heathy controls (HCs) matched for age and gender underwent MRI. The CI status of patients was measured using the MoCA, and we classify those with a score of 28 or above as the SLE cognitive normal group (SLE-NC). 3D T1-weighted, ASL and resting-state functional (rs-fMRI) sequences were obtained. Seed-based functional connectivity (FC) was calculated using the cerebral blood flow (CBF) results. Compared with SLE-NC, patients with SLE-CI had higher CBF in the left hippocampus, thalamus, and cerebellum crus II and lower CBF in the left frontal lobe. Secondary analyses revealed that compared with patients with SLE-NC, patients with SLE-CI had increased FC of the left insula gyrus when the left cerebellum crus II was set as the seed region and decreased FC in the homolateral para-hippocampus when the left hippocampus was set as the seed region. These structural, functional, and network changes may serve as potential biomarkers for cognitive impairment in SLE-CI patients.

Abstract Background This study aimed to identify characteristics associated with cognitive impairment in older individuals with obstructive sleep apnoea (OSA) using the Addenbrooke’s Cognitive Examination-Revised (ACE-R) that could aid in stratifying those at higher risk for impairment. Methods We analysed existing cross-sectional datasets that measured the performance of 89 adult patients (aged 50–85 years) with OSA on the ACE-R cognitive test. Receiver operating characteristic curves and logistic regression analysis were utilised to identify associations between impairment status and various factors, including demographic characteristics, self-reported sleepiness, cognitive complaints, and OSA severity. Results According to established thresholds (ACE-R ≤ 88), 36% of participants were cognitively impaired. When adjusted for age and education, the strongest factors associated with impairment status were prior measures of arousal index (cut-off: ≥28events/hr, OR: 5.67, p

Abstract Background With the aging of society, cognitive impairment in elderly people is becoming increasingly common and has caused major public health problems. The screening of cognitive impairment in elderly people and its related influencing factors can aid in the development of relevant intervention and improvement strategies. Methods In this study, stratified random cluster sampling was used to conduct a cross-sectional survey of elderly individuals aged 65 years in Chengdu, Sichuan Province, through an electronic questionnaire from November 2022 to November 2023. Descriptive analysis and logistic regression analysis were used to investigate cognitive impairment and its relevant influencing factors. Results Among the 16,609 elderly people, 7524 (45.3%) were males and 9085 (54.7%) were females, with an average age of 73.6 ± 6.5 years (age range 65–101 years). The average years of education was 5.9 ± 6.2 years, and the proportion of individuals with cognitive impairment was 13.1%. With increasing age, the risk of cognitive impairment increased significantly. The risk factors for cognitive impairment in elderly individuals included advanced age, hypertension, heart disease, diabetes, cerebrovascular disease, depressive symptoms, and anxiety symptoms, while the protective factors included higher education level, married status, and greater life satisfaction. Conclusion Cognitive impairment in elderly individuals in Chengdu is serious. We can intervene in and improve cognitive impairment in elderly people by controlling blood pressure and blood sugar, treating depressive and anxiety symptoms and developing community colleges for elderly people and increasing satisfaction with life.

Abstract Objective Evidence of the overall estimated prevalence of post-intensive care cognitive impairment among critically ill survivors discharged from intensive care units at short-term and long-term follow-ups is lacking. This study aimed to estimate the prevalence of the post-intensive care cognitive impairment at time to 12 months discharged from intensive care units. Methods Electronic databases including PubMed, Cochrane Library, EMBASE, CINAHL Plus, Web of Science, and PsycINFO via ProQuest were searched from inception through July 2024. Studies that reported on cognitive impairment among patients discharged from intensive care units with valid measures were included. Data extraction and risk of bias assessment were performed independently for all included studies according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses reporting guidelines. Newcastle–Ottawa Scale was used to measure risk of bias. Data on cognitive impairment prevalence were pooled using a random-effects model. The primary outcome was pooled estimated proportions of prevalence of the post-intensive care cognitive impairment. Results In total, 58 studies involving 347,940 patients were included. The pooled post-intensive care cognitive impairment prevalence rates at the follow-up timepoints 12 months were 49.8% [95% Prediction Interval (PI), 39.9%–59.7%, n = 19], 45.1% (95% PI, 34.8%–55.5%, n = 23), 47.9% (95% PI, 35.9%–60.0%, n = 16), 28.3% (95% PI, 19.9%–37.6%, n = 19), and 30.4% (95% PI, 18.4%–43.9%, n = 7), respectively. Subgroup analysis showed that significant differences of the prevalence rates between continents and study designs were observed. Conclusions The prevalence rates of post-intensive care cognitive impairment differed at different follow-up timepoints. The rates were highest within the first three months of follow-up, with a pooled prevalence of 49.8% at less than one month, 45.1% at one to three months, and 47.9% at three to six months. No significant differences in prevalence rates between studies that only included coronavirus disease 2019 survivors. These fundings highlight the need for further research to develop targeted interventions to prevent or manage cognitive impairment at short-term and long-term follow-ups.

Abstract Background Although physical activity (PA) has been linked to cognitive health, the nuanced relationships between different dimensions of PA and cognitive impairment remain inconclusive. This study investigated associations between late-life PA levels, midlife-to-late-life activity patterns, and cognitive impairment in Chinese older adults, considering potential moderation by apolipoprotein E (APOE) ε4 genotype. Methods We analyzed baseline data from 6,899 participants (median age 68 years, 55.78% female) in the West China Health and Aging Cohort study, with 6,575 participants having APOE genotyping data. Late-life PA and midlife-to-late-life activity patterns were assessed using the Global Physical Activity Questionnaire and a standardized question, respectively. Cognitive function was evaluated using the Chinese version of Mini-Mental State Examination. Logistic regression models were used to examine associations. Results Compared to low PA level, moderate (odds ratio [OR] = 0.74, 95% confidence interval [CI] = 0.55 ~ 0.99) and high PA levels (OR = 0.60, 95%CI = 0.48 ~ 0.75) were associated with lower risk of cognitive impairment. Engaging in work-, transport-, recreation-related, and moderate-intensity PA were each significantly associated with lower cognitive impairment risk. Maintaining activity levels from midlife to late life was associated with lower cognitive impairment risk compared to decreasing levels (OR = 0.75, 95%CI = 0.60 ~ 0.94). These associations were more pronounced in APOE ε4 non-carriers, with an interaction observed between APOE ε4 genotype and recreation-related PA (P-value = 0.04). Conclusions Our findings underscore the multifaceted benefits of PA in mitigating cognitive impairment risk among older Chinese adults. Public health strategies should focus on promoting overall late-life PA levels, especially moderate-intensity PA, and maintaining activity levels comparable to midlife, with potential for personalized interventions based on genetic risk profiles.

