Narrative review uncovers cellular and molecular pathways linking traumatic brain injury to Alzheimer's disease, highlighting interconnected neuroinflammatory and vascular cascades.
Key Points
To review the biological mechanisms linking mild, moderate, and severe traumatic brain injury to the subsequent pathogenesis of Alzheimer's disease.
Narrative synthesis of preclinical and clinical evidence investigating post-injury neurodegeneration.
Evaluation of interconnected cascades across neuroinflammation, amyloid-beta clearance, tau phosphorylation, and vascular integrity.
Acute neuroinflammation triggered by brain trauma frequently transitions into chronic neurotoxicity, impairing natural neuroprotective responses.
Trauma disrupts amyloid-beta homeostasis via impaired clearance and overproduction, while altered kinase and phosphatase activities promote hyperphosphorylated tau and neurofibrillary tangle formation.
Disruption of the blood–brain barrier facilitates peripheral immune cell infiltration and blood-derived protein entry, driving oxidative stress and synaptic dysfunction.