A comparison between tau and amyloid-β cerebrospinal fluid biomarkers in chronic traumatic encephalopathy and Alzheimer disease
Year: 2022
Type: article
Study design: Observational Study
Abstract: Background Cerebrospinal fluid (CSF) tau and beta-amyloid levels in chronic traumatic encephalopathy (CTE), a disease which can be clinically indistinguishable from Alzheimer’s disease (AD), are largely unknown. We examined postmortem CSF analytes among participants with autopsy confirmed CTE and AD. Methods In this cross-sectional study 192 participants from the Boston University AD Research Center, VA-BU-CLF Center, and Framingham Heart Study (FHS) had post-mortem CSF collected at autopsy. Participants were divided into pathological groups based on AD and CTE criteria, with 61 CTE participants (18 low, 43 high stage), 79 AD participants (23 low, 56 intermediate to high), 11 participants with CTE combined with AD, and 41 participants lacking both CTE and AD neuropathology. The Meso Scale Discovery immunoassay system was utilized to measure amyloid-beta (Aβ1-40, Aβ1-42), total tau (t-tau), and phosphorylated tau (p-tau181 and p-tau231). CSF analytes were then compared across the pathological groups: no CTE/no AD (control), Low CTE, Low AD, High CTE, Intermediate/High AD, and AD+CTE. Results Among the Low disease state groups, the Low CTE group had significantly higher levels of p-tau231 versus the control group and compared to the Low AD group. The Low CTE group was also found to have significantly lower levels of Aβ1-42 compared to the control group. The high CTE group had higher levels of p-tau231 and lower levels of Aβ1-42 compared to Intermediate/High AD group. Conclusions Importantly, p-tau231 and Aβ1-42 were predictors of diagnosis of CTE vs. control and CTE vs. AD. Increased CSF p-tau231 is a promising potentially sensitive biomarker of CTE, and CSF Aβ1-42 needs further investigation in CTE.
Source: Alzheimer s Research & Therapy
Authors: Katherine W. Turk, Alexandra Geada, Victor E. Alvarez, Weiming Xia, Jonathan D. Cherry, Raymond Nicks, Gaoyuan Meng, Sarah Daley, Yorghos Tripodis, Bertrand R. Huber, Andrew E. Budson, Brigid Dwyer, Neil W. Kowall, Robert C. Cantu, Lee E. Goldstein, Douglas I. Katz, Robert A. Stern, Michael L. Alosco, Jesse Mez, Ann C. McKee, Thor D. Stein
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,590
Awards: Traumatic Brain Injury and Repetitive Head Impacts: Contributions to AD/ADRD and CTE Neuropathology and Resulting Clinical Syndromes, G1156429883, G1353455142, G1949952796, G232440474, G245591028, G2630878680, G278200998, G2832038100, G3082176553, G3209124882, G3314419202, G3405256882, G3638081280, G3863744514, G388207060, G4300776172, G4728830014, G490679232, G4976486911, G500195777, G5034879460, Genetic and Neuropsychological Heterogeneity in Alzheimer's Disease, G5616488268, G5641610277, G6150795155, G6246110153, G6279095307, G6550790558, G6726222290, G7310125909, G7543333412, Age-Associated Lipidomic Changes in Alzheimer's Disease, Boston University Alzheimer's Disease Center, Age-Associated Lipidomic Changes in Alzheimer's Disease, G818144582, G8273196722, Precision Monitoring and Assessment in the Framingham Study: Cognitive, MRI, Genetic and Biomarker Precursors of AD & Dementia, Tau Pathology in CTE vs. Alzheimer's Disease: Microvasculopathy and Neuroinflammation, G955521001
OpenAlex ID: W4220712090