Background: Dementia is a chronic progressive illness with significant impairment in a person’s functioning ability. The currently available treatment options for dementia are limited in modifying disease progression. Non-invasive brain stimulation techniques such as transcranial direct current stimulation (tDCS) are emerging as potential treatment options for cognitive as well as behavioral symptoms in dementia. The objective of this systematic review and meta-analysis is to assess the efficacy of tDCS on cognitive function in mild cognitive impairment (MCI) and dementia due to neurodegenerative disorders to provide an update on the existing evidence considering an increasing number of trials using tDCS. Methods: The study was conducted according to the Preferred Reporting Items for Systematic Review and Meta-Analyses guidelines with a prespecified protocol registered in PROSPERO (CRD42024503852). The study selection was made through a search on databases such as PubMed, Ovid MEDLINE, APA PsycInfo, and Cochrane trials registry and a gray literature search on ClinicalTrials.gov. All randomized controlled trials that have used tDCS as a standalone intervention for cognitive impairment were included in the present study. Risk of bias (RoB) was assessed by the Cochrane RoB2 tool. Meta-analysis of outcomes was performed using RevMan software version 5.4. Pooled estimates of standardized mean difference (SMD) and 95% confidence interval (CI) were obtained for global cognition (primary outcome) and other domain-specific cognitive outcomes. Results: A total of 24 studies were finally included in the review. Most of the studies had “some concerns” with regard to the overall RoB. A total of 164 subjects in the true tDCS group and 151 subjects in the sham tDCS groups out of eight studies were analyzed for global cognitive outcome, giving a pooled SMD (95% CI) of 0.80 (0.35, 1.26), giving an overall effect of Z = 3.45 (P < 0.001), with I2 value of 72%, favoring true tDCS. On a sub-group analysis, a significant improvement was noted in the Alzheimer’s dementia group but not MCI. Discussion: The study findings suggest that tDCS is effective in improving global cognition in participants with Alzheimer’s dementia but not MCI. Owing to a smaller number of studies, the domain-specific cognitive outcomes could not be assessed effectively. There was a wide heterogeneity in the included studies in terms of tDCS stimulation protocols.

Multimorbidity accelerates cognitive decline and leads to an increased risk of cognitive impairment. However, existing studies have mainly explored the cognitive status of patients with a single or specific chronic disease, and the patient with multimorbidity remains to be urgently explored. The present study describes the epidemiological characteristics of cognitive impairment in multimorbidity, summarizes the influencing factors, organizes the association patterns between multimorbidity and cognitive impairment, elucidates the mechanisms underlying their occurrence, and finally proposes preventive and control strategies. The findings of this study are intended to serve as a valuable reference for future efforts in preventing and treating cognitive impairment in multimorbidity.

Aluminium chloride (AlCl3) is a prevalent environmental pollutant found in food and drinking water. Epidemiological studies suggest a strong link between AlCl3 exposure and neurodegenerative disorders, especially Alzheimer’s disease (AD). AlCl3 disrupts normal brain function, potentially leading to oxidative stress, inflammatory responses, and cognitive decline, all of which are implicated in AD pathology. This review compiled and analysed data from 59 studies, accessed through academic databases such as Google Scholar, PubMed, Springer, Science Direct, Wiley, Scopus, and Research Gate. The focus was specifically on the neurotoxic effects of AlCl₃, drawing insights into its impact on brain structure, function, and behaviour. Findings from the reviewed studies reveal that AlCl3 exposure leads to increased aluminium accumulation in brain tissues, resulting in structural damage and neurotoxic effects. This accumulation affects cognitive functions and behaviour, with histological analyses showing signs of neurodegeneration. Behavioural changes and impaired cognitive abilities observed in animal and cellular models suggest that AlCl3 disrupts neural pathways critical to learning and memory. The evidence indicates a significant association between AlCl3 exposure and neurodegenerative damage, especially in the context of AD. This review emphasizes the need for further research into AlCl3's neurotoxic mechanisms to clarify its role in AD and other neurodegenerative diseases. Enhanced understanding may help develop preventive measures and regulations to mitigate the health risks posed by aluminium exposure in daily life.

Abstract Background Patients with steatotic liver disease may show mild cognitive impairment. Rats with mild liver damage reproduce this cognitive impairment, which is mediated by neuroinflammation that alters glutamate neurotransmission in the hippocampus. Treatment with extracellular vesicles (EV) from mesenchymal stem cells (MSC) reduces neuroinflammation and improves cognitive impairment in different animal models of neurological diseases. TGFβ in these EVs seems to be involved in its beneficial effects. The aim of this work was to assess if MSCs-EVs may improve cognitive impairment in rats with mild liver damage and to analyze the underlying mechanisms, assessing the effects on hippocampal neuroinflammation and neurotransmission. We also aimed to analyze the role of TGFβ in the in vivo effects of MSCs-EVs. Methods Male Wistar rats with CCl4-induced mild liver damage were treated with EVs from unmodified MSC or with EVs derived from TGFβ—silenced MSCs and its effects on cognitive function and on neuroinflammation and altered neurotransmission in the hippocampus were analysed. Results Unmodified MSC-EVs reversed microglia activation and TNFα content, restoring membrane expression of NR2 subunit of NMDA receptor and improved object location memory. In contrast, EVs derived from TGFβ—silenced MSCs did not induce these effects but reversed astrocyte activation, IL-1β content and altered GluA2 AMPA receptor subunit membrane expression leading to improvement of learning and working memory in the radial maze. Conclusions EVs from MSCs with TGFβ silenced induce different effects on behavior, neuroinflammation and neurotransmitter receptors alterations than unmodified MSC-EVs, indicating that the modification of TGFβ in the MSC-EVs has a notable effect on the consequences of the treatment. This work shows that treatment with MSC-EVs improves learning and memory in a model of mild liver damage and MHE in rats, suggesting that MSC-EVs may be a good therapeutic option to reverse cognitive impairment in patients with steatotic liver disease.

Abstract The maintenance of cognitive function is essential for quality of life and health outcomes in later years. Cognitive impairment, however, remains an undervalued long-term complication of type 2 diabetes by patients and providers alike. The burden of sustained hyperglycemia includes not only cognitive deficits but also the onset and progression of dementia-related conditions, including Alzheimer’s disease (AD). Recent research has shown that the brain maintains an independent glucose “microsystem”—evolved to ensure the availability of fuel for brain neurons without interruption by transient hypoglycemia. When this milieu is perturbed, brain hyperglycemia, brain glucotoxicity, and brain insulin resistance can ensue and interfere with insulin signaling, a key pathway to cognitive function and neuronal integrity. This newly understood brain homeostatic system operates semi-autonomously from the systemic glucoregulatory apparatus. Large-scale clinical studies have shown that systemic dysglycemia is also strongly associated with poorer cognitive outcomes, which can be mitigated through appropriate clinical management of plasma glucose levels. Moreover, these studies demonstrated that glucose-lowering agents are not equally effective at preventing cognitive dysfunction. Glucagon-like peptide-1 (GLP-1) receptor analogs and sodium glucose cotransporter 2 inhibitors (SGLT2is) appear to afford the greatest protection; metformin and dipeptidyl peptidase 4 inhibitors (DPP-4is) also significantly improved cognitive outcomes. Sulfonylureas (SUs) and exogenous insulin, on the other hand, do not provide the same protection and may actually worsen cognitive outcomes. In the creation of a treatment plan, comorbid cognitive conditions should be considered. These efficacious treatments create a new gold standard of managing hyperglycemia—one which is consistent with the “complication-centric prescribing” mandates issued in type 2 diabetes treatment guidelines. The increasing longevity enjoyed by our populace places the onus on clinical care to play the “long game” in using targeted treatments for glucose control in patients with, or at risk for, cognitive decline to maintain cognitive wellness later in life. This article reviews critical emerging data for scientists and trialists and translates new enhancements in patient care for practitioners.

