Abstract
INTRODUCTION
The recent introduction of seed amplification assays (SAAs) detecting misfolded α-synuclein, a pathology-specific marker for Lewy body disease (LBD), has allowed the in vivo identification and phenotypic characterization of patients with co-occurring Alzheimer’s disease (AD) and LBD since the early clinical or even preclinical stage.
METHODS
We reviewed studies with an in vivo biomarker-based diagnosis of AD-LBD copathology.
RESULTS
Studies in large cohorts of cognitively impaired individuals have shown that cerebrospinal fluid (CSF) biomarkers detect the coexistence of AD and LB pathology in approximately 20%–25% of them, independently of the primary clinical diagnosis. Compared to those with pure AD, AD-LBD patients showed worse global cognition, especially in attentive/executive and visuospatial functions, and worse motor functions. In cognitively unimpaired individuals, concurrent AD-LBD pathologies predicted longitudinal cognitive progression with faster worsening of global cognition, memory, and attentive/executive functions.
DISCUSSION
Future research studies aiming for a better precision medicine approach should develop SAAs further to reach a quantitative evaluation or staging of each underlying pathology using a single biofluid sample.
Highlights
α-Synuclein seed amplification assays (SAAs) provide a specific marker for Lewy body disease (LBD).
SAAs allow for the in vivo identification of co-occurring LBD in patients with Alzheimer’s disease (AD).
AD-LBD coexist in 20-25% of cognitively impaired elderly individuals, and ∼8% of those asymptomatic.
Compared to pure AD, AD-LBD causes a faster worsening of cognitive functions.
AD-LBD is associated with worse attentive/executive, memory, visuospatial and motor functions.
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This post is Copyright: Simone Baiardi,
Oskar Hansson,
Johannes Levin,
Piero Parchi | June 22, 2024