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Introduction: Neurofibromatosis type 1 (NF type 1) is an autosomal dominant disease with typical clinical manifestations, such as skin lesions, Lisch nodules, optic pathway gliomas, and neurofibromas, caused by the mutation of the NF1 gene. Visual evoked potentials (VEP) present a measure of the electrophysiological response of visual cortex to a visual stimulus. The role of VEP in the pathophysiology of NF type 1 is very complex and requires additional research. The Aim: We examined the differences between NF type 1 patients with normal and altered VEP and analyzed the correlation between the prolongation of P100 latency and disease severity. Materials and Methods: Two groups were formed: a control group and a study group with NF type 1 patients. Based on the control group analysis, a threshold value for a normal VEP finding of 116 ms was obtained, and it was used to divide the study group into subgroups with normal and altered VEP. We proceeded with examining the differences in clinical manifestations of the disease between the subgroups, after which we checked if there is a correlation between the prolongation of the P100 latency and the severity of the clinical picture according to the Riccardi scale. Statistical analysis was performed using the Pearson chi-square test and the Spearman correlation test in the program SPSS 28.0, with levels of statistical significance p = 0.05 and p = 0.001. Results: In the group with the abnormal VEP we found a statistically significant more frequent occurrence of optic tract glioma (p = 0.008), tumors (p = 0.032), epilepsy (p = 0.043), and cognitive disorders (p = 0.028), while the other clinical signs had an equal prevalence in both groups. A moderately strong correlation (rs = 0.665) was observed between the prolongation of P100 latency and the severity of the clinical picture. Conclusion: Our results showed the important role of VEP in the description of clinical phenotypes of NF type 1. The authors of the study propose VEP to be included in the diagnostic algorithms designed for patients with NF type 1. [ABSTRACT FROM AUTHOR]

(R, S)- and (S)-ketamine have made significant progress in the treatment of treatment-resistant depression (TRD) and have become a research focus in recent years. However, they both have risks of psychomimetic effects, dissociative effects, and abuse liability, which limit their clinical use. Recent preclinical and clinical studies have shown that (R)-ketamine has a more efficient and lasting antidepressant effect with fewer side effects compared to (R, S)- and (S)-ketamine. However, a recent small-sample randomized controlled trial found that although (R)-ketamine has a lower incidence of adverse reactions in adult TRD treatment, its antidepressant efficacy is not superior to the placebo group, indicating its antidepressant advantage still needs further verification and clarification. Moreover, an increasing body of research suggests that (R)- ketamine might also have significant applications in the prevention and treatment of medical fields or diseases such as cognitive disorders, perioperative anesthesia, ischemic stroke, Parkinson's disease, multiple sclerosis, osteoporosis, substance use disorders, inflammatory diseases, COVID-19, and organophosphate poisoning. This article briefly reviews the mechanism of action and research on antidepressants related to (R)-ketamine, fully revealing its application potential and development prospects, and providing some references and assistance for subsequent expanded research. [ABSTRACT FROM AUTHOR]

IntroductionAir pollution is a significant contributor to morbidity and mortality globally and has been linked to an increased risk of dementia. Previous studies within the Betula cohort in Northern Sweden have demonstrated associations between air pollution and dementia, as well as distinctive metabolomic profiles in dementia patients compared to controls. This study aimed to investigate whether air pollution is associated with quantitative changes in metabolite levels within this cohort, and whether future dementia status would modify this association.MethodsBoth short-term and long-term exposure to air pollution were evaluated using high spatial resolution models and measured data. Air pollution from vehicle exhaust and woodsmoke were analyzed separately. Metabolomic profiling was conducted on 321 participants, including 58 serum samples from dementia patients and a control group matched for age, sex, and education level, using nuclear magnetic resonance spectroscopy.ResultsNo statistically significant associations were found between any metabolites and any measures of short-term or long-term exposure to air pollution. However, there were trends potentially suggesting associations between both long-term and short-term exposure to air pollution with lactate and glucose metabolites. Notably, these associations were observed despite the lack of correlation between long-term and short-term air pollution exposure in this cohort. There were also tendencies for associations between air pollution from woodsmoke to be more pronounced in participants that would later develop dementia, suggesting a potential effect depending on urban/rural factors.DiscussionWhile no significant associations were found, the trends observed in the data suggest potential links between air pollution exposure and changes in lactate and glucose metabolites. These findings provide some new insights into the link between air pollution and metabolic markers in a low-exposure setting. However, addressing existing limitations is crucial to improve the robustness and applicability of future research in this area. The pronounced associations in participants who later developed dementia may indicate an influence of urban/rural factors, warranting further investigation.

IntroductionNeurofibromatosis type 1 (NF type 1) is an autosomal dominant disease with typical clinical manifestations, such as skin lesions, Lisch nodules, optic pathway gliomas, and neurofibromas, caused by the mutation of the NF1 gene. Visual evoked potentials (VEP) present a measure of the electrophysiological response of visual cortex to a visual stimulus. The role of VEP in the pathophysiology of NF type 1 is very complex and requires additional research.The AimWe examined the differences between NF type 1 patients with normal and altered VEP and analyzed the correlation between the prolongation of P100 latency and disease severity.Materials and methodsTwo groups were formed: a control group and a study group with NF type 1 patients. Based on the control group analysis, a threshold value for a normal VEP finding of 116 ms was obtained, and it was used to divide the study group into subgroups with normal and altered VEP. We proceeded with examining the differences in clinical manifestations of the disease between the subgroups, after which we checked if there is a correlation between the prolongation of the P100 latency and the severity of the clinical picture according to the Riccardi scale. Statistical analysis was performed using the Pearson chi-square test and the Spearman correlation test in the program SPSS 28.0, with levels of statistical significance p = 0.05 and p = 0.001.ResultsIn the group with the abnormal VEP we found a statistically significant more frequent occurrence of optic tract glioma (p = 0.008), tumors (p = 0.032), epilepsy (p = 0.043), and cognitive disorders (p = 0.028), while the other clinical signs had an equal prevalence in both groups. A moderately strong correlation (rs = 0.665) was observed between the prolongation of P100 latency and the severity of the clinical picture.ConclusionOur results showed the important role of VEP in the description of clinical phenotypes of NF type 1. The authors of the study propose VEP to be included in the diagnostic algorithms designed for patients with NF type 1.

