Alterations in the physiological mechanisms of synapsis in alzheimer's
Alteraciones de los mecanismos fisiológicos de la sinapsis en la enfermedad de alzheimer
DOI:
https://doi.org/10.57188/Keywords:
Alzheimer Disease; Synapses; Neurodegenerative Diseases; Neuroinflammatory Processes; Biomarkers. (Source: MeSH-NLM)Abstract
Alzheimer's disease (AD) is the leading cause of dementia and is characterized by early synaptic dysfunction that precedes neurodegeneration and cognitive decline. This review aimed to analyze the available scientific evidence on alterations in the physiological mechanisms of synapses involved in AD progression, focusing on changes in synaptic proteins, structural synaptic remodeling, oxidative stress, and glial activation. A narrative review of the literature was conducted using studies published in indexed biomedical journals, emphasizing recent evidence on synaptic physiology, biomarkers, and molecular mechanisms of AD. Current evidence indicates that synaptic proteins, including SNAP-25, PSD-95, neurogranin, β-synuclein, and NPTX2, are sensitive biomarkers of synaptic dysfunction. In addition, synaptic density loss, dendritic spine degeneration, and alterations in glutamatergic and GABAergic neurotransmission are early events strongly associated with cognitive impairment. Oxidative stress, mitochondrial dysfunction, and persistent activation of microglia and astrocytes further promote neuroinflammation and complement-mediated elimination of functional synapses. Collectively, these mechanisms play a central role in AD pathophysiology and represent promising biomarkers and therapeutic targets for early diagnosis and interventions aimed at preserving synaptic integrity.
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Copyright (c) 2026 Piero Felix Raul Castro Sanchez, Pedro Valentin Ferre Pantigoso, Tatiana Alexandra Flores Cotrina, Jose Carlos Carrera Huaman, Oscar Lenin W López Amaya
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