Abstract The association between migraine and cognitive function has been studied during the last decade, however, this relationship is not well established. As migraine prevalence is highest between the ages of 30–40, aligning with some of our most productive years, we must understand cognitive changes within this disorder. Cognitive impairment potentially limits social and professional interactions, thus negatively impacting quality of life. Therefore, we will review the relationship between prevalent migraine and cognition. Cognitive dysfunction has been reported to be the second largest cause of disability, after pain, in migraine patients. While subjective patient reports on cognition consistently describe impairment, findings for objective neuropsychological assessments vary. Many studies report worse cognitive performance in the ictal phase compared to controls, which can persist into the postictal period, although whether this continues in the interictal period has been understudied. There is limited consensus as to whether cognition differs in migraine with aura versus migraine without aura, and while many studies do support cognitive impairment in chronic migraine, it remains uncertain as to whether this is more debilitating than the cognitive difficulties experienced by those with episodic migraine. To date, objective assessment of neurological abnormalities that may underlie cognitive impairment through neuroimaging has been underutilized. There is limited consensus as to whether cognitive impairment is a characteristic specific to migraine, whether it is driven by a combination of factors including co-morbidities such as anxiety, depression, or vascular dysfunction, treatment, or whether it is a more general characteristic of pain disorders. Overall, increasing numbers of studies support cognitive impairment in migraine patients. Future studies should consider longitudinal study designs to assess cognition across different migraine phases and subtypes of the disorder, including migraine with aura and chronic migraine, as well as controlling for important confounders such as treatment use.

Abstract Background An increase in choroid plexus (CP) volume may be associated with cognitive decline in older individuals without dementia. In this study, we aimed to clarify whether CP volume can serve as an imaging marker of cognitive decline, determine how strongly CP volume is associated with cognitive decline, and explore factors associated with CP volume in older adults. Methods We measured CP volume, brain parenchyma, and cerebrospinal fluid (CSF) spaces associated with disproportionately enlarged subarachnoid space hydrocephalus (DESH), an imaging feature of normal-pressure hydrocephalus, in community-dwelling older adults aged ≥ 65 years without dementia. Results In 1,370 participants, lower Mini-Mental State Examination (MMSE) scores were significantly associated with higher CP volume, even after adjusting for DESH-related CSF space and brain parenchymal volume. CP volume was more strongly associated with MMSE scores than DESH-related CSF space and brain parenchymal volume. History of smoking, white matter hyperintensity, enlarged perivascular spaces, age, body mass index, and diabetes mellitus were also associated with increased CP volume. Conclusions CP volume may be a highly sensitive imaging marker of cognitive decline in community-dwelling older adults without dementia, as it is linked to cognitive decline independently of brain parenchyma and CSF volumes. Our findings emphasize the importance of investigating CP volume increase to maintain cognitive function in older individuals. Accordingly, further longitudinal studies are required.

Abstract Background An enriched understanding is necessary concerning the association between hypertension and cognitive impairment in older adults, particularly regarding the potential underlying mechanisms at a biological level. This study aimed to explore the mediating role of methylmalonic acid (MMA) in the hypertension-cognition link in the older population. Methods A total of 2762 adults (age > = 60 years) from the National Health and Nutrition Examination Survey (NHANES) 2011–2014 participated. Cognitive function was assessed using a combination of the Animal Fluency Test (AFT), the Digit Symbol Substitution Test (DSST), and the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) Word List Learning Test. Self-reported hypertension diagnosis, antihypertensive medications use, and blood pressure examinations were used to identify hypertension. Serum MMA (sMMA) levels were collected. Weighted multiple linear regressions and mediation analysis were applied. A subgroup analysis by sex and age was performed. Results After adjusting for potential confounding factors, we observed a significant mediating effect of the sMMA level in the hypertension-cognition link, accounting for 11.14% (95% CI 4.09%-14.00%, p = 68) to address MMA-related cognitive decline.

Abstract Background The number of people reaching old age is rising, bringing an increase in age-related diseases like cardiovascular conditions and cognitive dysfunction. Cognitive impairment (CI) impacts various brain functions, affecting daily activities and quality of life. Metabolic syndrome (MetS), a cluster of cardiovascular risk factors, has been implicated in CI. This study examines the prevalence of MetS and CI among older adults in Calabar Metropolis and the associated risk factors. Methods This study was conducted in Calabar Metropolis, Cross River State, Nigeria, with 236 older adults (aged 65 years and above) selected via a multi-stage sampling technique. Informed consent was obtained from all participants. Physical examinations and biomarker assessments included measurements of blood pressure, height, weight, waist and hip circumference, fasting plasma glucose, cholesterol, triglycerides, and high-density lipoprotein (HDL) levels. MetS was defined according to the NCEP Adult Treatment Panel III criteria. CI was assessed using the Mini-Cog™ test, with scores ≤ 3 indicating poor cognitive status. Data analysis utilized SPSS version 26.0, employing chi-square tests and binary logistic regression. Significance was set at p

Abstract Introduction Dementia, an increasingly critical public health concern in low and middle-income countries, is associated with lower socioeconomic status, early cognitive impairment, and elevated dementia-related mortality risk. This study seeks to estimate the prevalence of cognitive impairment, investigate its links with social indicators, and visualize social gradients across different regions in Colombia. Methods Secondary data analysis from the SABE 2015 survey, multinomial regression analyses, and equiplot graphs. Results A sample of 23,694 individuals 60 years or older from Colombia. Higher risks were observed among individuals with dark skin color (OR 1.27; 95%CI: 1.10 – 1.47), lower educational levels (OR 3.01; 95%CI:2.04 – 4.42) and reading illiteracy (OR 2.14; 95%CI: 1.87 – 2.46). Inequity patterns were identified by region of residence and income. Discussion This study underscores the need for targeted interventions aimed at reducing health inequities. The results highlight the higher prevalence rates of cognitive impairment among socially disadvantaged individuals.

Long COVID, or post-acute sequelae of SARS-CoV-2 infection, includes a variety of enduring symptoms that endure beyond the acute phase of the illness, impacting multiple facets of patients’ psychological and physical health. The persistent symptoms encompass fatigue, breathing difficulties, musculoskeletal pain, and cognitive impairments, which can significantly affect daily functioning and overall quality of life. The objective of this study was to create and validate the accuracy of the Post-COVID Cognitive Impairment Scale, which is used to evaluate cognitive impairments resulting from a COVID-19 infection. This study was conducted in Iran between January and September 2023. It consisted of three phases: developing the scale, evaluating its content validity with experts, and validating its structure with 454 participants using exploratory and confirmatory factor analysis. The exploratory factor analysis revealed two variables, namely memory and attention, which accounted for 40.38% of the variation. Confirmatory factor analysis verified the model’s fit, with indices indicating satisfactory alignment: CMIN/DF = 2.80, RMSEA = 0.06, SRMR = 0.05, CFI = 0.93, and TLI = 0.92. The factor loadings were statistically significant (p < 0.001), and Cronbach’s Alpha values indicated strong internal consistency (working memory = 0.81, attention = 0.80). These results affirm the Post-COVID Cognitive Impairment Scale is a valid and reliable instrument for evaluating cognitive deficiencies in individuals with long COVID. Its application in clinical and research environments aids in the prompt detection and tracking of the treatment of such impairments.