Recently, there has been increasing attention on the impact of acupuncture on the dysregulated neural circuits in different disease. This has led to new understandings of how acupuncture works. This review presents a comprehensive analysis of research that have examined the impact of acupuncture on abnormal neural circuits associated with pain, anxiety, Parkinson’s disease, addiction disorders, cognitive problems, and gastrointestinal disorders. These studies have shown that acupuncture’s therapeutic effects are mediated by specific brain areas and neurons involved in neural circuit mechanisms, emphasising its wide-ranging influence. The positive impacts of acupuncture can be ascribed to its ability to modify the functioning of neurocircuits in various physiological conditions. Nevertheless, contemporary studies on acupuncture neural circuits frequently overlook the comprehensive circuit mechanism including the periphery, central nervous system, and target organ. Additionally, the scope of diseases studied is restricted. Future study should focus on broadening the range of diseases studied and exploring the neural circuit mechanisms of these diseases in depth in order to enhance our understanding of acupuncture’s neurobiological impacts.

IntroductionDuring the pandemic, the Cognitive Disorders Unit of San Raffaele Hospital (Milan, Italy) offered patients the opportunity to undergo neuropsychological evaluations and cognitive training through telemedicine.MethodWe conducted an investigation to assess how patients responded to this option and to determine if telemedicine could ensure continuity of care.ResultsBetween October 2019 and May 2022, a total of 5,768 telemedicine appointments and 8,190 in-person outpatient appointments were conducted, resulting in an increase in the rate of telemedicine activity from 16.81% in January 2020 to 23.21% in May 2022. Peaks in telemedicine activity reached 85.64% in May 2020 and 83.65% in February 2021, both representing a significant portion of the total activity. Interestingly, there was a notable positive correlation between telemedicine activity and the worsening of the Italian pandemic (r = 0.433, p = 0.027).DiscussionDuring the peaks of contagion, the total number of visits remained stable, highlighting that telemedicine effectively served as a valuable and efficient tool to ensure continuity of care for vulnerable patients. This was evident from the integration of remote visits with in-person appointments.

Introduction: Metformin has shown good efficacy in the management of antipsychotic-induced metabolic syndrome (MetS) in patients with schizophrenia or schizoaffective disorders. Its ability to induce antidepressant behavioural effects and improve cognitive functions has also been investigated: yet information has not been systematized. The aim of this study was therefore to investigate the effects of metformin on cognitive and other symptom dimension in schizophrenic patients treated with antipsychotics through a systematic review and meta-analysis. Methods: We searched PubMed, ClinicalTrials.Gov, Embase, PsycINFO, and WHO ICTRP database up to February 2022, Randomised Controlled Trials (RCT) evaluating patients diagnosed with schizophrenia and related disorders, who were treated with metformin as add-on therapy to antipsychotics for the treatment of weight gain and in which changes in psychiatric symptoms and cognitive functions were evaluated. Results: A total of 19 RCTs met the inclusion criteria. Meta-analysis was performed on 12 eligible studies. We found a positive trend after 24 weeks of treatment in schizophrenic patients with stable conditions [SMD (95%CI) = -0.40 (-0.82;0.01), OR (95%CI) = 0.5 (-2.4;3.4)]. Better performance was detected in the Brief Assessment of Cognition in Schizophrenia and Positive and Negative Syndrome Scale (PANSS) with low heterogeneity among studies. One study reported changes in BACS-verbal memory subdomain in favour of placebo [MD (95%CI) = -16.03 (-23.65;8.42)]. Gastrointestinal disorders, xerostomia, and extrapyramidal syndrome were the most reported adverse effects. Psychiatric adverse events were also described: in particular, symptoms attributable to a relapse of schizophrenia. Conclusion: Some degree of efficacy was found for Metformin in improving cognitive and other symptom dimensions in patients with Schizophrenia. Given the clinical relevance of this potential pharmacological effect, longer specific studies using adequate psychometric scales are strongly recommended. Likewise, how metformin acts in this context needs to be evaluated in order to enhance its efficacy or find more efficacious drugs. [ABSTRACT FROM AUTHOR]

Non-invasive, non-pharmacological interventions utilizing virtual reality (VR) represent a promising approach to enhancing cognitive function in patients with degenerative cognitive disorders. Traditional "pen and paper" therapies often lack the practical engagement in everyday activities that older individuals encounter in their environment. These activities pose both cognitive and motor challenges, underscoring the necessity of understanding the outcomes of such combined interventions. This review aimed to assess the advantages of VR applications that integrate cognitive-motor tasks, simulating instrumental activities of daily living (iADLs). We systematically searched five databases-Scopus, Web of Science, Springer Link, IEEE Xplore, and PubMed, from their inception until January 31, 2023. Our review revealed that motor movements, coupled with VRbased cognitive-motor interventions, activate specific brain areas and foster improvements in general cognition, executive function, attention, and memory. VR applications that meld cognitive-motor tasks and simulate iADLs can offer significant benefits to older adults. Enhanced cognitive and motor performance can promote increased independence in daily activities, thereby contributing to improved quality of life. [ABSTRACT FROM AUTHOR]

Audio frequency magnetic fields (20 Hz−20 kHz) are magnetic fields in extremely low frequency-very low frequency (ELF-VLF) bands that are present near audio equipment and acoustic transducers. These devices transform and operate the electrical signal from the recordings or other devices into acoustic and audio signals. The cognitive influence of sound and noise has been widely studied and recognized since the times of ancient Rome; however, the cognitive effects of the magnetic fields of these frequencies have not been studied. Due to the extensive use of audio devices that use this type of transducer near the temporal–parietal area, we believe that it is of interest to study their impact on short-term memory or working memory (WM) and to analyze their potential as they operate as a transcranial magnetic stimulation. In this study, a mathematical model and an experimental tool are introduced to analyze memory performance. The model dissociates the reaction time of a cognitive task. We analyze the model in data from a group of 65 young, healthy subjects. WM is assessed in our experimental setup by means of the Sternberg test (ST), whereby during the ST, one subgroup was exposed to an audio frequency magnetic stimulus, and the other subgroup received a sham stimulus. The magnetic stimulus was ∼0.1 µT and was applied to both sides of the head at the frontal cortex near the temporal–parietal area, which is where WM is expected to be located. The ST records reaction times when determining whether an object displayed on the computer screen is one of the objects to be remembered. The results are analyzed within the mathematical model and changes are observed, including the deterioration of WM, which could affect 32% of its operability. [ABSTRACT FROM AUTHOR]

