Evidence map›Paper›PMID 39863324›Full record

ArticleThe journal of prevention of Alzheimer's disease2025

Distinct CSF α-synuclein aggregation profiles associated with Alzheimer's disease phenotypes and MCI-to-AD conversion.

Yanfei Ding, Lingbing Wang, Jun Liu, Yulei Deng, Yang Jiao, Aonan Zhao, Alzheimer's Disease Neuroimaging Initiative (ADNI)

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Article in The journal of prevention of Alzheimer's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

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5citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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5 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Yanfei DingDepartment of Neurology and Institute of Neurology, Ruijin Hospital affiliated to the Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
Lingbing WangDepartment of Neurology and Institute of Neurology, Ruijin Hospital affiliated to the Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
Jun LiuDepartment of Neurology and Institute of Neurology, Ruijin Hospital affiliated to the Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
Yulei DengDepartment of Neurology and Institute of Neurology, Ruijin Hospital affiliated to the Shanghai Jiaotong University School of Medicine, Shanghai 200025, China. Electronic address: dyl10786@rjh.com.cn.
Yang JiaoDepartment of Neurology and Institute of Neurology, Ruijin Hospital affiliated to the Shanghai Jiaotong University School of Medicine, Shanghai 200025, China. Electronic address: drjiaoyang@163.com.
Aonan ZhaoDepartment of Neurology and Institute of Neurology, Ruijin Hospital affiliated to the Shanghai Jiaotong University School of Medicine, Shanghai 200025, China. Electronic address: aonanzhao@gmail.com.
Alzheimer's Disease Neuroimaging Initiative (ADNI)The ADNI is detailed in Supplemental Acknowledgments.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundα-Synuclein (α-Syn) pathology is present in 30-50 % of Alzheimer's disease (AD) patients, and its interactions with tau proteins may further exacerbate pathological changes in AD. However, the specific role of different aggregation forms of α-Syn in the progression of AD remains unclear.

objectivesTo explore the relationship between various aggregation types of CSF α-Syn and Alzheimer's disease progression.

designWe conducted a retrospective analysis of data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) to examine the association between different α-Syn aggregation forms-Syn0 (no detectable α-Syn aggregates) and Syn1 (α-Syn aggregates detected, resembling those found in Parkinson's disease)-with the pathological and clinical features of AD. Additionally, we evaluated their potential as predictors of conversion from mild cognitive impairment (MCI) to AD.

settingThe ADNI database.

participantsA total of 250 participants, including 70 cognitively normal controls, 119 patients diagnosed with MCI, and 61 patients diagnosed with AD. MEASUREMENTS: Pearson correlation was employed to assess the relationship between α-Syn levels and cerebrospinal fluid (CSF) biomarkers, including total tau (T-tau), phosphorylated tau (p-tau), and amyloid-β

resultsCompared with controls, overall MCI and AD patients had elevated α-Syn levels. Notably, in the α-Syn0 group, α-Syn levels were increased in the MCI patients and further increased in AD patients, whereas in the α-Syn1 group, α-Syn levels did not significantly differ across diagnostic groups. Both in the α-Syn0 and α-Syn1 groups, α-Syn levels were found to correlate more strongly with CSF tau levels than with Aβ

conclusionsCSF α-Syn is associated with tau pathology and neurodegeneration in Alzheimer's disease. The distinct aggregation profiles of α-Syn serve as valuable biomarkers, offering insights into differing prognoses in AD and aiding in the prediction of early disease progression.

Indexed as

alpha-SynucleinAlzheimer DiseaseCognitive DysfunctionAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersDisease ProgressionFemaleHumansMalePhenotypeRetrospective Studiestau Proteinsalpha-SynucleinAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer's diseaseCerebrospinal fluidMild cognitive impairmentα-Synuclein

Identifiers

PMID39863324
PMCPMC12184058

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