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Introduction: Hemodialysis (HD) patients have significant burden of cerebral ischemic pathology noted on brain imaging. These ischemic type lesions maybe due to cerebral hypoperfusion that may be occurring during blood pressure (BP) fluctuations commonly noted during HD sessions. We evaluated changes in cerebral perfusion and measured an index of cerebral autoregulation (CA index) during HD to identify potential risk factors for intradialytic decline in cerebral perfusion and impaired cerebral autoregulation. Methods: In this cross‐sectional study, we included HD patients age 50 years or older receiving conventional in‐center HD. We measured cerebral perfusion during HD, using cerebral oximetry, and calculated the correlation between cerebral perfusion and BP during HD as an index of CA. We measured the association between potential risk factors for intradialytic decline in cerebral perfusion and CA index. Findings: We included 32 participants and 118 HD sessions in our analysis. The mean ± SD decline in cerebral oxygen saturation during HD was 6.5% ± 2.9% with a relative decline from baseline values of 9.2% ± 4.4%. Greater drop in systolic BP (SBP) during HD was associated with decline in cerebral oxygen saturation, p = 0.02. Impaired CA index was noted in 37.3% of HD sessions. Having diabetes and >20 mmHg drop in SBP during HD were associated with increased (worse) CA index with an increase of 0.24 95%CI [0.06, 0.41] for diabetes and increase of 0.43 95%CI [0.27, 0.56] for a >20 mmHg drop in SBP during HD. Discussion: Cerebral perfusion can decline during HD and is associated with changes in systemic BP. This may be due to impaired cerebral autoregulation in HD patients. Risk factors for worse CA index include diabetes and >20 mmHg drop in SBP during HD. This study highlights the risk of intradialytic decline in cerebral perfusion and impaired cerebral autoregulation in HD patients. [ABSTRACT FROM AUTHOR]

Background: Physicians may soon be able to diagnose Alzheimer's disease (AD) in its early stages using fluid biomarkers like amyloid. However, it is acknowledged that additional biomarkers need to be characterized which would facilitate earlier monitoring of AD pathogenesis., Objective: To determine if a potential novel inflammation biomarker for AD, symmetric dimethylarginine, has utility as a baseline serum biomarker for discriminating prodromal AD from cognitively unimpaired controls in comparison to cerebrospinal fluid amyloid-β42 (Aβ 42 )., Methods: Data including demographics, magnetic resonance imaging and fluorodeoxyglucose-positron emission tomography scans, Mini-Mental State Examination and Functional Activities Questionnaire scores, and biomarker concentrations were obtained from the Alzheimer's Disease Neuroimaging Initiative for a total of 146 prodromal AD participants and 108 cognitively unimpaired controls., Results: Aβ 42 ( p  = 0.65) and symmetric dimethylarginine ( p  = 0.45) were unable to predict age-matched cognitively unimpaired controls and prodromal AD participants. Aβ 42 was negatively associated with regional brain atrophy and hypometabolism as well as cognitive and functional decline in cognitively unimpaired control participants ( p  < 0.05) that generally decreased in time. There were no significant associations between Aβ 42 and symmetric dimethylarginine with imaging or neurocognitive biomarkers in prodromal AD patients., Conclusions: Correlations were smaller between Aβ 42 and neuropathological biomarkers over time and were absent in prodromal AD participants, suggesting a plateau effect dependent on age and disease stage. Evidence supporting symmetric dimethylarginine as a novel biomarker for AD as a single measurement was not found., Competing Interests: The authors have no conflicts of interest to report., (© 2023 – The authors. Published by IOS Press.)