Review of brain-aging mechanisms and their proposed links to Alzheimer's and Parkinson's pathology
This review describes brain aging as coordinated changes across many biological processes that may raise neuronal vulnerability, and it examines how these age-related alterations may relate to Alzheimer's and Parkinson's disease. Much of the mechanistic evidence comes from animal and cellular models. [1]
Automatic summary · not editorially reviewed
The key findings
The review describes brain aging as coordinated changes across multiple biological processes rather than a single pathological event. [1]
Age-related biological alterations may increase susceptibility to Alzheimer's and Parkinson's disease, and disease proteins may interact with age-related inflammation, metabolic dysfunction and proteostasis loss. [1]
Much of the mechanistic evidence comes from animal and cellular models, so further longitudinal and human studies are needed. [1]
The source at a glance
- Study type / format
- Review (abstract)
- Population / context
- Brain aging and its proposed links to Alzheimer's and Parkinson's disease pathology, as covered in a review
- Summary based on
- Study abstract
- Original publication
- September 21, 2026
Brain aging as many interacting processes
The review states that brain aging is a major risk factor for neurodegenerative disorders and is associated with a progressive loss of neuronal homeostasis. It does not describe brain aging as the result of a single pathological event. Instead, it lists coordinated changes across processes such as neuroinflammation, impaired proteostasis, mitochondrial dysfunction, neurotransmission deficit, cellular senescence, gut microbiota dysbiosis, extracellular vesicle dysregulation, nutrient-sensing disturbances and metabolic drift. These processes are said to interact at molecular, cellular and systemic levels and may progressively increase neuronal vulnerability to neurodegenerative pathology.
Supporting source [1]
Proposed links to Alzheimer's and Parkinson's proteins
According to the abstract, age-related biological alterations may increase susceptibility to Alzheimer's disease and Parkinson's disease. Disease-associated proteins, including amyloid-β, tau and α-synuclein, may interact with age-related inflammation, metabolic dysfunction and loss of proteostasis. The review examines the evidence for these mechanisms, their interactions and their relevance to normal brain aging, Alzheimer's disease and Parkinson's disease. The wording is cautious: these are proposed interactions and possible increases in susceptibility, not established causes.
Supporting source [1]
Animal and cellular evidence limits human conclusions
The abstract notes that much of the current mechanistic evidence derives from animal and cellular models. It therefore calls for further longitudinal and human studies to better understand how these mechanisms operate during human brain aging and in neurodegenerative diseases. This is a review of evidence, not a new human study, and the abstract does not report sample sizes, follow-up periods or measured outcomes. The described mechanisms should not be read as proven causes of human disease or as a basis for personal health decisions.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The abstract reports no sample sizes, follow-up periods or measured outcomes, and it states that much of the mechanistic evidence derives from animal and cellular models. Proposed interactions are not established causes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Yi H, Qin H, Goon JA, Makpol S, Tan JK. · europepmc.org · September 21, 2026