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2% to 92.6%. When predicting performance using a more comprehensive battery of criterion neuropsychological tests, we identified less then 22 as the most accurate MoCA cut score to identify a clinically relevant level of impairment and less then 24 to identify milder cognitive impairment. [https://www.selleckchem.com/products/ttk21.html Epigenetic Reader Domain activator] Conclusions Our findings suggest that a MoCA cut score of less then 26 carries a risk of misdiagnosis of cognitive impairment, and scores in the range of less then 22 to less then 24 are more reliable for identifying cognitive impairment.Background Semantic dementia (SD) is characterized by progressive semantic anomia extending to a multimodal loss of semantic knowledge. Although often considered an early-onset dementia, SD also occurs in later life, when it may be misdiagnosed as Alzheimer disease (AD). Objective To evaluate late-onset SD in comparison to early-onset SD and to AD. Methods We identified 74 individuals with SD and then compared those with late-onset SD (≥65 years of age) to those with early-onset SD ( less then 65) on demographic and clinical features. We also compared a subgroup of 23 of the late-onset SD individuals with an equal number of individuals with clinically probable AD. Results Twenty-six (35.1%) of the SD individuals were late onset, and 48 (64.9%) were early onset. There were no differences between the two groups on clinical measures, although greater asymmetry of temporal involvement trended to significance in the late-onset SD group. Compared to the 23 AD individuals, the subgroup of 23 late-onset SD individuals had worse performance on confrontational naming, irregular word reading, and face recognition; however, this subgroup displayed better verbal delayed recall and constructions. The late-onset SD individuals also experienced early personality changes at a time when most individuals with AD had not yet developed behavioral changes. Conclusions Approximately one-third of SD individuals may be late onset, and the differentiation of late-onset SD from AD can lead to better disease management, education, and prognosis. SD may be distinguished by screening for disproportionate changes in reading, face recognition, and personality.Background Sustained cognitive testing is used to detect cognitive fatigability and is often considered a substitute for subjective cognitive fatigue (CF). However, the relationship between cognitive fatigability and subjective CF in people with multiple sclerosis (PwMS) remains undetermined. Objective To explore potential associations between fatigability induced by sustained cognitive testing and subjective CF in PwMS. Methods We gave 120 PwMS and 60 demographically matched, healthy individuals the Beck Depression Inventory-FastScreen (BDI-FS) to measure mood and the Modified Fatigue Impact Scale to measure CF. In addition, we used the Quotient ADHD Test, a sustained attention test, to measure cognitive fatigability. We also explored potential correlations between the individuals' performance on the sustained attention test and thalamic volume using recent MRI scans. Results Forty-one (34.2%) of the PwMS exhibited cognitive fatigability. These 41 were found to be significantly older (P=0.006), had been diagnosed with the disease for longer (P=0.03), had higher scores (P less then 0.001) on the Expanded Disability Status Scale, and had reduced thalamic volume (P=0.04) compared with the 79 (65.8%) PwMS not exhibiting cognitive fatigability. The PwMS exhibiting cognitive fatigability scored similarly on the BDI-FS (P=0.21) and self-reported similar rates of CF (P=0.62) as the PwMS not exhibiting cognitive fatigability. Conclusion Cognitive fatigability induced by sustained cognitive testing is not an accurate clinical alternative to subjective CF. This study provides evidence to support cognitive fatigability and CF in PwMS as two distinct concepts.Background Cognitive impairment is often identified in individuals with bipolar disorder and is associated with their functional impairment. However, there is controversy surrounding potential classification methods for impairment in cognitive measures. Objective To examine the proportion of cognitive measures indicating impairment of attention, processing speed, memory, visuoconstructional abilities, and executive functions in individuals with bipolar disorder type I (euthymic) and healthy controls, using a strict criterion for defining impairment. Methods We gave 43 individuals with bipolar disorder type I and 17 healthy controls a comprehensive clinical and neuropsychological assessment. All scores were standardized using means and standard deviations according to age. Impaired performance in all cognitive measures was determined using a distribution-based threshold of z=±1645. The effects of the sociodemographic and clinical variables on cognitive performance were examined using multiple stepwise backward regression analyses. Results Clinically significant cognitive impairment was observed more frequently in the bipolar disorder group, compared to controls, on all measures. From participant factors, we found that level of education and number of manic episodes predicted variation in more cognitive measure scores. Discussion The use of population-based norms to standardize cognitive measures, and a strict criterion to define cognitive impairment, in individuals with bipolar disorder type 1 and healthy controls resulted in a prevalence of impairment in cognitive domains' frequencies of deficits that fell within the ranges previously reported in meta-analyses. Conclusions Clinically introducing population norms and a stringent cognitive impairment criterion can facilitate more accurate measures of cognitive impairment in individuals with bipolar disorder.Multiple sclerosis (MS) is the most common inflammatory neurologic disease in young adults. Its pathological mechanisms include demyelination, neurodegeneration, and synaptopathy. Cognitive deficits occur in up to 65% of individuals with MS and affect both nonsocial (eg, information processing speed, memory, and executive functions) and social (ie, emotion recognition, theory of mind, and empathy) cognitive domains. In the last 3 decades, there has been a growing interest in social cognition and its relationship with neuropsychological, sociodemographic, and disease characteristics in individuals with MS. Uncovering the neuropathological correlates of social cognitive deficits is now a crucial aim that would also help us better understand the underlying mechanisms of social cognition. We reviewed 11 neuroimaging studies to investigate social cognition in MS. These studies focused mainly on facial emotion recognition and theory of mind, with the findings suggesting that a disrupted cortico-subcortical network forms the basis of social deficits involving both domains.