The major pathological hallmarks in the brain of AD patients are neuronal loss, synaptic dysfunction, and plaque deposition, which primarily consists of Amyloid-脙聨脗虏 (A脙聨脗虏) peptide and neurofibrillary tangles (NFT脙垄芒聜卢芒聞垄s) composed of phosphorylated tau protein. A脙聨脗虏 aggregation is widely regarded as the chief component in the pathogenesis of AD. A脙聨脗虏 deposition primarily occurs in cortical regions responsible for memory and learning as well as in the small blood vessels of the meninges and cerebral cortex. Oxidative stress and mitochondrial dysfunction are also key contributors to the pathological cascade leading to AD. Researchers have attempted to delineate the biological processes by which the neuropathology following TBI may elicit a pathogenic cascade contributing to the progression of AD and other NDs.
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Last date updated on March, 2025