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Obsessive-compulsive disorder (OCD) frequently co-occurs with various psychiatric conditions and may impact as many as one-fifth of individuals diagnosed with bipolar disorder (BD). Despite the expanding body of literature on the coexistence of OCD and BD, there is a notable lack of comprehensive data pertaining to the distinct features of obsessive-compulsive symptoms that define this comorbidity. To bridge this knowledge gap, we conducted a systematic search of PubMed/MEDLINE, Scopus, EMBASE, and PsycINFO until August 7th, 2023. We performed random-effects meta-analyses to compare individuals with both OCD and BD to those with OCD in terms of OCD symptomatology as well as the specific categories of obsessions and compulsions. Out of the 10,393 records initially screened, 17 studies were ultimately incorporated into the qualitative assessment, with 15 of them being included in the quantitative analysis. Individuals with OCD and BD experienced fewer lifetime contamination obsessions (OR=0.71; 95 %CI=0.53, 0.95; p = 0.021) and more sexual obsessions (OR=1.77; 95 %CI=1.03, 3.04; p = 0.04) compared to individuals with OCD without BD. No significant difference was observed for other types of obsessions or compulsions or for the severity of OCD symptoms, although BD type may play a role according to meta-regression analyses. The detection of the presence of sexual or contamination obsessions through a detailed interview may be the focus of clinical attention when assessing OCD in the context of comorbid BD. Sub-phenotyping complex clinical presentation of comorbid psychiatric disorders can aid in making more informed decisions when choosing an appropriate treatment approach., Competing Interests: Declaration of Competing Interest EV has received grants and served as consultant, advisor, or CME speaker for the following entities: AB-Biotics, AbbVie, Angelini, Biogen, Biohaven, Boehringer-Ingelheim, Celon Pharma, Compass, Dainippon Sumitomo Pharma, Ethypharm, Ferrer, Gedeon Richter, GH Research, Glaxo-Smith Kline, Idorsia, Janssen, Lundbeck, Medincell, Novartis, Orion Corporation, Organon, Otsuka, Rovi, Sage, Sanofi-Aventis, Sunovion, Takeda, and Viatris, outside the submitted work; GF has received CME-related honoraria, or consulting fees from Angelini, Janssen-Cilag and Lundbeck; GF's work is supported by a fellowship from "La Caixa" Foundation (ID 100010434 fellowship code LCF/BQ/DR21/11880019). All other authors have no conflicts to declare., (Copyright © 2023. Published by Elsevier B.V.)

Objective: Mutations in the valosin-containing protein (VCP) gene cause autosomal dominant multisystem proteinopathy 1 (MSP1), characterized by a variable combination of inclusion body myopathy (IBM), Paget's disease of bone (PDB), and frontotemporal dementia (FTD). Here we report a novel VCP missense mutations in an Italian family with FTD as the prevalent manifestation and compare our results with those described in the literature., Methods: We described the clinical, molecular, and imaging data of the studied family. We also conducted a systematic literature search with the aim of comparing our findings with previously reported VCP-related phenotypes., Results: A novel heterozygous VCP missense mutation (c 0.473 T > C/p.Met158Thr) was found in all the affected family members. The proband is a 69-year-old man affected by progressive muscle weakness since the age of 49. Muscle MRI showed patchy fatty infiltration in most muscles, and STIR sequences revealed an unusual signal increase in distal leg muscles. At age 65, he presented a cognitive disorder suggestive of behavioral variant FTD. A bone scintigraphy also revealed PDB. The patient's mother, his maternal aunt and her daughter had died following a history of cognitive deterioration consistent with FTD; the mother also had PDB. No relatives had any muscular impairments. Reviewing the literature data, we observed a different sex distribution of VCP-related phenotypes, being FTD prevalence higher among women as compared to men (51.2 % vs 31.2 %) and IBM prevalence higher among men as compared to women (92.1 % vs 72.8 %)., Discussion: This study broadened our clinical, genetic, and imaging knowledge of VCP-related disorders., Competing Interests: Declaration of Competing Interest The authors declare no competing interests., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Advantages and limits of the use of cholinesterase inhibitors (ChEI) in Alzheimer's disease (AD) are well established. Their effects result from an increase in extracellular acetylcholine (ACh) whose hydrolysis is prevented by cholinesterase inhibition. In this way, the cholinergic deficit which characterizes AD may be corrected. This overview discusses which components of the cognitive process are improved by ChEI administration. In animal experiments, the increase in ACh release, detected in brain areas during behavioral tasks designed to tax attentional processes, demonstrates that an activation of cholinergic neurons underlies arousal and attention. Since arousal and attention depend on activation of the forebrain cholinergic system, it is to be expected that the loss of cholinergic neurons occurring in AD may lead to impairment of the attentional processes. Indeed, a consensus exists that attention is the first non-memory domain to be affected in AD, before deficits in language and visuo-spatial functions. The difficulties with daily living, which occur even in mild AD, may be related to attentional deficits. ChEIs, by restoring the cholinergic activity, should improve attention. If the cognitive changes resulting from ChEI treatment in AD patients are assessed with appropriate tests or selected items of the scales, a predominant effect on attention and executive functions emerges. In a group of 121 subjects with mild to moderate AD, (MMSE score 21.88 ± 3.63) followed in the Alzheimer Unit in Florence, after a year of treatment with standard doses of ChEIs, it was observed a stabilization of the disease, characterized by no changes of the tests evaluating attention and executive functions but a worsening of those involving memory mechanisms. These findings suggest that ChEI treatment preserves attention more than memory. Finally, the electrophysiological and neurochemical mechanisms through which the activation of the cholinergic forebrain neurons enhance attention and create the condition for information acquisition are reviewed., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

