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Alzheimer's disease pathogenesis

Alzheimer's disease (AD), also known as senile dementia, is a chronic degenerative disease of the central nervous system, often onset in old age or pre-senile age, with insidious onset. The main clinical manifestations of AD include progressive memory loss and acquired knowledge loss, personality changes accompanied by a variety of behavioral and mental disorders such as life and work. AD brings a heavy burden to the society and family. It is the fourth disease that seriously threatens the life and health of the elderly after cardiovascular disease, cancer and stroke. It has become a hot issue faced by geriatrics in the world.


According to the 2018 Global Alzheimer's Disease Report published by the International Alzheimer's Association, a new case of dementia occurs every 3 seconds around the world. In 2018, 50 million people worldwide were living with dementia. By 2050, that number is expected to reach 152 million. The global cost of dementia treatment and care is estimated to increase from $1 trillion in 2018 to $2 trillion in 2030.


Alzheimer's disease pathogenesis

The main pathological features of AD are cerebral cortical atrophy, neuronal loss, senile plaque (SP) formed by deposition of beta amyloid peptide (Aβ) in the hippocampus, and microtubule-associated protein (microtubule-associated protein) in brain neurons. Neurofibrillary tangles (NFTs) formed by hyperphosphorylation of tau protein. The etiology and pathogenesis of AD are still unclear. The hypothesis involving amyloid protein and microtubule-related protein, the hypothesis of cholinergic damage, the hypothesis of gene mutation, the hypothesis of free radical damage, and the hypothesis of inflammation are the main pathogenesis at present.