ArticleScientific reports2025
Synaptic markers are associated with cognitive decline after accounting for amyloid burden among an at-risk Alzheimer's disease cohort.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Plasma proteomic signatures of preclinical Alzheimer's disease in clinically unimpaired older adults.Molecular neurodegeneration · 2026Article
- Review
- Integrating functional network topology, synaptic density, and tau pathology to predict cognitive decline in amnestic mild cognitive impairment.Journal of neurology · 2026Article
- BDNF-amyloid-Frontiers in molecular neuroscience · 2026Review
- Plasma proteomic signatures of preclinical Alzheimer's disease biomarkers and memory in clinically unimpaired older adults.medRxiv : the preprint server for health sciences · 2025Article
- Cerebrospinal fluid markers link to synaptic plasticity responses and Alzheimer's disease genetic pathways.Molecular neurodegeneration · 2025Article
- Plasma Neurofilament Light Chain in Patients Affected by Alzheimer's Disease with Different Rate of Progression: A Retrospective Study on an ADNI Cohort.Brain sciences · 2025Article
- Increased Synapse Elimination by Inflammatory Cells Contributes to Long-lasting Post-Stroke Memory Dysfunction in Old Mice.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Amyloid burden impacts cognitive decline in the pre-dementia stages of Alzheimer's disease (AD), but there remains significant variability in cognitive trajectories that may be explainable by markers of synaptic function and neurodegeneration. Leveraging longitudinal data from two harmonized, at-risk but predominantly unimpaired cohorts, we examined how several proteins measured from cerebrospinal fluid (CSF) differ by amyloid status, cognitive status, and impact cognitive decline measured using a Preclinical Alzheimer's Cognitive Composite. Four hundred and thirty-four individuals provided CSF biomarkers of amyloid-beta42 (ab42), phosphorylated tau (181), from which we identified Aβ + individuals using a cutoff based on a p-tau181/Aβ42 ratio. Other markers of neurodegeneration (N) included neurofilament light, neurogranin, SNAP-25, and NPTX2. Most biomarkers of N were higher in the Aβ + group and lower in cognitively unimpaired individuals, though NPTX2 exhibited the opposite pattern. Even in the face of Aβ+, NPTX2 was higher in individuals who showed slower rates of cognitive decline, suggesting NPTX2 may be associated with cognitive resilience. Moreover, a SNAP-25/NPTX2 ratio of synaptic dysfunction explained more variance in cognitive decline than other biomarkers alone. This work provides support for potentially useful biomarkers of synaptic function implicated in the clinical syndrome of AD, aiding in future diagnosis and staging efforts.
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