A 46-year-old woman who presented with prosopagnosia was clinically evaluated. Results of neuropsychological measures showed severe impairment in oral naming with anomia and a marked deficit in naming and recognition of famous faces. The clinical diagnosis was semantic dementia (SD). Genetic testing revealed a missense mutation V363I in exon 12 of the microtubule-associated protein tau (MAPT) gene. This is the description of an association between a mutation in the MAPT gene and a case of SD. The same mutation was recently described in a case of progressive non-fluent aphasia, but the prominent presenting feature in tau gene mutation cases is the behavioral variant of frontotemporal dementia, with typical symmetrical frontotemporal atrophy., (2010 Elsevier B.V. All rights reserved.)

To evaluate whether inflammation-like mechanisms present in the brain of Alzheimer's disease (AD) patients are reflected in the periphery, the expression of CD11b in peripheral blood neutrophils and the expression and activity of inflammatory markers in cultured skin fibroblasts were examined. We found significantly higher levels of CD11b in neutrophils from sporadic AD patients than in controls and this elevation was positively correlated with disease severity and progression rate of mental decline. Cultured skin fibroblasts from familial (FAD) and sporadic AD patients and from controls were immunopositive for both isoforms of cyclooxygenase with no differences between groups. In unstimulated culture, the production of prostaglandin-E2 in the medium was significantly higher in fibroblasts from sporadic AD and FAD patients than in controls, and this elevation was reverted by the addition of 25 microM of ibuprofen. Our findings provide further evidence of the presence of inflammatory and immuno-related markers in the periphery of AD patients and support those studies indicating the beneficial effects of anti-inflammatory therapy in AD.

Background and Purpose: The majority of studies on neuropsychological complications after cardiac surgery used the raw variation of selective tests scores to define the occurrence of cognitive decline. We prospectively estimated the frequency of cognitive impairment after cardiac surgery, with a particular emphasis on persistent and clinically relevant cognitive decline. Possible baseline and operative predictors were also evaluated., Methods: An extensive neuropsychological battery was administered to 110 patients (mean age 64.1+/-9.4 years; 70.9% males) undergoing cardiac surgery before and 6 months after the operation. After evaluating the variations in the cognitive performances, two independent neuropsychologists ranked the patients as unchanged-improved, mildly-moderately deteriorated, or severely deteriorated, using a global and functionally oriented judgement. The degree of the impairment was determined in relation to its impact on everyday life activities., Results: Ten patients (9.1%) were ranked as severely deteriorated, 22 (20%) as mildly-moderately deteriorated, and 78 (70.9%) as unchanged-improved. Cognitively impaired patients were older (p=0.031), more often females (p=0.005), with a low education level (p=0.013). At multivariate analysis, female gender (odds ratio (OR) 6.14, 95% confidence interval (95% CI) 2.16-17.50), baseline use of beta-blockers (OR 4.55, 95% CI 1.30-15.92), and PaO2 at arrival in intensive care unit (OR for 1 mm Hg increment 1.012, 95% CI 1.004-1.020) were significant predictors of cognitive impairment of any degree. Positive predictors of severe cognitive impairment were history of hypertension (OR 5.33, 95% CI 1.03-27.64) and PaO2 at arrival intensive care unit (OR for 1 mm Hg increment 1.020, 95% CI 1.006-1.035), while education was protective (OR per year of increment 0.53, 95% CI 0.31-0.90)., Conclusions: A considerable proportion of cardiac surgery patients may undergo clinically relevant cognitive impairment. The knowledge of variables influencing cognitive outcome is essential for the adoption of preventive measures.

The ever greater emphasis on the application of a standard work-up in the clinical diagnosis of dementia -- and Alzheimer's Disease (AD) in particular -- has made it easier to identify potentially treatable and/or reversible cases. The aim of this paper is to update the issue of treatable and reversible dementias.