Abstract Background Exercise is a promising nonpharmacological intervention to delay the progression of cognitive impairment and improve physical function and sleep quality in patients, but the evidence remains inconclusive. Aims To compare the therapeutic efficacy of an exercise intervention on physical performance, sleep efficiency, and quality of life in older adults with cognitive impairment. Design A three-arm randomized controlled trial. Methods This study recruited 81 older adults with mild to moderate cognitive impairment at a nursing home from December 2020 to July 2021. Participants were screened and randomized into three groups: a tai chi intervention group (n = 27), a conventional exercise intervention group (n = 27), and a waitlist control group with no intervention (n = 27). The intervention groups underwent 12 weeks of exercise intervention. Participants were assessed at weeks 0, 6, and 12. The primary outcome was the Short Physical Performance Battery score, and the secondary outcomes were sleep efficiency and quality of life. Statistical analysis was conducted with generalized estimating equations (GEEs). Results The mean age of the participants was 81.0 ± 7.4 years. The GEE analysis revealed that the Short Physical Performance Battery score, sleep efficiency, and quality of life were significantly higher in both intervention groups than in the control group at week 12, and physical performance improved significantly more in the tai chi group than in the conventional exercise group. Conclusions Both exercise interventions improved physical performance, sleep efficiency, and quality of life in older adults with mild to moderate cognitive impairment. According to our results, tai chi may be a more effective therapeutic approach for cognitive impairment than conventional exercise. Trial registration University Hospital Medical Information Network number UMIN000042051. Registered 01/12/2020.

Abstract Background Dementia poses a significant burden on healthcare systems. Early identification of individuals at risk for cognitive decline is crucial. The retina, an extension of the central nervous system, reflects neurodegenerative changes. Optical coherence tomography (OCT) is a non-invasive tool for assessing retinal health and has shown promise in predicting cognitive decline. However, prior studies produced mixed results. Methods This study investigated a large cohort (n = 490) of Asian individuals attending memory clinics. Participants underwent comprehensive neuropsychological testing annually for five years. Retinal thickness was measured by OCT at baseline. We assessed the association between baseline retinal thickness and subsequent cognitive decline. Results Participants with a significantly thinner macular ganglion cell-inner plexiform layer (GCIPL) at baseline (≤ 79 μm) had a 38% greater risk of cognitive decline compared to those who did not (≥ 88 μm; p = 0.037). In a multivariable model accounting for age, education, cerebrovascular disease status, hypertension, hyperlipidemia, diabetes and smoking, thinner GCIPL was associated with an increased risk of cognitive decline (hazard ratio = 1.14, 95% CI = 1.01–1.30, p = 0.035). Retinal nerve fiber layer (RNFL) thickness was not associated with cognitive decline. Conclusions This study suggests that OCT-derived macular GCIPL thickness may be a valuable biomarker for identifying individuals at risk of cognitive decline. Our findings highlight GCIPL as a potentially more sensitive marker compared to RNFL thickness for detecting early neurodegenerative changes. Trial registration number and name of the trial registry National Healthcare Group Domain-Specific Review Board (NHG DSRB) reference numbers DSRB Ref: 2018/01368. Name of the trial: Harmonisation project.

Abstract Background Age-related decline in physical and cognitive capacity increases older adults’ risk of disability, long-term care placement, and mortality rate. Functional training, which uses activities of daily living or simulated movements to complete activities as the intervention medium, could be more effective than rote exercise, which uses repetitive movements without added purpose, in preventing late-life disability in older people. With a growing number of studies in this area, systematically studying the effect of functional training is needed. The purpose of this systematic review was to examine the effects of functional training on the outcomes of activities of daily living, physical functioning, and cognitive function in community-dwelling older adults. Methods Literature published between January 2010 and April 2024 in 10 electronic databases were searched and screened. This timeframe was established to include studies published within the last 15 years. Each identified article was screened and reviewed by two authors independently. The methodological quality of the included studies was evaluated using the PEDro Scale. Key findings were synthesized according to participants’ characteristics and intervention types. Results The review included 32 studies. In the general community-dwelling older adult population (20 studies), studies that applied functional training as a single-component approach showed a positive effect on activities of daily living. However, the training effect on balance and mobility was not superior to that of other exercise programs. Moreover, the effect was mixed when functional training was combined with other intervention components. In older adults with mild cognitive impairment (5 studies), Simulated Functional Tasks Exercise, a single-component training, consistently demonstrated positive effects on the activities of daily living and cognitive functions. In older adults with dementia (4 studies) or frailty (3 studies), the effect was mixed across the single- and multi-component approaches. Conclusion Functional training alone is effective in preventing late-life disability in general community-dwelling older adults. When training activities challenge both motor and cognitive abilities, the effect seems to improve the performance of activities of daily living and cognitive functions in older adults with mild cognitive impairment. Additional studies of functional training in older adults with cognitive impairment or frailty are recommended.

Abstract Disruptions in cognitive function have been reported in individuals undergoing haemodialysis and those with chronic kidney disease. This pilot study protocol primarily assesses the feasibility and acceptability of using mobile cognitive gaming apps for patient-led cognitive training during haemodialysis sessions. The protocol consists of three phases: (1) reviewing and evaluating available cognitive gaming apps, (2) conducting focus groups/interviews with people with kidney disease to determine app preferences, and (3) undertaking a quasi-experimental randomised controlled trial to compare cognitive outcomes between a patient-led app intervention group and a standard care control group over four months. Primary outcomes will include changes in cognitive test scores [Montreal Cognitive Assessment (MoCA), Modified Mini-Mental State Exam (3MSE), Rapid Objective Working Memory Assessment (ROWMA)], while secondary outcomes will encompass quality of life measures [Patient-Reported Outcomes Measurement (PROM) Kidney Disease Quality of Life Short Form (KDQoL-SF™) v 1.3, Patient-Reported Outcomes Measurement Information System (PROMIS) Global Health Instrument, European Quality of Life Five Dimension (EQ-5D)]. If demonstrated to be effective, this novel method of utilising gamified cognitive training applications could potentially mitigate cognitive decline and improve the well-being of people receiving haemodialysis without necessitating significant clinical resources. The findings from this research will guide the development of a larger definitive randomised trial in the future.