Cognitive impairment is the core precursor to dementia and other cognitive disorders. Current hypotheses suggest that they share a common pathological basis, such as inflammation, restricted neurogenesis, neuroendocrine disorders, and the destruction of neurovascular units. Fibroblast growth factors (FGFs) are cell growth factors that play essential roles in various pathophysiological processes via paracrine or autocrine pathways. This system consists of FGFs and their receptors (FGFRs), which may hold tremendous potential to become a new biological marker in the diagnosis of dementia and other cognitive disorders, and serve as a potential target for drug development against dementia and cognitive function impairment. Here, we review the available evidence detailing the relevant pathways mediated by multiple FGFs and FGFRs, and recent studies examining their role in the pathogenesis and treatment of cognitive disorders and dementia. [ABSTRACT FROM AUTHOR]

IntroductionMetformin has shown good efficacy in the management of antipsychotic-induced metabolic syndrome (MetS) in patients with schizophrenia or schizoaffective disorders. Its ability to induce antidepressant behavioural effects and improve cognitive functions has also been investigated: yet information has not been systematized. The aim of this study was therefore to investigate the effects of metformin on cognitive and other symptom dimension in schizophrenic patients treated with antipsychotics through a systematic review and meta-analysis.MethodsWe searched PubMed, ClinicalTrials.Gov, Embase, PsycINFO, and WHO ICTRP database up to February 2022, Randomised Controlled Trials (RCT) evaluating patients diagnosed with schizophrenia and related disorders, who were treated with metformin as add-on therapy to antipsychotics for the treatment of weight gain and in which changes in psychiatric symptoms and cognitive functions were evaluated.ResultsA total of 19 RCTs met the inclusion criteria. Meta-analysis was performed on 12 eligible studies. We found a positive trend after 24 weeks of treatment in schizophrenic patients with stable conditions [SMD (95%CI) = -0.40 (−0.82;0.01), OR (95%CI) = 0.5 (−2.4;3.4)]. Better performance was detected in the Brief Assessment of Cognition in Schizophrenia and Positive and Negative Syndrome Scale (PANSS) with low heterogeneity among studies. One study reported changes in BACS-verbal memory subdomain in favour of placebo [MD (95%CI) = -16.03 (-23.65;8.42)]. Gastrointestinal disorders, xerostomia, and extrapyramidal syndrome were the most reported adverse effects. Psychiatric adverse events were also described: in particular, symptoms attributable to a relapse of schizophrenia.ConclusionSome degree of efficacy was found for Metformin in improving cognitive and other symptom dimensions in patients with Schizophrenia. Given the clinical relevance of this potential pharmacological effect, longer specific studies using adequate psychometric scales are strongly recommended. Likewise, how metformin acts in this context needs to be evaluated in order to enhance its efficacy or find more efficacious drugs.

Non-invasive, non-pharmacological interventions utilizing virtual reality (VR) represent a promising approach to enhancing cognitive function in patients with degenerative cognitive disorders. Traditional “pen and paper” therapies often lack the practical engagement in everyday activities that older individuals encounter in their environment. These activities pose both cognitive and motor challenges, underscoring the necessity of understanding the outcomes of such combined interventions. This review aimed to assess the advantages of VR applications that integrate cognitive-motor tasks, simulating instrumental activities of daily living (iADLs). We systematically searched five databases–Scopus, Web of Science, Springer Link, IEEE Xplore, and PubMed, from their inception until January 31, 2023. Our review revealed that motor movements, coupled with VR-based cognitive-motor interventions, activate specific brain areas and foster improvements in general cognition, executive function, attention, and memory. VR applications that meld cognitive-motor tasks and simulate iADLs can offer significant benefits to older adults. Enhanced cognitive and motor performance can promote increased independence in daily activities, thereby contributing to improved quality of life.

Audio frequency magnetic fields (20 Hz−20 kHz) are magnetic fields in extremely low frequency-very low frequency (ELF-VLF) bands that are present near audio equipment and acoustic transducers. These devices transform and operate the electrical signal from the recordings or other devices into acoustic and audio signals. The cognitive influence of sound and noise has been widely studied and recognized since the times of ancient Rome; however, the cognitive effects of the magnetic fields of these frequencies have not been studied. Due to the extensive use of audio devices that use this type of transducer near the temporal–parietal area, we believe that it is of interest to study their impact on short-term memory or working memory (WM) and to analyze their potential as they operate as a transcranial magnetic stimulation. In this study, a mathematical model and an experimental tool are introduced to analyze memory performance. The model dissociates the reaction time of a cognitive task. We analyze the model in data from a group of 65 young, healthy subjects. WM is assessed in our experimental setup by means of the Sternberg test (ST), whereby during the ST, one subgroup was exposed to an audio frequency magnetic stimulus, and the other subgroup received a sham stimulus. The magnetic stimulus was ~0.1 μT and was applied to both sides of the head at the frontal cortex near the temporal–parietal area, which is where WM is expected to be located. The ST records reaction times when determining whether an object displayed on the computer screen is one of the objects to be remembered. The results are analyzed within the mathematical model and changes are observed, including the deterioration of WM, which could affect 32% of its operability.

Background: The Cognitive Functioning Self-Assessment Scale (CFSS) was developed to allow the self-assessment of perceived cognitive functioning. It has been tested with satisfactory reliability and validity but was not available for the Chinese population. This study aimed to adapt and validate the Chinese version of the CFSS for community-dwelling adults. Methods: A cross-sectional study of a sample of 1,002 Chinese adults from the general population was conducted online (July–August 2022). The Chinese version of the CFSS with 18 items was created through translation, cognitive debriefing, and psychometric evaluation. Exploratory factor analysis (EFA) was performed on the first half of the randomly split sample. A model derived from EFA was confirmed by confirmatory factor analysis (CFA) in the second half of the sample. The model fits were further evaluated with and without subgrouping by age, gender, and education level. Internal consistency was assessed using Cronbach’s alpha (α) and McDonald’s omega hierarchical coefficients (ωH). Results: EFA (n = 460) revealed a three-factor solution, including spatio-temporal orientation, attention, and memory, which explained 51% of the total variance. The second-order CFA (n = 510) demonstrated a good fit: CFI = 0.951, TLI = 0.944, RMSEA = 0.054, SRMR = 0.040. A second-order multiple-group analysis showed that the structure was invariant by age, gender, and education level. The total CFSS score was significantly associated with the Chinese version of the nine-item Patient Health Questionnaire (r = 0.56, p< 0.001) and the Chinese version of the seven-item General Anxiety Disorder (r = 0.53, p<0.001). The internal consistency reliability was satisfactory, with α = 0.94 and ωH = 0.84. The item-total correlation coefficients ranged from 0.58 to 0.72. Conclusion: The Chinese version of the CFSS possesses good item characteristics, satisfactory validity, and reliability for assessing self-reported cognitive functioning among community-dwelling adults. It is a feasible and appropriate self-assessment instrument to examine cognitive functioning in the Hong Kong Chinese population, which contributes to monitoring and developing strategies to prevent and manage cognitive impairment and disorders for the public’s cognitive health and well-being. [ABSTRACT FROM AUTHOR]

