ArticleFrontiers in neurology2025
GAP-43 is associated with faster amyloid-associated neurodegeneration and cognitive decline in Alzheimer's disease.
Article in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- A combined neuronal extracellular vesicle-haematology panel for clinical stratification of Alzheimer's disease and dementia.Metabolic brain disease · 2026Article
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4 authors.
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Abstract
Background: It has been proposed that amyloid-β (Aβ) deposition may trigger neurodegeneration and cognitive decline. The elevated levels of presynaptic growth-associated protein 43 (GAP-43) in cerebrospinal fluid (CSF) were significantly associated with Alzheimer's disease (AD). To examine whether GAP-43 was associated with faster amyloid-associated neurodegeneration or cognitive decline, it was necessary to further explore whether Aβ deposition affected CSF GAP-43 through inflammation. Methods: A total of 671 participants from Alzheimer's Disease Neuroimaging Initiative (ADNI) were enrolled with available baseline CSF GAP-43, microglia activation [measured by CSF soluble triggering receptor expressed on myeloid cells (sTREM2) and progranulin (PGRN)], neurodegeneration (measured by CSF t-tau), and Aβ pathology (measured by amyloid-PET). To compare CSF GAP-43 levels across different Aβ and clinical stages, the analysis of variance (ANOVA) and Bonferroni Results: Compared with the amyloid- (A-) group, CSF GAP-43 was significantly higher at baseline in the amyloid+ (A+) group. When stratified by diagnosis, similar results were observed in A+ cognitively normal (CN) and A+ mild cognitive impairment (MCI), compared with A-CN or A-MCI participants. We found that baseline of CSF GAP-43 was positively related to CSF sTREM2, PGRN, amyloid-PET and t-tau, whereas it was negatively associated with cognition. Besides, CSF GAP-43 mediated the faster progression of amyloid-associated neurodegeneration and cognitive decline. Furthermore, the mediation analysis revealed that CSF sTREM2/PGRN was related to CSF t-tau mediated by CSF GAP-43 in the A+ group. Conclusion: Our findings provided evidence that CSF GAP-43 was related to the accelerated amyloid-associated neurodegeneration, and further contributed to cognitive decline. We also demonstrated that Aβ deposition may act as a trigger for synaptic dysfunction by promoting inflammation.
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