Jiang Wang,1,2,&ast; Aizhang Zhu,1,2,&ast; Jie Chen,3,&ast; Rui Zeng,4,&ast; Siyi Wang,1,2 Lihuan Chen,5 Ying Chen,1,2 Qianqian Min,1,2 Wei Li,4,6 Dongmei Ye,4 Ruohan Wu,1,2 Fayi Xie,4 Tenghui Fan,4 Ke Zhu,4 Wan Zhu,4 Hongmei Hu,1 Conghua Wang,3 Xiaoming Zhang3 1School of Basic Medicine, Jinggangshan University, Ji’an, Jiangxi, People’s Republic of China; 2Online Collaborative Research Center for Evidence-Based Medicine Ministry of Education, Jinggangshan University Branch, Ji’an, Jiangxi, People’s Republic of China; 3Department of Emergency, The People’s Hospital of Baoan Shenzhen, Shenzhen, Guangdong, People’s Republic of China; 4School of Clinical Medicine, Jinggangshan University, Ji’an, Jiangxi, People’s Republic of China; 5School of Chinese Medicine, Jinggangshan University, Ji’an, Jiangxi, People’s Republic of China; 6Clinical Medical Research Center, Affiliated Hospital of Jinggangshan University, Jiangxi Province Key Laboratory of Organ Development and Epigenetics, Clinical College of Jinggangshan University, Ji’an, Jiangxi, 343009, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Hongmei Hu; Xiaoming Zhang, Email huhongmei1218@126.com; zhangmuxi0310@163.comBackground: The interplay between cognitive frailty and depression remains inadequately understood, with a paucity of evidence from prospective cohort studies. Our study aims to elucidate the relationship between cognitive frailty and the risk of incident depression.Methods: Utilizing data from the China Health and Retirement Longitudinal Study (CHARLS) spanning 2011, 2013, and 2015, subjects were classified according to cognitive frailty criteria established by an international consensus panel. Multiple logistic regression models were employed to examine the cross-sectional and longitudinal associations between frailty, cognitive impairment, cognitive frailty, and depression. Subgroup analyses and interaction tests were conducted to identify potential effect modifiers.Results: In 2011, the study encompassed 4514 participants, with 2330 individuals followed up through 2015. Cross-sectional analyses revealed that participants classified in frailty, cognitive impairment, and cognitive frailty exhibited multivariable-adjusted odds ratios (ORs) for depression of 1.87 (95% CI 1.60– 2.18; P < 0.001), 1.97 (95% CI 1.58– 2.47; P < 0.001), and 3.38 (95% CI 2.66– 4.29; P < 0.001), respectively, compared to no diseased group. Longitudinal analyses from 2011 to 2015 indicated that participants in frailty, cognitive impairment, and cognitive frailty had multivariable-adjusted ORs of 1.28 (95% CI 1.05– 1.58; P = 0.0165), 1.39 (95% CI 1.01– 1.91; P = 0.0411), and 1.57 (95% CI 1.05– 2.35; P = 0.0273), respectively, for new-onset depression relative to no diseased group.Limitations: The definition of depression relied solely on self-reported data.Conclusion: In the middle-aged and elderly Chinese population, patients with cognitive frailty have a higher risk of depression than those with only frailty and cognitive impairment. This may suggest that health care providers should pay more attention to the mental health of those patients with cognitive frailty.Keywords: cognitive frailty, cognitive impairment, physical frailty, depression, CHARLS

Introduction: Skin lesions observed concomitantly with increasing functional dependency and/or cognitive impairment can lead to significant additional challenges. In this study, we aimed to assess the relationship between functional dependency, cognitive status, and skin lesions in elderly individualsMethods: Individuals presenting to the geriatric outpatient clinic of a tertiary reference center were included in a cross-sectional study. The level of dependency was determined using the Katz Index of Independence in Activities of Daily Living (ADL) and the Lawton-Brody Instrumental Activities of Daily Living (IADL) scale, classifying individuals as "totally dependent," "partially dependent," or "independent." Cognitive status was assessed using the Standardized Mini-Mental State Examination (MMSE), with scores of 24 and above considered "normal."Results: Of the 228 individuals included in the study, 63.60% were male, with a mean age of 76.20 (±7.10) years. The three most commonly observed skin findings in the study group were scar (43.90%), xerosis (40.40%), and dermatophytosis (36.40%). It was revealed that the occurrence of xerosis, infection-related lesions, eczema, diabetic foot ulcers, decubitus ulcers, and pruritus was statistically significantly lower in individuals with "totally independent" ADL, "totally independent" IADL, and/or "normal" cognitive function assessed by MMSE.Conclusion: There is a significant relationship between functional and cognitive status and the occurrence of skin lesions in elderly individuals. Certain skin lesions such as xerosis, infection-related lesions, eczema, diabetic foot ulcers, decubitus ulcers, and pruritus may be particularly common in elderly individuals who are functionally dependent and/or have impaired cognitive functions and should be taken into consideration in clinical practice.

Abstract Fibrinogen (FBG) has been discovered to be associated with cognitive impairment (CI) and dementia. However, the exact correlation between FBG levels and CI after acute ischemic stroke (AIS) remains uncertain. Plasma FBG levels were measured in 398 patients with AIS who underwent comprehensive neuropsychological evaluation. To assess the correlation of FBG with global cognitive function, physical status, anxiety, depression, and psychiatric symptoms. Multifactorial logistic regression was used to analyze risk factors for CI. Constructed and plotted a nomogram graph to visualize the CI prediction model. The model was further evaluated for discrimination, calibration, and clinical utility. The results indicate that plasma FBG levels are significantly elevated in patients with CI compared to those with non-cognitive impairment (NCI). Analysis of the overall population reveals that elevated FBG levels are correlated with both reduced cognitive function and decreased activity status. After adjusting for other influencing factors, high FBG levels were identified as a risk factor for the incidence of CI. We developed an intuitive and valid predictive model for CI, demonstrating its suitability for clinical application. In conclusion, our study demonstrates that plasma FBG serves as a potential biomarker of CI following AIS, offering a novel perspective for the identification of CI.

Abstract Multiple Sclerosis (MS), a neuroinflammatory disease of the central nervous system, is one of the commonest causes of non-traumatic disability among young adults. Impaired cognition arises as an impactful symptom affecting more than 50% of the patients and with substantial impact on social, economic, and individual wellbeing. Despite the lack of therapeutic strategies, many efforts have been made to understand the mechanisms behind cognitive impairment in MS patients. Here, we aimed to investigate whether microglia-derived synaptic elimination and immune interactions are exacerbated in MS patients with impaired cognition when compared to non-demented controls (NDC) and cognitively preserved MS patients, that may clarify the role of immune cell interplay in MS cognitive deficits. Postmortem hippocampal samples were obtained from NDCs and MS patients. Sixteen MS patients were categorized based on their cognitive status: preserved cognition (MSCP) and impaired cognition (MSCI). Immunohistochemistry studies were conducted to explore the density of microglia, their role in synaptic engulfment, and their interaction with CD8+ immune cells in the context of cognitive impairment in MS. In high synaptic density hippocampal regions, MSCI patients exhibited a massive presence of microglia cells actively engulfing both excitatory and inhibitory synapses, accompanied by morphological alterations. Additionally, there was an increased expression of the complement protein C1q particularly localized at inhibitory synapses within microglia cells, suggesting a preferential engulfment of complement-tagged inhibitory synapses in MSCI patients. Furthermore, in hippocampal lesions of MSCI patients, we detected a significant infiltration of microglia and CD8 T cells that may be contributing to the smouldering MS and cognitive deterioration. These findings demonstrate that cognitive deficits occurring in MS are associated with microglia engulfment of C1q-tagged inhibitory synapses, which may be driven by direct or indirect stimulation from CD8+ T cells.

Artificial intelligence (AI) has revolutionized ophthalmology by aiding in the diagnosis, prognosis, and treatment planning of various eye diseases. However, AI’s potential extends beyond ocular conditions. By analyzing eye-related biomarkers, AI can utilize the eye as a window into the body’s systemic health. This field, known as oculomics, leverages AI and deep learning algorithms to process vast amounts of data from imaging techniques such as fundus photography, optical coherence tomography (OCT), OCT angiography, infrared iris imaging, slit-lamp photography, and external eye photography. AI-powered analysis of these images can predict systemic diseases such as Alzheimer’s, Parkinson’s, cardiovascular disease, cerebrovascular disease, chronic kidney disease, and liver disease. Retinal changes —including alterations in the retinal nerve fiber layer, ganglion cell layer, and retinal vessels —serve as valuable indicators of these conditions. Additionally, AI can estimate age, sex, body composition, and other health parameters from eye images. While the potential of AI in oculomics is promising, challenges such as access to ophthalmic imaging, data quality, and the need for rigorous validation must be addressed to ensure its widespread adoption and clinical utility. Nevertheless, AI holds the potential to transform healthcare by enabling early detection, noninvasive screening, and personalized treatment for a wide range of systemic diseases.

