TITLE:
Synaptic Plasticity in Alzheimer’s Disease: Bridging Molecular Data and Computational Models
AUTHORS:
Evan Zou, R. Antonio Herrera
KEYWORDS:
Alzheimer’s Disease, Synaptic Plasticity, Synaptic Dysfunction, Neurodegeneration, Computational Modeling
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.16 No.12,
December
17,
2025
ABSTRACT: Neurodegenerative disorders, most notably Alzheimer’s disease (AD), are marked by progressive cognitive decline and widespread neuronal loss. A growing body of evidence indicates that synaptic dysfunction occurs early in AD and serves as a key driver of memory impairment rather than a secondary symptom. Central to this dysfunction is synaptic plasticity (SP)—the ability of synapses to modify their strength in response to patterns of neuronal signaling. By strengthening or weakening connections, SP enables the brain to encode experience, support flexible behavior, and maintain cognitive adaptability. Disruption of SP has therefore been identified as a core pathological mechanism underlying AD progression. This review aims to first summarize the basic mechanisms of synaptic plasticity and then synthesize recent findings on how SP is regulated and dysregulated in Alzheimer’s disease. By highlighting current knowledge gaps and unresolved questions, it seeks to identify key directions for future research. Clarifying how major forms of SP are altered in AD may offer crucial insight into the mechanisms of memory impairment and potential therapeutic targets.