Neurocognitive disorders (NCDs) include complex and multifactorial diseases that affect many patients. The 5-hydroxytryptamine (5-HT) neuron system plays an important role in NCDs. Existing studies have reported that para-chlorophenylalanine (PCPA), a 5-HT scavenger, has a negative effect on cognitive function. However, we believe that PCPA may result in NCDs through other pathways. To explore this possibility, behavioral tests were performed to evaluate the cognitive function of PCPA-treated mice, suggesting the appearance of cognitive dysfunction and depression-like behavior. Furthermore, 16S rRNA and metabolomic analyses revealed that dysbiosis and acetate alternation could be related to PCPA-induced NCDs. Our results suggest that not only 5-HT depletion but also dysbiosis and acetate alternation contributed to PCPA-related NCDs. Specifically, the latter promotes NCDs by reducing short-chain fatty acid levels. Together, these findings provide an alternative perspective on PCPA-induced NCDs. [ABSTRACT FROM AUTHOR]

The main goal of the present study is to investigate visual and verbal short-term memory side to side with sentence comprehension in Catalan-speaking subjects with aphasia in comparison with subjects without brain damage. We aim to examine whether there are any significant correlations between their performance on short-term memory and comprehension tasks in order to evaluate the hypothesis that linguistic and memory deficits in aphasia are the result of a dysfunction of a common mechanism, usually short-term memory. Eigthy-four control subjects and twelve individuals suffering from different types of aphasia were assessed using the Catalan version of the Comprehensive Aphasia Test (CAT-CAT), which includes one recognition task and two digit and word span tests to evaluate visual and verbal short-term memory, respectively, as well as a sentence-to-picture comprehension task. The results showed that the performance of subjects with aphasia was significantly low on all tasks. Yet, the logistic regression analysis revealed that the magnitude of the differences between the control and experimental group varied across subtests, and that visual short-term memory was better preserved than verbal memory. The results also showed that there were no significant correlations between memory and language comprehension, which rules out the hypothesis that the deficits observed are due to a common underlying mechanism. Individual variation was also observed, specially on memory subtests, which suggest that memory impairments cannot explain the comprehension deficit in aphasia. [ABSTRACT FROM AUTHOR]

Neurocognitive disorders (NCDs) include complex and multifactorial diseases that affect many patients. The 5-hydroxytryptamine (5-HT) neuron system plays an important role in NCDs. Existing studies have reported that para-chlorophenylalanine (PCPA), a 5-HT scavenger, has a negative effect on cognitive function. However, we believe that PCPA may result in NCDs through other pathways. To explore this possibility, behavioral tests were performed to evaluate the cognitive function of PCPA-treated mice, suggesting the appearance of cognitive dysfunction and depression-like behavior. Furthermore, 16S rRNA and metabolomic analyses revealed that dysbiosis and acetate alternation could be related to PCPA-induced NCDs. Our results suggest that not only 5-HT depletion but also dysbiosis and acetate alternation contributed to PCPA-related NCDs. Specifically, the latter promotes NCDs by reducing short-chain fatty acid levels. Together, these findings provide an alternative perspective on PCPA-induced NCDs.

The main goal of the present study is to investigate visual and verbal short-term memory side to side with sentence comprehension in Catalan-speaking subjects with aphasia in comparison with subjects without brain damage. We aim to examine whether there are any significant correlations between their performance on short-term memory and comprehension tasks in order to evaluate the hypothesis that linguistic and memory deficits in aphasia are the result of a dysfunction of a common mechanism, usually short-term memory. Eigthy-four control subjects and twelve individuals suffering from different types of aphasia were assessed using the Catalan version of the Comprehensive Aphasia Test (CAT-CAT), which includes one recognition task and two digit and word span tests to evaluate visual and verbal short-term memory, respectively, as well as a sentence-to-picture comprehension task. The results showed that the performance of subjects with aphasia was significantly low on all tasks. Yet, the logistic regression analysis revealed that the magnitude of the differences between the control and experimental group varied across subtests, and that visual short-term memory was better preserved than verbal memory. The results also showed that there were no significant correlations between memory and language comprehension, which rules out the hypothesis that the deficits observed are due to a common underlying mechanism. Individual variation was also observed, specially on memory subtests, which suggest that memory impairments cannot explain the comprehension deficit in aphasia.

ObjectivesThe aim of this meta-analysis was to assess the quantitative associations between fruit and vegetable intake and cognitive disorders in older adults.DesignA meta-analysis.Setting and ParticipantsWe used the PubMed, Web of Science and Scopus databases for a literature search to 12 April 2022. We preliminarily retrieved 11,759 studies, 16 of which met the inclusion criteria including six cross-sectional studies, nine cohort studies and one case-control study, incorporating 64,348 participants and 9,879 cases.MethodsUsing the three databases, we identified observational studies exploring the association. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a random effects model.ResultsSixteen studies were included in the meta-analysis, and the results showed that increased fruit and vegetable consumption in older adults was associated with a decline in the prevalence of cognitive disorders (OR: 0.79, 95% CI: 0.76–0.83). Moreover, intake of fruits (OR: 0.83, 95% CI: 0.77–0.89) and vegetables (OR: 0.75, 95% CI: 0.70–0.80) alone were both associated with a lower prevalence of cognitive disorders. Subgroup analyses indicated that the intake of fruits and vegetables was associated with the prevalence of cognitive impairment (OR: 0.72, 95% CI: 0.76–0.80) and dementia (OR: 0.84, 95% CI: 0.78–0.91) but not Alzheimer’s disease (OR: 0.88, 95% CI: 0.76–1.01).Conclusion and ImplicationsOur meta-analysis provides evidence that the intake of fruits and vegetables is inversely proportional and linearly associated with the prevalence of cognitive disorders in older adults. Future research is required to further investigate the preventive effects of the frequency, quantity, and duration of eating vegetables and fruits on cognitive disorders in older adults.