Abstract Background There is limited population-based evidence on the prevalence of cognitive impairment in Mexico, a country with a rapidly aging population and where key risk factors, such as diabetes and obesity, are common. This study describes the distribution of cognitive impairment in adults from Mexico City. Methods This cross-sectional population-based study included participants from the Mexico City Prospective Study which recruited 150,000 adults aged ≥ 35 years in 1998–2004. In 2015–2019 about 10,000 survivors were resurveyed with identical information from the original survey and additional assessments including a cognitive assessment. The main analyses included those aged 50–89 years with complete cognitive assessment and covariate data at resurvey. Cognitive impairment was defined by a score ≤ 24 on the Mini Mental State Examination (MMSE). The distribution of MMSE scores and cognitive impairment by age, sex, and major disease risk factors (diabetes, hypertension, and adiposity) was analyzed among those with complete MMSE data and some degree of self-reported formal education. Results Of the 9,288 participants aged 50–89 years at the 2015–2019 resurvey with complete data, 8,197 reported having at least some years of formal education. Among these (mean age 66 years; 31% men), their mean MMSE score was 26.2 (SD 3.6) points, 1,941 (24%) had cognitive impairment, their mean body-mass index (BMI) was 28.6 (SD 5.5) kg/m2, 3,008 (37%) had hypertension and 2,467 (30%) had diabetes. The sex- and district-standardised prevalence of cognitive impairment increased strongly with age, from 10% in those 50–59 years to 55% in those aged 80–89. At any given age, the prevalence of cognitive impairment was higher in women than in men. After accounting for the effects of age, sex, and district there was little difference in the prevalence of cognitive impairment between participants with or without diabetes, hypertension, overweight or obesity (BMI ≥ 25 km/m2), or high levels of fat mass. Conclusions In this population of adults aged 50–89 years from Mexico City, the prevalence of cognitive impairment was high, particularly among women. The extent to which cognitive impairment relates to health outcomes in this population needs to be investigated.

Xiangbo Yan,1,2 Wanqing Liu,3 Danyang Li,1 Qiang Huang,1 Jianlin Wu,1 Qing Zhang1 1Imaging Department, Affiliated Zhongshan Hospital Dalian University, Dalian, People’s Republic of China; 2Faculty of Medicine, Dalian University of Technology, Dalian, People’s Republic of China; 3Department of Radiology, West China Second University Hospital, Sichuan University, Chengdu, People’s Republic of ChinaCorrespondence: Qing Zhang, Imaging Department, Affiliated Zhongshan Hospital, Dalian University, Dalian, 116001, People’s Republic of China, Tel +86 15566978288, Email zhangqingsmile@163.comPurpose: Previous studies have found that obstructive sleep apnea (OSA) can induce cognitive impairment (CI). However, the exact mechanisms of CI development in patients with OSA remains unclear. We investigated the neuropathological basis of CI development by examining changes in cerebral blood perfusion.Patients and Methods: Thirty-five patients with untreated OSA (15 with CI and 20 without CI [NCI]) and 15 good sleepers (GS) diagnosed using polysomnography were recruited. All participants underwent resting state brain scans in a Siemens 3.0 Tesla magnetic resonance imaging scanner with a pulsed arterial spin labeling sequence and completed a battery of neuropsychological tests.Results: Compared to the regional cerebral blood flow (rCBF) values in the GS group, both the CI and NCI groups exhibited lower rCBF values in the bilateral inferior temporal, left lingual, and right medial and paracingulate gyri, as well as higher rCBF values in the bilateral middle frontal gyrus (p < 0.05 in all cases). Compared to the rCBF values in the NCI group, the CI group had lower rCBF values in the bilateral inferior temporal and left lingual gyri, and higher rCBF values in the right rectus and right middle orbital frontal gyri (p < 0.05 in all cases). In the CI group, rCBF values in the bilateral inferior temporal (right, p = 0.025; left, p = 0.005) and left lingual gyri (p = 0.018) were positively associated with the delayed memory scores, and rCBF values in the left inferior temporal gyrus positively correlated with the attention scores (p = 0.011).Conclusion: Regions with abnormal perfusion in the NCI and CI groups were mostly memory-related. Blood perfusion in the bilateral inferior temporal and left lingual gyri decreased in the following order: GS > OSA-NCI > OSA-CI. These findings provide blood perfusion-level insights into the neuropathological basis of OSA-CI development.Keywords: Obstructive sleep apnea, cognitive impairment, cerebral blood flow, memory function, arterial spin labeling

Kai Zhang,1 Dandi Ma,1 Yunxiao Wu,2 Zhifei Xu1 1Clinical Department of National Clinical Research Center for Respiratory Diseases, Beijing Children’s Hospital, Capital Medical University, National Center for Children’s Health, Beijing, 100045, People’s Republic of China; 2Department of Otolaryngology, Head and Neck Surgery, Beijing Children’s Hospital, Capital Medical University, National Center for Children’s Health, Beijing, 100045, People’s Republic of ChinaCorrespondence: Zhifei Xu, Clinical Department of National Clinical Research Center for Respiratory Diseases, Beijing Children’s Hospital, Beijing, 100045, People’s Republic of China, Email zhifeixu@aliyun.comPurpose: Chronic intermittent hypoxia (CIH) is considered one of the main pathophysiological mechanisms of obstructive sleep apnea (OSA). CIH can further lead to cognitive dysfunction by inducing processes such as neuroinflammation and oxidative stress. The hippocampus is primarily associated with cognitive functions such as learning and memory. This study aimed to explore the effects of CIH on cognitive function and hippocampal neurons in mice and to reveal its potential molecular mechanisms.Methods: SPF-grade C57BL/6J mice (n=36) were selected as subjects and divided into control, mild CIH, and severe CIH groups (12 mice per group). Cognitive function was assessed using the Morris water maze test, and hippocampal neuron numbers and morphological changes were observed using HE staining and Nissl staining. Additionally, differential genes and pathways were revealed through RNA sequencing (RNA-seq) and bioinformatics analysis. We examined oxidative stress-related biochemical markers in the hippocampal tissue and used Western Blot to verify changes in the expression of potential key genes. Statistical analyses were performed using ANOVA and post hoc tests to ensure robust comparisons between groups.Results: CIH mice exhibited significant cognitive impairment, including decreased learning and memory abilities. The severe CIH group had a longer escape latency compared to the mild CIH group (p < 0.001) and the control group (p < 0.01), while the mild CIH group took longer than the control group (p < 0.01). In the probe test, the severe CIH group showed a significant decrease in platform crossings (p < 0.01) and target quadrant dwell time (p < 0.05), while the mild CIH group exhibited a reduction in target quadrant dwell time (p < 0.05). Abnormal hippocampal neuron morphology was observed, with a significant reduction in hippocampal neurons (p < 0.05). RNA-seq analysis revealed numerous differentially expressed genes, mainly enriched in biological processes such as inflammation and oxidative stress, as well as multiple signaling pathways. Specifically, downregulated LepR, SIRT1, and Nrf2 genes were found to exacerbate oxidative stress and neuroinflammation, impairing neuronal integrity and cognitive function. Further validation showed increased oxidative stress levels in hippocampal tissue and downregulation of key gene expression. Western blot analysis confirmed significantly reduced expression of LepR (p < 0.01), SIRT1 (p < 0.001), and Nrf2 (p < 0.001) in the severe CIH group.Conclusion: While oxidative stress and inflammation are well-established mechanisms in CIH-induced cognitive impairment, our study provides novel insights by identifying the specific roles of LepR, SIRT1, and Nrf2 in this process. The downregulation of these key genes suggests potential new targets for therapeutic intervention. Importantly, the differential expression patterns observed in varying degrees of hypoxia severity highlight the potential for tailored therapeutic strategies that modulate these pathways in response to the intensity of hypoxic exposure. These findings offer unique opportunities for developing targeted therapies aimed at mitigating CIH-related cognitive decline and neural damage. However, a key limitation of this study is the exclusive use of animal models, which may not fully replicate human pathophysiology. Further studies are needed to validate these findings in clinical settings and to explore the regulatory relationships between the key genes involved.Keywords: obstructive sleep apnea, chronic intermittent hypoxia, cognitive impairment, hippocampal neurons, RNA sequencing, oxidative stress, inflammation