The aim of this study was to establish the presence and the consistency of different cognitive profiles in AD patients taking into consideration the severity of mental impairment. Therefore we stratified 679 neuropsychological observations on 119 probable AD patients followed longitudinally on the basis of overall degree of cognitive impairment. To compare performance on tests with different score ranges we transformed raw test scores into coefficients; to summarize our results in terms of language versus visuo-spatial performance we computed indices of prevalent impairment of performance (IPIP) by subtracting the coefficients for constructional praxis from coefficients for language-related tests. Finally, we converted these indices into z-scores for each level of mental decline to identify patients with generalized, language (L) or visuo-spatial (V) prevalent impairment. The latter, 30% of the sample, can be detected at all stages of dementia. There was a higher percentage of males among language impaired patients (P<0.05). Approximately half of patients with L/V prevalent impairment continued to show such a focality when followed longitudinally. The groups did not differ in the annual rate of cognitive decline.

The aim of this 7-year inception cohort study was to determine the prognostic value of plateaux in cognitive decline in the course of Alzheimer's disease (AD) as well as their impact on the rate of progression of cognitive impairment. From a consecutive sample of 106 outpatients participating in a longitudinal study on AD, we selected 31 with a mild degree of mental deficit at presentation and a disease duration of at least 3 years when included into the study. All underwent extensive clinico-neuropsychological testing about every 6 months and there were no drop-outs. Mean period of follow-up lasted 6.8 (SD 2.9) years. Nineteen patients displayed a plateau, where a plateau refers to a patient's remaining on a mild level of cognitive decline for more than two years. Survival curves (Kaplan-Meier method) showed that patients with plateaux reached several end-points--very severe functional or cognitive impairment, urinary incontinence, death--significantly later than patients without (p < 0.04). Patients with plateaux showed a smaller cognitive loss (p < 0.01) in terms of the mean annual rate of progression of mental decline. In conclusion plateaux in an early stage of Alzheimer's Disease served to identify patients with a more favourable course.

We examined selective MRI features (localization and degree of white matter abnormalities, cortical and subcortical atrophy) in relation to cognitive decline in patients with cerebrovascular disease (CVD) and leukoaraiosis (LA). We enrolled 6 female and 18 male CVD patients (mean age 66.2 +/- 6.6 years) whose Magnetic Resonance Images (MRI) revealed LA and who displayed a history of stroke or TIA; none showed signs of cortical infarcts or normal pressure hydrocephalus. Two blind raters independently scored MRI scans with a high level of agreement. All patients underwent extensive clinico-neuropsychological assessment upon admission to the study and 19 were followed for an average of 48 +/- 7.6 months. Twelve patients were initially classified as non-demented and 12 as demented. Three years later, one in the former group had become demented and mental impairment had worsened for 6 patients in the latter group; these 7 subjects were labeled as "decliners". Ventricular indexes were significantly higher in the demented group and correlated with severity of mental impairment, while the degree of LA was similar in demented and non-demented subjects. Neither white matter lesions nor sulcal and ventricular enlargement differed statistically between decliners and non-decliners.

Some CSF protein abnormalities have been proposed as a possible marker for vascular dementia. We studied the CSF protein levels and albumin ratio in 21 patients (mean age 64.04 +/- 7.5) with progressive bilateral motor impairment, and a CT picture of leucoaraiosis. Seven of these patients also presented with dementia. Twenty-seven Alzheimer's disease patients (mean age 59.59 +/- 5.30) without leucoaraiosis were taken as controls. We also evaluated the correlations of the albumin ratio values with the diagnosis of dementia, the severity of cognitive impairment, the degree of cerebral atrophy and presence of infarcts on CT, and the abnormalities in CSF circulation, found on isotopic cisternography, in the leucoaraiosis group. After controlling for age and sex, the patients with leucoaraiosis showed greater CSF albumin levels (0.27 g/l +/- 0.11 vs. 0.21 g/l +/- 0.06; covariance analysis P = 0.066), CSF IgG values (4.68 mg/100 ml +/- 1.45 vs. 2.85 mg/100 ml +/- 1.03; covariance analysis P < 0.001), and a higher albumin ratio (0.0078 +/- 0.0027 vs. 0.0058 +/- 0.0019; covariance analysis P = 0.013) than those with Alzheimer's disease. The variations of these parameters were not apparently related to the presence of dementia in the leucoaraiosis group. A significantly higher albumin ratio was observed in patients with a slowed CSF circulation compared to those with normal CSF circulation (0.0086 +/- 0.0028 vs. 0.0059 +/- 0.0019; covariance analysis P = 0.05). We conclude that, independently from the presence of dementia, patients with leucoaraiosis have CSF abnormalities consistent with functional blood-brain barrier alterations.