Human cytomegalovirus (HCMV) infection is very common in the human population all around the world. Although the majority of HCMV infections are asymptomatic, they can cause neurologic deficits. Previous studies have shown that immediate early protein 2 (IE2, also known as UL122) of HCMV is related with the cognitive disorder mechanism. Due to species isolation, a HCMV-infected animal model could not be established which meant a study into the long-term effects of IE2 on neural development could not be carried out. By establishing HCMV-UL122-Tg mice (UL122 mice), we explored the cognitive behavior and complexity of neuron changes in this transgenic UL122 mice that could consistently express IE2 protein at different ages (confirmed in both 6- and 12-month-old UL122 mice). In the Morris water maze, cognitive impairment was more pronounced in 12-month-old UL122 mice than in 6-month-old ones. At the same time, a decrease of the density of dendritic spines and branches in the hippocampal neurons of 12-month-old mice was observed. Moreover, long-term potentiation was showed to be impaired in 12-month-old UL122 mice. The expressions of several synaptic plasticity-regulated molecules were reduced in 12-month-old UL122 mice, including scaffold proteins postsynaptic density protein 95 (PSD95) and microtubule-associated protein 2 (MAP2). Binding the expression of IE2 was increased in 12-month-old mice compared with 6-month-old mice, and results of statistical analysis suggested that the cognitive damage was not caused by natural animal aging, which might exclude the effect of natural aging on cognitive impairment. All these results suggested that IE2 acted as a pathogenic regulator in damaging synaptic plasticity by downregulating the expression of plasticity-related proteins (PRPs), and this damage increased with aging. [ABSTRACT FROM AUTHOR]

Human cytomegalovirus (HCMV) infection is very common in the human population all around the world. Although the majority of HCMV infections are asymptomatic, they can cause neurologic deficits. Previous studies have shown that immediate early protein 2 (IE2, also known as UL122) of HCMV is related with the cognitive disorder mechanism. Due to species isolation, a HCMV-infected animal model could not be established which meant a study into the long-term effects of IE2 on neural development could not be carried out. By establishing HCMV-UL122-Tg mice (UL122 mice), we explored the cognitive behavior and complexity of neuron changes in this transgenic UL122 mice that could consistently express IE2 protein at different ages (confirmed in both 6- and 12-month-old UL122 mice). In the Morris water maze, cognitive impairment was more pronounced in 12-month-old UL122 mice than in 6-month-old ones. At the same time, a decrease of the density of dendritic spines and branches in the hippocampal neurons of 12-month-old mice was observed. Moreover, long-term potentiation was showed to be impaired in 12-month-old UL122 mice. The expressions of several synaptic plasticity-regulated molecules were reduced in 12-month-old UL122 mice, including scaffold proteins postsynaptic density protein 95 (PSD95) and microtubule-associated protein 2 (MAP2). Binding the expression of IE2 was increased in 12-month-old mice compared with 6-month-old mice, and results of statistical analysis suggested that the cognitive damage was not caused by natural animal aging, which might exclude the effect of natural aging on cognitive impairment. All these results suggested that IE2 acted as a pathogenic regulator in damaging synaptic plasticity by downregulating the expression of plasticity-related proteins (PRPs), and this damage increased with aging.

Different factors seemingly account for the emergence of present-day languages in our species. Human self-domestication has been recently invoked as one important force favoring language complexity mostly via a cultural mechanism. Because our self-domestication ultimately resulted from selection for less aggressive behavior and increased prosocial behavior, any evolutionary or cultural change impacting on aggression levels is expected to have fostered this process. Here, we hypothesize about a parallel domestication of humans and dogs, and more specifically, about a positive effect of our interaction with dogs on human self-domestication, and ultimately, on aspects of language evolution, through the mechanisms involved in the control of aggression. We review evidence of diverse sort (ethological mostly, but also archeological, genetic, and physiological) supporting such an effect and propose some ways of testing our hypothesis.

Different factors seemingly account for the emergence of present-day languages in our species. Human self-domestication has been recently invoked as one important force favoring language complexity mostly via a cultural mechanism. Because our self-domestication ultimately resulted from selection for less aggressive behavior and increased prosocial behavior, any evolutionary or cultural change impacting on aggression levels is expected to have fostered this process. Here, we hypothesize about a parallel domestication of humans and dogs, and more specifically, about a positive effect of our interaction with dogs on human self-domestication, and ultimately, on aspects of language evolution, through the mechanisms involved in the control of aggression. We review evidence of diverse sort (ethological mostly, but also archeological, genetic, and physiological) supporting such an effect and propose some ways of testing our hypothesis. [ABSTRACT FROM AUTHOR]

In summary, the 17 studies published in this Research Topic provide evidence on the connection between hearing loss and cognitive disorders. A case-control study first reported that hearing impairment in older adults was strongly associated with the likelihood of having dementia - raising the hypothesis that hearing impairment may contribute to dementia risk (Uhlmann et al., [12]). Their study examined the reliability of the visual-auditory interaction in pre-lingually deaf children with CIs and demonstrated that the CI-induced activation of mirror neurons could explain deficiencies in the classical cross-modal interaction. Keywords: hearing loss; cognitive disorders; behavior detection; cochlear implant; neuroimaging EN hearing loss cognitive disorders behavior detection cochlear implant neuroimaging 1 3 3 05/19/22 20220516 NES 220516 Overall, 466 million people worldwide are estimated to be living with hearing loss. [Extracted from the article]

Kidney transplantation is a serious event that involves profound psychological, relational and social changes both for the patient and his family context. Assessment of personality profile, awareness of disease, family and social support of the patient candidate for kidney transplantation are necessary because factors not adequately considered, can influence the success of the transplant and alter the psychological stability of the patient. The present study aims to provide a systematic review of the literature of the last twelve years (2006–2018), focusing in particular on patient’s readiness level and illness management and on possible psychopathology. Sixty-two studies were examined. Based on the Downs and Black checklist, most studies (n = 32) were of high quality; 15 of which related to lifestyle, health education, and therapeutic adherence in post-renal transplantation, 17 studies concerned the possible existence of psychopathology and cognitive impairment of renal deceased transplanted subjects. The literature used has shown that the population of kidney transplant patients is exposed to a high risk of psychiatric disorders with repercussions on the quality of life and the risk of rejection. Therefore, an adequate pre-transplant psychosocial assessment is necessary, which allows a more in-depth knowledge of the candidate to plan coping strategies and possible post-transplant psychotherapy.