Zhifeng Chen,1– 4 Yulin Shang,5 Yanru Ou,1– 4 Li Zhou,1– 4 Ting Liu,1– 4 Subo Gong,6 Xudong Xiang,7 Yating Peng,1– 4 Ruoyun Ouyang1– 4 1Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People’s Republic of China; 2Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, People’s Republic of China; 3Clinical Medical Research Center for Pulmonary and Critical Care Medicine in Hunan Province, Changsha, Hunan, 410011, People’s Republic of China; 4Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan, 410011, People’s Republic of China; 5Ophthalmology and Otorhinolaryngology, Zigui Country Hospital of Traditional Chinese Medicine, Yichang, Hubei, 443600, People’s Republic of China; 6Department of Geriatrics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People’s Republic of China; 7Department of Emergency, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People’s Republic of ChinaCorrespondence: Yating Peng; Ruoyun Ouyang, Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University 139 Middle Renmin Road, Changsha, Hunan, 410011, People’s Republic of China, Email pengyating2011@csu.edu.cn; ouyangruoyun@csu.edu.cnBackground: OSA can cause cognitive impairment (CI). The aim of this study was to investigate whether miR-20a-5p in exosomes derived from bEnd3 cells with IH mediates intercellular crosstalk and induces CI through hippocampal neuronal cell pyroptosis.Materials and Methods: BEnd3-derived exosomes were isolated from the normal oxygen control group (NC-EXOS) and IH group (IH-EXOS). In vitro, exosomes were cocultured with HT22 cells. Meanwhile, in vivo, exosomes were injected into mice via the caudal vein. The spatial memory ability of mice was tested by MWM method to evaluate the effect of exosomes on the cognitive function of mice. Adults diagnosed with OSA underwent the MoCA and ESS tests to assess cognitive function and daytime sleepiness. Spearman’s rank correlation analysis was used to evaluate the correlation between miR-20a-5p and candidate proteins and clinical parameters. Transfection using small interfering RNAs, miRNA mimics, and plasmids to evaluate the role of miR-20a-5p and its target genes. Dual luciferase reporter gene assay was used to confirm the binding of miR-20a-5p to its target gene.Results: IH could cause pyroptosis and inflammation in bEnd3 cells, and promote the expression of miR-20a-5p. Isolated IH-EXOS induced increased pyroptosis and activation of inflammatory response in vitro and in vivo, accompanied by increased expression of miR-20a-5p. In addition, IH-EXOS led to decreased learning and memory ability in mice. Interestingly, AHI was higher and MoCA scores were lower in severe OSA compared to healthy comparisons. In addition, miR-20a-5p and GSDMD were positively correlated with AHI but negatively correlated with MoCA in severe OSA. IH-induced exosomes were rich in miR-20a-5p, and these exosomes were found to deliver miR-20a-5p to HT22 cells, playing a key role in the induction of OSA-CI by directly targeting MFN2.Conclusion: Exosome miR-20a-5p from IH-stimulated bEnd3 cells can promote OSA-CI by increasing HT22 cells pyroptosis through its target MFN2.Keywords: exosome, OSA, cognitive impairment, miR-20a-5p, MFN2, GSDMD

The article presents a clinical case of rehabilitation of a patient with moderate cognitive and motor impairment after a COVID-associated stroke. The patient received a complex of rehabilitation measures with daily individualized cognitive training. By the end of the course of medical rehabilitation, the set goals were achieved: the patient learned to make simple decisions on her own, perform separately assigned tasks, independently attend physical therapy classes, physiotherapy, a canteen, walk around the room without the use of aids, climb to the 2nd floor without shortness of breath. The patient showed an improvement in cognitive functions: motor, dynamic and constructive praxis, object gnosis, visual-constructive skills, attention, abstract thinking and speech.

Cognitive impairment is one of the key manifestations of chronic cerebrovascular diseases. Among the factors contributing to their development are microcirculatory disturbances, changes in blood rheological properties, endothelial dysfunction and oxidative stress. This review is devoted to the analysis of the clinical application potential of the nonspecific phosphodiesterase inhibitor pentoxifylline (Vasonit®) in the therapy of patients with chronic cerebral ischaemia in order to correct haemorheological and haemodynamic factors. Data from experimental and clinical studies indicating the possibility and pathogenetic validity of the use of pentoxifylline (Vasonit®) in the complex therapy of cognitive disorders associated with chronic cerebrovascular diseases are considered. The authors describe their own experience of using Vasonit® in a patient with vascular cognitive impairment.

Changteng Zhang,1,2,&ast; Ying Su,1,2,&ast; Xianzheng Zeng,3 Xiaoyu Zhu,1,2 Rui Gao,1,2 Wangyang Liu,1,2 Runzi Du,1,2 Chan Chen,1,2 Jin Liu1,2 1Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, People’s Republic of China; 2The Research Units of West China (2018RU012)-Chinese Academy of Medical Sciences, West China Hospital, Sichuan University, Chengdu, People’s Republic of China; 3Department of Pain Management, West China Hospital, Sichuan University, Chengdu, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Chan Chen, Email chenchan@scu.edu.cn; xychenchan@gmail.comBackground: Cognitive impairment (CI) is frequently observed in patients with chronic pain (CP). CP progression increases the risk of dementia and accelerates Alzheimer’s disease pathogenesis. However, risk diagnostic models and biomarkers for CP-related CI remain insufficient. Previous research has highlighted the relationships between several complete blood count parameters for CP or CI-related diseases, such as Alzheimer’s disease, while the specific values of complete blood count parameters in CP-related CI patients remain unclear. This study aimed to explore the correlation between complete blood count parameters and CP-related CI to establish a risk diagnostic model for the early detection of CP-related CI.Methods: This cross-sectional study was conducted at West China Hospital, Sichuan University. The Montreal Cognitive Assessment (MoCA) was used to classify patients into either the CP with CI group or the CP without CI group. Univariate analysis and multivariate logistic regression analysis were used to screen the related factors of CP-related CI for constructing a risk diagnostic model, and the model was evaluated using receiver operating characteristic (ROC) curve analysis.Results: The study ultimately included 163 eligible patients. Based on analysis, age (OR, 1.037 [95% CI, 1.007– 1.070]; P=0.018), duration of pain (OR, 2.546 [95% CI, 1.099– 6.129]; P=0.032), VAS score (OR, 1.724 [95% CI, 0.819– 3.672]; P=0.153), LMR (OR, 0.091 [95% CI, 0.024– 0.275]; P< 0.001), absolute neutrophil value (OR, 0.306 [95% CI, 0.115– 0.767]; P=0.014), and lymphocyte percentage (OR, 6.551 [95% CI, 2.143– 25.039]; P=0.002) were identified as critical factors of CP-related CI. The diagnostic model was evaluated by the ROC curve, demonstrating good diagnostic value with an area under the curve (AUC) of 0.803, a sensitivity of 0.603 and a specificity of 0.871.Conclusion: The risk diagnostic model developed in this study for CP-related CI has significant value and enables clinicians to customize interventions based on each patient’s needs.Keywords: cognitive impairment, chronic pain, diagnostic model, complete blood count parameters, risk factors

