In vivo detection of Alzheimer's and Lewy body disease concurrence : Clinical implications and future perspectives
Baiardi, Simone ; Hansson, Oskar LU
; Levin, Johannes
and Parchi, Piero
(2024)
In Alzheimer's and Dementia
20(8).
p.5757-5770
- 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... (More)
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.
(Less)
- author
- Baiardi, Simone
; Hansson, Oskar
LU
; Levin, Johannes
and Parchi, Piero
- organization
- publishing date
- 2024-08
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- dementia, Lewy body disease, prions, real-time quaking-induced conversion, RT-QuIC, synuclein
- in
- Alzheimer's and Dementia
- volume
- 20
- issue
- 8
- pages
- 14 pages
- publisher
- Wiley
- external identifiers
-
- pmid:38955137
- scopus:85196623142
- ISSN
- 1552-5260
- DOI
- 10.1002/alz.14039
- language
- English
- LU publication?
- yes
- id
- a2e662db-0140-4431-b972-e3405643d0a7
- date added to LUP
- 2024-09-04 10:48:51
- date last changed
- 2025-12-12 06:23:56
@article{a2e662db-0140-4431-b972-e3405643d0a7,
abstract = {{<p>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.</p>}},
author = {{Baiardi, Simone and Hansson, Oskar and Levin, Johannes and Parchi, Piero}},
issn = {{1552-5260}},
keywords = {{dementia; Lewy body disease; prions; real-time quaking-induced conversion; RT-QuIC; synuclein}},
language = {{eng}},
number = {{8}},
pages = {{5757--5770}},
publisher = {{Wiley}},
series = {{Alzheimer's and Dementia}},
title = {{In vivo detection of Alzheimer's and Lewy body disease concurrence : Clinical implications and future perspectives}},
url = {{http://dx.doi.org/10.1002/alz.14039}},
doi = {{10.1002/alz.14039}},
volume = {{20}},
year = {{2024}},
}