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Plasma Biomarker Predicts Cognitive Decline in Preclinical Alzheimer Disease
Plasma P-tau217 significantly predicted longitudinal cognitive decline in people with preclinical Alzheimer disease, according to study results published in JAMA Neurology.
“Alzheimer disease pathology starts with a prolonged phase of β-amyloid (Aβ) accumulation without symptoms. The duration of this phase differs greatly among individuals,” researchers explained in the study. “While this disease phase has high relevance for clinical trial designs, it is currently unclear how to best predict the onset of clinical progression.”
The study investigated various plasma biomarkers for predicting cognitive decline in Aβ-positive participants without cognitive impairment using data from 2 prospective longitudinal cohort studies: the Swedish BioFINDER-1 study and the Wisconsin Registry for Alzheimer Prevention (WRAP) study. Aβ pathology was defined via cerebrospinal fluid Aβ42/40 in BioFINDER-1 and by Pittsburgh Compound B positron emission tomography in WRAP. A total 171 participants were included in the main analysis.
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Among 119 participants from BioFINDER-1, the best marker to predict cognitive decline on the modified Preclinical Alzheimer Cognitive Composite and the Mini-Mental State Examination over a median 6 years was plasma P-tau217, according to the study. The results were validated in 52 participants from the WRAP study.
Additionally, baseline plasma P-tau217 was associated with conversion to Alzheimer disease in the BioFINDER-1 cohort, the study found.
In simulated hypothetical clinical trials of Aβ-positive individuals without cognitive impairment, the inclusion of plasma P-tau217 led to large reductions in sample sizes. Consequently, researchers believe that adding plasma P-tau217 could increase the power of trials in the earliest stages of Alzheimer’s disease.
“These findings,” the authors concluded, “suggest that plasma P-tau217 may be used as a complement to cerebrospinal fluid or positron emission tomography for participant selection in clinical trials of novel disease-modifying treatments.”
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