Abstract Background Atherosclerosis plays a crucial role in the progression of cardiovascular disease, which is still a major global health concern. Its onset and advancement are significantly influenced by inflammation, especially when it comes to the immune system’s relationship with hypercholesterolemia. Effective serum biomarkers for atherosclerosis are still elusive, despite continuous research into anti-inflammatory therapies. Both monocytes and high-density lipoprotein play important roles in inflammatory and antioxidant processes, while high-density lipoprotein cholesterol (HDL-C) provides protective benefits, and monocytes are involved in the development of atherosclerotic plaque. The monocyte to high-density lipoprotein ratio (MHR) has emerged as a promising predictor of cardiovascular events, potentially more sensitive than each one’s individual levels. Studies have investigated the relationship between MHR and cardiovascular events in a number of diseases, such as acute coronary syndrome and chronic kidney disease. This study investigates the associations between MHR, atherosclerosis, arteriosclerosis, and cognitive impairment in elderly Egyptian populations, exploring its potential as a diagnostic marker and its role in predicting cognitive decline in diabetic individuals. Comprehending this intricate correlation is essential for developing preventive measures and targeted interventions for preventing cardiovascular disease and cognitive deterioration in the geriatrics. Results The study included 100 participants, 50 with type 2 diabetes and 50 nondiabetic, with a mean age of 67 years. Significant negative correlations were found between MHR and the 3MS test (r: − 0.353, p = 0.012) and (r: − 0.170, p = 0.238) and between carotid femoral PWV and the 3MS test in diabetics and in nondiabetics (r: − 0.453, p = 0.001) in both groups, suggesting a potential link between MHR and cognitive impairment. Conclusion This study highlights the complex relationship between monocyte to HDL-C ratio (MHR), atherosclerosis, and cognitive function in the elderly. Positive correlations were found between MHR and carotid intima-media thickness and carotid femoral PWV, suggesting a role for MHR in atherosclerosis. Notably, a negative correlation between MHR and cognitive function in diabetic individuals suggests a potential link between MHR and cognitive decline.

Abstract Background Subjective Cognitive Decline (SCD) is recognized as a risk stage for future cognitive impairment and dementia. The criteria for SCD include normal performance on neuropsychological testing; however, there is a lack of consensus regarding standard score cut-offs for neuropsychological tests to define cognitive impairment and to differentiate between SCD and Mild Cognitive Impairment (MCI). This study aimed to assess the frequency of SCD diagnosis using various neuropsychological definitions of cognitive normality and to characterize the sociodemographic and neuropsychological features of SCD patients diagnosed under these criteria. Methods The Cognitive Complaints Cohort (CCC) participants were diagnosed following Subjective Cognitive Decline Initiative (SCD-I) criteria. Normal cognitive performance was defined by the absence of Mild Cognitive Impairment (MCI) according to the five sets of MCI neuropsychologically based criteria defined by Jak and Bondi. Descriptive statistics were used to analyze sociodemographic, clinical, and neuropsychological data. A bootstrap methodology was employed to estimate the mean and 95% confidence intervals (CI) for specific parameters of interest, namely the SMC scale (subjective memory complaints scale), Mini-Mental State Examination (MMSE), Blessed Dementia Rating Scale – first part (BDRS first part), and Geriatric Depression Scale (GDS). Results Among the 1268 subjects included, the prevalence of SCD diagnosis exhibited substantial variation across SCD-I criteria using different neuropsychological definitions of cognitive normality (ranging from 16.4 to 81.3%). When using the most conservative criteria to define cognitive impairment (2 tests within a cognitive domain > 1.5 SD below age-adjusted means), the resulting Conservative SCD group had poorer global cognitive function (MMSE: mean 27.15, 95% CI 27.00-27.31), whereas when using the most liberal criteria to define cognitive impairment (only one test > 1 SD below age-adjusted means) the resulting Liberal SCD group had superior performance in daily-life functioning (BDRS first part: mean 0.30, 95% CI 0.23–0.38). However, subjective cognitive complaints and neuropsychiatric symptoms did not significantly differ among SCD diagnostic groups. Conclusions The utilization of diagnostic criteria using distinct neuropsychological definitions of cognitive normality significantly impacts the frequency of SCD diagnosis and characterizes different patient populations. Consequently, it is essential to specify the criterion when diagnosing a SCD patient and to understand the risks and benefits of using different criteria to define cognitive impairment.

Abstract Background Hospitalized older patients with cognitive impairment (CI) experience poor outcomes and high rates of hospital acquired complications (HACs). This study investigated the effectiveness of a multimodal hospital CI identification and education program. Method A prospective stepped-wedge, cross-sectional, continuous-recruitment, hybrid effectiveness-Implementation study was conducted in acute hospitals in four Australian states/territories. The intervention, the Dementia Care in Hospitals Program (DHCP) provided: clinical/ non-clinical hospital staff CI awareness support and education; CI screening for older patients and a bedside alert—the Cognitive Impairment Identifier (CII). The primary outcome was change in the rate of the combined risk of four HACs (urinary tract infection, pneumonia, new onset delirium, pressure injury). Results Participants were patients aged 65 years and over admitted for 24 h or more over a 12-month period between 2015–2017 (n = 16,789). Of the 11,309 (67.4%) screened, 4,277 (37.8%) had CI. HACs occurred in 27.4% of all screened patients and were three times more likely in patients with CI after controlling for age and sex (RR = 3.03; 95%CI:2.74–3.27). There was no significant change in HAC rate for patients with CI (RR = 1.084; 95%CI: 0.93; 1.26). In the intervention period the raw HAC rate for all screened patients was 27.0%, which when adjusted for age and sex suggested a small reduction overall. However, when adjusted for hospital site, this reduction in HAC risk not statistically significant (RR = 0.968; 95%CI:0.865–1.083). There was considerable interhospital variation in intervention implementation and outcomes which explains the final non-significant effect. Conclusion For patient with CI the implementation of the DCHP did not result in a reduction in HAC rates. Education for hospital staff regarding cognitive impairment screening, care support, carer engagement and bedside alerts, using the DCHP, can be feasibly implemented in acute hospitals. Reducing high frequency HACs in older hospital patients with CI, warrants further research. Trial Registration. The trial was registered retrospectively with the Australian New Zealand Clinical Trials Registry (ANZCTR) ACTRN12615000905561 on 01/09/2015 with 92 patients (0.8% of total sample) recruited in the baseline and none in the intervention before registration submission.