The initiation of hemodialysis is associated with an accelerated decline of cognitive function and an increased incidence of cerebrovascular accidents and white matter lesions. Investigators have hypothesized that the repetitive circulatory stress of hemodialysis induces ischemic cerebral injury, but the mechanism is unclear. We studied the acute effect of conventional hemodialysis on cerebral blood flow (CBF), measured by [O]HO positron emission tomography-computed tomography (PET-CT). During a single hemodialysis session, three [O]HO PET-CT scans were performed: before, early after the start of, and at the end of hemodialysis. We used linear mixed models to study global and regional CBF change during hemodialysis. Twelve patients aged ≥65 years (five women, seven men), with a median dialysis vintage of 46 months, completed the study. Mean (±SD) arterial BP declined from 101±11 mm Hg before hemodialysis to 93±17 mm Hg at the end of hemodialysis. From before the start to the end of hemodialysis, global CBF declined significantly by 10%±15%, from a mean of 34.5 to 30.5 ml/100g per minute (difference, -4.1 ml/100 g per minute; 95% confidence interval, -7.3 to -0.9 ml/100 g per minute; =0.03). CBF decline (20%) was symptomatic in one patient. Regional CBF declined in all volumes of interest, including the frontal, parietal, temporal, and occipital lobes; cerebellum; and thalamus. Higher tympanic temperature, ultrafiltration volume, ultrafiltration rate, and pH significantly associated with lower CBF. Thus, conventional hemodialysis induces a significant reduction in global and regional CBF in elderly patients. Repetitive intradialytic decreases in CBF may be one mechanism by which hemodialysis induces cerebral ischemic injury.

The Alzheimer's disease-related cerebral glucose metabolic covariance pattern identified by SSM/PCA analysis was highly sensitive and specific for Alzheimer's disease. This method is expected to be helpful in the early diagnosis of Alzheimer's disease in clinical practice.

Neuropsychological tests, particularly for episodic memory, are used to classify patients in memory clinics. Still, the differential diagnosis between dementia of the Alzheimer’s disease type (Dementia‐AD), mild cognitive impairment (MCI), or major depressive disorder (MDD) is challenging. However, impairments in other domains, such as emotion recognition, an aspect of social cognition, might have additional value in distinguishing Dementia‐AD from MCI and MDD and hence signal progression of neurodegeneration. We evaluated this in patients visiting a memory clinic. Sixty healthy controls (HC) and 143 first time attendants of an academic hospital memory clinic who were eventually classified as Dementia‐AD (n = 45), MCI (n = 47), MDD (n = 27), or No Impairment (NI, n = 24) were included. We assessed group differences in Emotion Recognition (Ekman 60 Faces Test (EFT)) and episodic memory (Dutch Rey Auditory Verbal Learning Test (RAVLT)). With multinomial and binomial regression analysis, we assessed whether EFT was added to RAVLT in distinguishing patient groups. Dementia‐AD patients had significantly worse emotion recognition than HC, MCI, MDD, and NI groups, but no other between‐group differences were found. Episodic memory was impaired in Dementia‐AD and MCI patients. We found no memory impairments in the MDD and NI groups. Emotion recognition in addition to episodic memory was significantly better in predicting group membership than episodic memory alone. In conclusion, emotion recognition measurement had added value for differentiation between patients first visiting memory clinics, in particular in distinguishing Dementia‐AD from MCI. We recommend the standard inclusion of emotion recognition testing in neuropsychological assessment in memory clinics.

Objectives: To investigate the presence, nature and direction of the daily temporal association between depressive symptoms, cognitive performance and sleep in older individuals. Design, setting, participants: Single-subject study design in eight older adults with cognitive impairments and depressive symptoms. Measurements: For 63 consecutive days, depressive symptoms, working memory performance and night-time sleep duration were daily assessed with an electronic diary and actigraphy. The temporal associations of depressive symptoms, working memory and total sleep time were evaluated for each participant separately with time-series analysis (vector autoregressive modeling). Results: For seven out of eight participants we found a temporal association between depressive symptoms and/or sleep and/or working memory performance. More depressive symptoms were preceded by longer sleep duration in one person (r = 0.39; p < .001), by longer or shorter sleep duration than usual in one other person (B = 0.49; p < .001), by worse working memory in one person (B = −0.45; p = .007), and by better working memory performance in one other person (B = 0.35; p = .009). Worse working memory performance was preceded by longer sleep duration (r = −.35; p = .005) in one person, by shorter or longer sleep duration in three other persons (B = −0.76; p = .005, B = −0.61; p < .001; B = −0.34; p = .002), and by more depressive symptoms in one person (B = −0.25; p = .009). Conclusion: The presence, nature and direction of the temporal associations between depressive symptoms, cognitive performance and sleep differed between individuals. Knowledge of personal temporal associations may be valuable for the development of personalized intervention strategies in order to maintain their health, quality of life, functional outcomes and independence.