Kidney transplantation is a serious event that involves profound psychological, relational and social changes both for the patient and his family context. Assessment of personality profile, awareness of disease, family and social support of the patient candidate for kidney transplantation are necessary because factors not adequately considered, can influence the success of the transplant and alter the psychological stability of the patient. The present study aims to provide a systematic review of the literature of the last twelve years (2006–2018), focusing in particular on patient's readiness level and illness management and on possible psychopathology. Sixty-two studies were examined. Based on the Downs and Black checklist, most studies (n = 32) were of high quality; 15 of which related to lifestyle, health education, and therapeutic adherence in post-renal transplantation, 17 studies concerned the possible existence of psychopathology and cognitive impairment of renal deceased transplanted subjects. The literature used has shown that the population of kidney transplant patients is exposed to a high risk of psychiatric disorders with repercussions on the quality of life and the risk of rejection. Therefore, an adequate pre-transplant psychosocial assessment is necessary, which allows a more in-depth knowledge of the candidate to plan coping strategies and possible post-transplant psychotherapy. [ABSTRACT FROM AUTHOR]

Background: Convergence insufficiency (CI) in parkinsonian conditions causes disabling visual symptoms during near tasks and usually manifests as double vision. Since double vision is more common in patients who report cognitive symptoms, we sought to determine if symptomatic CI, as opposed to asymptomatic CI, could serve as a marker of cognitive impairment in parkinsonian disorders.Methods: Twenty-four participants with parkinsonian disorders (18 Parkinson's disease, 5 progressive supranuclear palsy, 1 multiple system atrophy) and objective findings of convergence insufficiency on neuro-ophthalmologic examination were included. Subjective visual symptoms and cognitive complaints were recorded, and the Self-Administered Gerocognitive Examination was used as a global cognitive screening measure.Results: 54.1% of parkinsonian participants had cognitive impairment, but there were no significant differences in the degree of convergence insufficiency, measured by near point of convergence (NPC), or cognitive outcomes between those with symptomatic CI, and asymptomatic CI. However, NPC was greater for those with cognitive impairment (x = 18.4 cm), compared to those who were cognitively intact (x = 12.5 cm, p = 0.003).Conclusions: Cognitive impairment commonly co-occurs in parkinsonian disorders with convergence insufficiency and is associated with significantly greater NPC distances. Clinicians should have a high index of suspicion for cognitive impairment in patients with objective findings of convergence insufficiency, whether symptomatic or not. Further investigation of convergence insufficiency in relationship to cognitive impairment in parkinsonian disorders is warranted, as there may be a shared mechanism of dysfunction.

Background/Aim: Current evidence in the literature supports associations between frailty, cognitive impairment, and dementia. The study aim was to describe the risk of cognitive disorders associated with physical frailty in older adults from community-based studies.Methods: We performed a systematic review and meta-analysis, using MEDLINE, PsycINFO, Scopus, and Web of Science as databases for the search. Cohort and longitudinal studies were included in qualitative analysis and quantitative synthesis. For inclusion, studies had to assess dementia and cognitive impairment as a primary or secondary outcome, and describe the prevalence of frailty among participants at baseline and follow-up.Results: Of the 2,210 studies retrieved by the systematic review, 6 relevant studies were included in a meta-analysis. Baseline frailty was significantly associated with an increased risk of geriatric cognitive disorders (pooled OR = 1.80, 95% CI = 1.11–2.92; p = 0.02). Heterogeneity across the studies was significant (I2 = 79%).Conclusions: The analyses confirmed that frail older adults were at higher risk of incident cognitive disorders than non-frail elders. Frailty status seems to be most associated with the risk of incident dementia. Frailty may represent a risk factor for dementia and could constitute a novel modifiable target in early cognitive impairment.

The purpose of this review study is to reveal a potential threat of one type of such widely used and freely distributed drugs, which are proton pump inhibitors that might be the cause of the onset of both dementia and depression. The authors performed a literature review of available studies on the research topic describing the adverse effect of proton pum inhibitors (PPIs) (omeprazole, esomeprazole, lansoprazole, dexlansoprazole, rabeprazole, pantoprazole, dexrabeprazole, ilaprazole). For a long time, PPIs were considered to be completely safe drug substances for both short and long-term use. In recent years, there have been a few contradictory studis of absolute safety, especially in patients, who have long been using PPIs. At this time when depression and dementia are rising in the population, this is a very worrying fact that needs to be highlighted, and which needs to be carefully studied and evaluated, ideally trying to prevent it. The findings of most research studies described in this review indicate that there is a direct association between the onset of dementia and depression on one side and the long-term use of PPIs on the other.

PDE9A is a cGMP-specific phosphodiesterase expressed in neurons throughout the brain that has attracted attention as a therapeutic target to treat cognitive disorders. Indeed, PDE9A inhibitors are under evaluation in clinical trials as a treatment for Alzheimer's disease and schizophrenia. However, little is known about the cGMP signaling cascades regulated by PDE9A. Canonical cGMP signaling in brain follows the activation of neuronal nitric oxide synthase (nNOS) and the generation of nitric oxide, which activates soluble guanylyl cyclase and cGMP synthesis. However, we show that in mice, PDE9A regulates a pool of cGMP that is independent of nNOS, specifically, and nitric oxide signaling in general. This PDE9A-regulated cGMP pool appears to be highly compartmentalized and independent of cGMP pools regulated by several PDEs. These findings provide a new foundation for study of the upstream and downstream signaling elements regulated by PDE9A and its potential as a therapeutic target for brain disease. [ABSTRACT FROM AUTHOR]

Background: Convergence insufficiency (CI) in parkinsonian conditions causes disabling visual symptoms during near tasks and usually manifests as double vision. Since double vision is more common in patients who report cognitive symptoms, we sought to determine if symptomatic CI, as opposed to asymptomatic CI, could serve as a marker of cognitive impairment in parkinsonian disorders. Methods: Twenty-four participants with parkinsonian disorders (18 Parkinson's disease, 5 progressive supranuclear palsy, 1 multiple system atrophy) and objective findings of convergence insufficiency on neuro-ophthalmologic examination were included. Subjective visual symptoms and cognitive complaints were recorded, and the Self-Administered Gerocognitive Examination was used as a global cognitive screening measure. Results: 54.1% of parkinsonian participants had cognitive impairment, but there were no significant differences in the degree of convergence insufficiency, measured by near point of convergence (NPC), or cognitive outcomes between those with symptomatic CI, and asymptomatic CI. However, NPC was greater for those with cognitive impairment (x = 18.4 cm), compared to those who were cognitively intact (x = 12.5 cm, p = 0.003). Conclusions: Cognitive impairment commonly co-occurs in parkinsonian disorders with convergence insufficiency and is associated with significantly greater NPC distances. Clinicians should have a high index of suspicion for cognitive impairment in patients with objective findings of convergence insufficiency, whether symptomatic or not. Further investigation of convergence insufficiency in relationship to cognitive impairment in parkinsonian disorders is warranted, as there may be a shared mechanism of dysfunction. [ABSTRACT FROM AUTHOR]

