ReviewBiogerontology2026
Synaptic aging and neurodegeneration: the role of synaptic vesicle dynamics and neurotransmitter imbalance.
Review in Biogerontology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic aging is a core manifestation of brain aging arising from the convergence of fundamental biological aging processes, including genomic instability, loss of proteostasis, mitochondrial dysfunction, oxidative stress, and chronic low-grade inflammation. As highly energy-dependent and protein-rich sites of neuronal communication, synapses are particularly vulnerable to age-associated molecular stress. Accumulating evidence indicates that age-related impairments in synaptic vesicle trafficking, recycling, and neurotransmitter homeostasis precede neuronal loss and represent early drivers of cognitive decline and neurodegeneration. Disruption of vesicle dynamics compromises neurotransmitter release, synaptic plasticity, and circuit stability, thereby accelerating synaptic failure. Dysregulation of key neurotransmitter systems, including acetylcholine, dopamine, glutamate, and γ-aminobutyric acid, further exacerbates synaptic dysfunction and cognitive impairment. These changes are driven by interconnected aging mechanisms, wherein impaired proteostasis promotes the accumulation of dysfunctional synaptic proteins, mitochondrial dysfunction limits ATP availability for vesicle mobilisation, and persistent neuroinflammation heightens synaptic vulnerability. Emerging evidence also implicates age-related blood-brain barrier disruption and gut-brain axis dysregulation as additional modulators of synaptic integrity via immune, metabolic, and neurochemical pathways. This review synthesises recent advances in understanding the molecular mechanisms of synaptic aging, with a focus on vesicle dynamics and neurotransmitter imbalance, and discusses therapeutic strategies aimed at enhancing synaptic resilience to promote healthy brain aging.
Indexed as
Identifiers
41663815What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.