ArticleNature communications2024
Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Synaptic biomarkers in Alzheimer's disease dementia and mild cognitive impairment: A systematic review and meta-analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Pooled it
- Sex-specific brain reserve and progression from mild cognitive impairment to Alzheimer's disease dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Elevated CSF GAP-43 is associated with reduced cerebral glucose metabolism and cognitive impairment in individuals with mild cognitive impairment.Brain imaging and behavior · 2026Article
- Artery tertiary lymphoid organs, neuro-immune interaction and their mediators in atherosclerosis.Basic research in cardiology · 2026Review
- Ratios of CSF proteins reflect cognitive function in ALS.Alzheimer's research & therapy · 2026Article
- Shaping the cognitive reserve: the role of lifelong enrichment and education in the Alzheimer's disease continuum.Frontiers in aging neuroscience · 2026Article
- Association of cerebrospinal fluid amphiphysin-1 levels with cognition and Alzheimer's disease pathology biomarkers.Frontiers in aging neuroscience · 2026Article
- Network Pharmacology, Molecular Docking, andCurrent topics in medicinal chemistry · 2026Article
- Plasma growth-associated protein 43 correlates with synaptic loss in Alzheimer's disease.Cell reports. Medicine · 2025Article
- Protective Effects of Socioeconomic Status and Lifestyle on Amyloid- and White Matter Hyperintensity-Related Longitudinal Brain Atrophy and Cognitive Decline.Annals of neurology · 2025Article
- Surface Problem: Unveiling Extracellular Vesicles Surface Markers and Their Implications for Central Nervous System Diseases' Diagnosis and Treatment.Molecular neurobiology · 2025Review
- Connectivity as a universal predictor of tau progression in atypical Alzheimer's disease.Brain : a journal of neurology · 2025Article
- Cerebrospinal fluid markers link to synaptic plasticity responses and Alzheimer's disease genetic pathways.Molecular neurodegeneration · 2025Article
- Reduced synaptic vesicle protein 2A in extracellular vesicles and brains of Alzheimer's disease: associations with Aβ, tau, synaptic proteins and APOE ε4.Translational neurodegeneration · 2025Article
- Association of pulse pressure with presynaptic dysfunction in older adults with Alzheimer's disease: a cohort study.Scientific reports · 2025Article
- From Amyloid to Synaptic Dysfunction: Biomarker-Driven Insights into Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Biomarkers and therapeutic strategies targeting microglia in neurodegenerative diseases: current status and future directions.Molecular neurodegeneration · 2025Review
- Higher Educational Attainment and Accelerated Tau Accumulation in Alzheimer Disease.JAMA neurology · 2025Article
- Unveiling blood biomarkers for neuronal hyperplasticity: Insights from AD molecular subtyping, a comprehensive review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Novel synaptic markers predict early tau pathology and cognitive deficit in an asymptomatic population at risk of Alzheimer's disease.Molecular psychiatry · 2025Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Alzheimer's disease, amyloid-beta (Aβ) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote tau spreading. Aβ induces aberrant synaptic activity, manifesting in increases in the presynaptic growth-associated protein 43 (GAP-43), which is closely involved in synaptic activity and plasticity. We therefore tested whether Aβ-related GAP-43 increases, as a marker of synaptic changes, drive tau spreading in 93 patients across the aging and Alzheimer's spectrum with available CSF GAP-43, amyloid-PET and longitudinal tau-PET assessments. We found that (1) higher GAP-43 was associated with faster Aβ-related tau accumulation, specifically in brain regions connected closest to subject-specific tau epicenters and (2) that higher GAP-43 strengthened the association between Aβ and connectivity-associated tau spread. This suggests that GAP-43-related synaptic changes are linked to faster Aβ-related tau spread across connected regions and that synapses could be key targets for preventing tau spreading in Alzheimer's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.