Purpose: Cognitive impairment in cancer patients induced, at least in part, by treatment are frequently observed and likely have negative impacts on patient quality of life. Such cognitive dysfunctions can affect attention, executive functions, and memory and processing speed, can persist after treatment, and their exact causes remain unclear. The aim of this review was to create an inventory and analysis of clinical studies evaluating biological markers and risk factors for cognitive decline in cancer patients before, during, or after therapy. The ultimate objectives were to identify robust markers and to determine what further research is required to develop original biological markers to enable prevention or adapted treatment management of patients at risk. Method: This review was guided by the PRISMA statement and included a search strategy focused on three components: "cognition disorders," "predictive factors"/"biological markers," and "neoplasms," searched in PubMed since 2005, with exclusion criteria concerning brain tumors, brain therapy, and imaging or animal studies. Results: Twenty-three studies meeting the criteria were analyzed. Potential associations/correlations were identified between cognitive impairments and specific circulating factors, cerebral spinal fluid constituents, and genetic polymorphisms at baseline, during, and at the end of treatment in cancer populations. The most significant results were associations between cognitive dysfunctions and genetic polymorphisms, including APOE-4 and COMT-Val; increased plasma levels of the pro-inflammatory cytokine, IL-6; anemia; and hemoglobin levels during chemotherapy. Plasma levels of specific hormones of the hypothalamo-pituitary-adrenal axis are also modified by treatment. Discussion: It is recognized in the field of cancer cognition that cancer and comorbidities, as well as chemotherapy and hormone therapy, can cause persistent cognitive dysfunction. A number of biological circulating factors and genetic polymorphisms, can predispose to the development of cognitive disorders. However, many predictive factors remain unproven and discordant findings are frequently reported, warranting additional clinical and preclinical longitudinal cohort studies, with goals of better characterization of potential biomarkers and identification of patient populations at risk and/or particularly deleterious treatments. Research should focus on prevention and personalized cancer management, to improve the daily lives, autonomy, and return to work of patients. [ABSTRACT FROM AUTHOR]

Cognitive abilities, such as memory, learning, language, problem solving, and planning, involve the frontal lobe and other brain areas. Not much is known yet about the molecular basis of cognitive abilities, but it seems clear that cognitive abilities are determined by the interplay of many genes. One approach for analyzing the genetic networks involved in cognitive functions is to study the coexpression networks of genes with known importance for proper cognitive functions, such as genes that have been associated with cognitive disorders like intellectual disability (ID) or autism spectrum disorders (ASD). Because many of these genes are gene regulatory factors (GRFs) we aimed to provide insights into the gene regulatory networks active in the human frontal lobe. Using genome wide human frontal lobe expression data from 10 independent data sets, we first derived 10 individual coexpression networks for all GRFs including their potential target genes. We observed a high level of variability among these 10 independently derived networks, pointing out that relying on results from a single study can only provide limited biological insights. To instead focus on the most confident information from these 10 networks we developed a method for integrating such independently derived networks into a consensus network. This consensus network revealed robust GRF interactions that are conserved across the frontal lobes of different healthy human individuals. Within this network, we detected a strong central module that is enriched for 166 GRFs known to be involved in brain development and/or cognitive disorders. Interestingly, several hubs of the consensus network encode for GRFs that have not yet been associated with brain functions. Their central role in the network suggests them as excellent new candidates for playing an essential role in the regulatory network of the human frontal lobe, which should be investigated in future studies.

Intracellular protein-protein interactions are dynamic processes requiring tightly regulated spatial and temporal checkpoints. But how are these spatial and temporal cues integrated to produce highly specific molecular response patterns? A helpful analogy to this process is that of a cellular map, one based on the fleeting localization and activity of various guide proteins that direct a wide array of interactions between key molecules. One such guide protein, Myristoylated alanine-rich substrate of protein kinase C (MARCKS) has recently emerged as an important component of this cellular map, governing a wide variety of protein interactions in every cell type within the brain. In addition to its well-documented interactions with the actin cytoskeleton, MARCKS has been found to interact with a number of other proteins involved in processes ranging from intracellular signaling to process outgrowth. Here we will explore these diverse interactions and their role in an array of brain-specific functions that have important implications for many neurological conditions.

Background: Corticobasal Syndrome (CBS) is a neurodegenerative disorder that overlaps both clinically and neuropathologically with Frontotemporal dementia and is characterized by apraxia, alien limb phenomena, cortical sensory loss, cognitive impairment, behavioural changes and aphasia. It has been recently demonstrated that transcranial direct current stimulation (tDCS) improves naming in healthy subjects and in subjects with language deficits.Objective: The aim of the present study was to explore the extent to which anodal transcranial direct current stimulation (anodal tDCS) over the parietal cortex (PARC) could facilitate naming performance in CBS subjects. Methods: Anodal tDCS was applied to the left and right PARC during object and action naming in seventeen patients with a diagnosis of possible CBS. Participants underwent two sessions of anodal tDCS (left and right) and one session of placebo tDCS. Vocal responses were recorded and analyzed for accuracy and vocal Reaction Times (vRTs). Results: A shortening of naming latency for actions was observed only after active anodal stimulation over the left PARC, as compared to placebo and right stimulations. No effects have been reported for accuracy.Conclusions: Our preliminary finding demonstrated that tDCS decreased vocal reaction time during action naming in a sample of patients with CBS. A possible explanation of our results is that anodal tDCS over the left PARC effects the brain network implicated in action observation and representation. Further studies, based on larger patient samples, should be conducted to investigate the usefulness of tDCS as an additional treatment of linguistic deficits in CBS patients.

Parkinson´s disease (PD) is not a single entity but rather a heterogeneous neurodegenerative disorder. The present study aims to conduct a critical systematic review of the literature to describe the main pharmacological treatment strategies to treat cognitive dysfunction and major depressive disorder in PD patients. We performed a search of articles cited in PubMed from 2004 to 2014 using the following MeSH terms (Medical subject headings) parkinson disease; Delirium, Dementia, Amnestic, Cognitive disorders and parkinson disease; depression; depressive disorder major; drug therapy. We found a total of 71 studies related to pharmacological treatment in cognitive dysfunction and 279 studies for pharmacological treatment in major depressive disorder. After fulfillment of all the inclusion and exclusion criteria, 13 articles remained for cognitive dysfunction and 11 for major depressive disorder, which are presented and discussed in this study. Further research into non-motor symptoms of PD may provide insights into mechanisms of neurodegeneration, and provide better quality of life by using rational drugs.

