Evidence map›Paper›PMID 41065931›Full record

ArticleNeurology and therapy2025

Cognitive Function and Proteomic Changes in Patients with Autoantibody-Positive Neurodegenerative Dementia.

Jin Gong, Chang Xu, Wenxian Sun, Heya Luan, Pin Wang, Xiaodong Han, Shaoqi Li, Cuibai Wei

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PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Jin Gong *College of Integrated Traditional Chinese and Western Medicine, Changchun University of Chinese Medicine, Changchun, China.
Chang Xu *Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, 45 Changchun Street, Beijing, 100053, China.
Wenxian Sun *Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, 45 Changchun Street, Beijing, 100053, China.
Heya LuanInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, 45 Changchun Street, Beijing, 100053, China.
Pin WangInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, 45 Changchun Street, Beijing, 100053, China.
Xiaodong HanInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, 45 Changchun Street, Beijing, 100053, China.
Shaoqi LiCollege of Integrated Traditional Chinese and Western Medicine, Changchun University of Chinese Medicine, Changchun, China.
Cuibai WeiInnovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, 45 Changchun Street, Beijing, 100053, China. weicb@xwhosp.org.

Funding

National Natural Science Foundation of China No.82471405STI2030-Major Projects No.2021ZD0201802
6 · The paper itself

Abstract

introductionNeurodegenerative dementia (ND) is characterized by progressive cognitive decline. The role of autoantibodies in ND remains controversial, as they may contribute to neurological damage or, under certain pathophysiological conditions, exert protective effects. In this study, we aimed to analyze the clinical characteristics of patients with autoantibody-positive ND and investigate potential molecular mechanisms using proteomics.

methodsThe study included 13 patients with autoantibody-positive ND (ND +), 13 with autoantibody-negative ND (ND -), and 13 cognitively normal controls. Differentially expressed proteins (DEPs) were identified through proteomic analysis. Bioinformatics approaches were employed to explore potential pathways and mechanisms. Multiple linear regression analysis was performed to examine the effects of DEPs on cognitive function and their interaction with autoantibody status.

resultsThe ND + and ND - groups displayed similar overall cognitive status, levels of depression or anxiety symptoms, and mental and behavioral abnormalities. The ND + group demonstrated better daily living abilities and superior frontal lobe cognitive function. Proteomic analysis identified 162 DEPs associated with autoantibodies enriched in pathways related to endocytosis, endoplasmic reticulum protein processing, tight junctions, and cellular adhesion. In the ND + group, β-arrestin-1 (ARRB1, β = 3.31, 95% CI: 1.56-5.05) and calpain-2 (CAPN2, β = 0.32, 95% CI: 0.09-0.55) were positively associated with Frontal Assessment Battery (FAB) scores, whereas no such associations were observed in the ND - group. Conversely, in the ND- group, UDP-glucose:glycoprotein glucosyltransferase 1 (UGGT1, β = - 2.38, 95% CI: -4.12 to-0.64) was negatively associated with FAB, with no corresponding effect in the ND + group.

conclusionThis exploratory study provides preliminary evidence of distinct clinical and molecular signatures in autoantibody-positive neurodegeneration. ARRB1 and CAPN2 may contribute to cognitive resilience in this group, while UGGT1 appears associated with cognitive decline in autoantibody-negative cases. Owing to the limited sample size, these findings should be considered hypothesis-generating and warrant validation in larger, independent cohorts before consideration as biomarkers or therapeutic targets.

Indexed as

AutoantibodiesNeurodegenerative dementiaNeuropsychological characteristicsProteomics

Identifiers

PMID41065931
PMCPMC12623529

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