ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Modeling presynaptic inhibition by the amyloid precursor protein demonstrates one potential mechanism for preventing runaway synaptic modification in Alzheimer's disease.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Cell-specific expression of APP and GABABrain research · 2026Article
- Oligodendrocytes show enriched expression of amyloid precursor protein and GABA B receptor isoform 1a.bioRxiv : the preprint server for biology · 2025Article
- Modeling presynaptic inhibition by the amyloid precursor protein demonstrates one potential mechanism for preventing runaway synaptic modification in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
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3 authors.
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Abstract
introductionPrevious simulations of Hebbian associative memory models inspired the malignant synaptic growth hypothesis of Alzheimer's disease (AD), which suggests that cognitive impairments arise due to runaway synaptic modification resulting from poor separation between encoding and retrieval.
methodsWe computationally model presynaptic inhibition by the recently identified interaction of soluble amyloid precursor protein alpha (sAPPα) with γ-aminobutyric acid type B receptor (GABA
resultsSimulations predict that the dual effect of sAPPα on long-term potentiation and presynaptic inhibition of glutamatergic synapses maintains effective associative memory function and prevents runaway synaptic modification. Moreover, computational modeling predicts that sAPPα, which interacts with the 1a isoform of GABA DISCUSSION: Molecular mechanisms that enhance presynaptic inhibition, such as sAPPα-GABA HIGHLIGHTS: Computational modeling of Hebbian associative memory provides a framework for understanding the functional basis of Alzheimer's disease. Soluble amyloid precursor protein (sAPPα) presynaptic activation of γ-aminobutyric acid B (GABA
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