Stroke often aggravated age-related cognitive impairments that strongly affect several aspects of quality of life. However, few studies are, to date, focused on rehabilitation strategies that could improve cognition. Among possible interventions, aerobic training is well known to enhance cardiovascular and motor functions but may also induce beneficial effects on cognitive functions. To assess the effectiveness of aerobic training on cognition, it seems necessary to know whether training promotes the neuroplasticity in brain areas involved in cognitive functions. In the present review, we first explore in both human and animal how aerobic training could improve cognition after stroke by highlighting the neuroplasticity mechanisms. Then, we address the potential effect of combinations between aerobic training with other interventions, including resistance exercises and pharmacological treatments. In addition, we postulate that classic recommendations for aerobic training need to be reconsidered to target both cognition and motor recovery because the current guidelines are only focused on cardiovascular and motor recovery. Finally, methodological limitations of training programs and cognitive function assessment are also developed in this review to clarify their effectiveness in stroke patients. [ABSTRACT FROM AUTHOR]

Cognitive abilities, such as memory, learning, language, problem solving, and planning, involve the frontal lobe and other brain areas. Not much is known yet about the molecular basis of cognitive abilities, but it seems clear that cognitive abilities are determined by the interplay of many genes. One approach for analyzing the genetic networks involved in cognitive functions is to study the coexpression networks of genes with known importance for proper cognitive functions, such as genes that have been associated with cognitive disorders like intellectual disability (ID) or autism spectrum disorders (ASD). Because many of these genes are gene regulatory factors (GRFs) we aimed to provide insights into the gene regulatory networks active in the human frontal lobe. Using genome wide human frontal lobe expression data from 10 independent data sets, we first derived 10 individual coexpression networks for all GRFs including their potential target genes. We observed a high level of variability among these 10 independently derived networks, pointing out that relying on results from a single study can only provide limited biological insights. To instead focus on the most confident information from these 10 networks we developed a method for integrating such independently derived networks into a consensus network. This consensus network revealed robust GRF interactions that are conserved across the frontal lobes of different healthy human individuals. Within this network, we detected a strong central module that is enriched for 166 GRFs known to be involved in brain development and/or cognitive disorders. Interestingly, several hubs of the consensus network encode for GRFs that have not yet been associated with brain functions. Their central role in the network suggests them as excellent new candidates for playing an essential role in the regulatory network of the human frontal lobe, which should be investigated in future studies. [ABSTRACT FROM AUTHOR]

Aim. To evaluate the ability of five clinimetric instruments to discriminate between subjects >60 years of age living at home versus those living in a residency.Methods. Trained nutritionists applied five instruments (Cognition/ Depression/ Functionality/ Nutrition/ Appetite) to 285 subjects with majorities of women (64%), aged

Kleine-Levin syndrome (KLS) is an episodic hypersomnia with cognitive disturbances such as confusion, apathy and derealisation. Hyperphagia and hyper sexuality occur in around 50% of cases. No evidence-based treatments have been established for Kleine Levin syndrome. Many drugs have been tried, most often with little success. Here a case with a striking response to lithium is presented.

Background: Corticobasal Syndrome (CBS) is a neurodegenerative disorder that overlaps both clinically and neuropathologically with Frontotemporal dementia (FTD) and is characterized by apraxia, alien limb phenomena, cortical sensory loss, cognitive impairment, behavioral changes and aphasia. It has been recently demonstrated that transcranial direct current stimulation (tDCS) improves naming in healthy subjects and in subjects with language deficits. Objective: The aim of the present study was to explore the extent to which anodal tDCS over the parietal cortex (PARC) could facilitate naming performance in CBS subjects. Methods: Anodal tDCS was applied to the left and right PARC during object and action naming in seventeen patients with a diagnosis of possible CBS. Participants underwent two sessions of anodal tDCS (left and right) and one session of placebo tDCS. Vocal responses were recorded and analyzed for accuracy and vocal Reaction Times (vRTs). Results: A shortening of naming latency for actions was observed only after active anodal stimulation over the left PARC, as compared to placebo and right stimulations. No effects have been reported for accuracy. Conclusions: Our preliminary finding demonstrated that tDCS decreased vocal reaction time during action naming in a sample of patients with CBS. A possible explanation of our results is that anodal tDCS over the left PARC effects the brain network implicated in action observation and representation. Further studies, based on larger patient samples, should be conducted to investigate the usefulness of tDCS as an additional treatment of linguistic deficits in CBS patients. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is not a single entity but rather a heterogeneous neurodegenerative disorder.The present study aims to conduct a critical systematic review of the literature to describe the main pharmacological strategies to treat cognitive dysfunction and major depressive disorder in PD patients. We performed a search of articles cited in PubMed from 2004 to 2014 using the following MeSH terms (Medical subject headings) "Parkinson disease"; "Delirium," "Dementia," "Amnestic," "Cognitive disorders," and "Parkinson disease"; "depression," "major depressive disorder," "drug therapy."We found a total of 71 studies related to pharmacological treatment in cognitive dysfunction and 279 studies for pharmacological treatment in major depressive disorder. After fulfillment of all the inclusion and exclusion criteria, 13 articles remained for cognitive dysfunction and 11 for major depressive disorder, which are presented and discussed in this study. Further research into non-motor symptoms of PD may provide insights into mechanisms of neurodegeneration, and provide better quality of life by using rational drugs. [ABSTRACT FROM AUTHOR]

A 54-year-old woman was referred to our Korsakoff Center because of extensive cognitive problems following acuteWernicke's encephalopathy (WE). She had a relatively short history of alcohol abuse and was found lying on the floor in her home by her son. After 5 days without treatment, she was diagnosed with WE in a general hospital. During the course of the disease, minimal change to the acute situation occurred, with chronic confusion, attention deficits, and incoherent behavior symptoms most notable unlike classical Korsakoff's syndrome. Neuropsychological assessment after 4 and 16 months after admission to the hospital revealed global cognitive decline, with striking impairments in attentional, executive, and memory functions.The present case study suggests that the state of confusion and the neuropsychological symptoms inWE can become chronic in case of very late treatment.We therefore recommend that confused alcoholics should receive appropriate parenteral thiamine according to the current clinical standards. [ABSTRACT FROM AUTHOR]

The author discusses the interaction of sensorimotor and multisensory integration in speech perception. Topics discussed include the visual speech perception of individual with autism spectrum disorder (ASD), the use of cued speech in person with hearing impairment, and the investigations on the interaction between the motor and auditory brain during the auditory speech perception using magnetoencephalography.