ArticleJournal of molecular neuroscience : MN2025
Elevated CSF GAP-43 in Mild Cognitive Impairment Linked to Cognitive Impairment Through Increased Amyloid-β Accumulation, with a Shift to Reduced Amyloid-β Accumulation in Alzheimer's Disease.
Article in Journal of molecular neuroscience : MN, 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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2 citing papers in PubMed.
- Developmental expression patterns of neuronal growth genes across human brain stages using Bgee transcriptomic data.IBRO neuroscience reports · 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
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Abstract
Growth-associated protein 43 (GAP-43), a key regulator of synaptic plasticity, neuronal growth, and memory, has recently been identified as a crucial biomarker for synaptic dysfunction in mild cognitive impairment (MCI) and Alzheimer's disease (AD) dementia. This study aimed to explore the mechanisms underlying GAP-43's role in cognitive impairment by examining the relationship between CSF GAP-43 levels and amyloid-β (Aβ) accumulation in brain regions like the frontal, temporal, and parietal lobes. This study included 332 participants sourced from the Alzheimer's Disease Neuroimaging Initiative (ADNI), categorized into three groups: 93 cognitively normal (CN), 218 with MCI, and 21 with AD dementia. Cognitive status was assessed with ADAS-Cog 13, CSF GAP-43 levels via ELISA, and Aβ accumulation using florbetapir PET imaging and Syngo.PET for SUVr values in key brain regions. The results revealed that CSF GAP-43 levels were highest in the AD dementia group, followed by the MCI group, and lowest in the CN group, with a significant difference (p < 0.001), indicating a link between elevated CSF GAP-43 and cognitive impairment. In MCI group, CSF GAP-43 positively correlated with Aβ accumulation in all regions: Globally (β = 0.362, p < 0.001), frontal (β = 0.388, p < 0.001), temporal (β = 0.382, p < 0.001), and parietal lobes (β = 0.344, p < 0.001). In contrast, the AD dementia group exhibited negative correlations between CSF GAP-43 levels and Aβ accumulation, significantly in the frontal (β = - 0.513, p = 0.035) and parietal lobes (β = - 0.513, p = 0.035), suggesting a shift in the CSF GAP-43-Aβ relationship in AD dementia. Mediation analysis, adjusted for age, gender, education, and ApoE ɛ4 status, revealed that elevated CSF GAP-43 is linked to increased cognitive impairment via increasing Aβ accumulation solely in MCI, with significant effects in global (β = 0.0894, CI: [0.0427, 0.1457]), frontal (β = 0.0895, CI: [0.0422, 0.1443]), temporal (β = 0.0941, CI: [0.0466, 0.1522]), and parietal (β = 0.0499, CI: [0.0100, 0.0945]) regions. Thus, elevated CSF GAP-43 may contribute to cognitive impairment by promoting Aβ accumulation in individuals with MCI, while in AD dementia, it may be associated with reduced Aβ accumulation, potentially reflecting a compensatory or disease-stage-dependent effect. This dynamic relationship suggests that GAP-43 could play a dual role in neurodegeneration, influencing Aβ pathology differently across disease stages.
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