The etiology of this disease includes degenerative and non-degenerative diseases, the former includes Alzheimer’s disease frontotemporal dementia, Lewy body dementia, Parkinson’s disease combined with dementia, disease Huntington’s disease Creutzfeldt-Jakob dementia, the latter includes vascular dementia, traumatic brain dementia, infectious dementia, normal pressure hydrocephalus dementia, dementia due to metabolic or toxic encephalopathy, craniocerebral tumor dementia, etc. Alzheimer’s disease is the most common Alzheimer’s disease is the most common cause, and vascular dementia is now generally considered to be the second most common cause, with other types of dementia being less common. The cause of Alzheimer’s disease is still unknown, but it may be related to genetic and environmental factors, and is generally disseminated. The significant decrease in acetylcholine and acetylcholine transferase is associated with the severity of dementia, increased number of senile plaques and neuronal fiber tangles. The familial disease is autosomal, with genetic specificity and amyloid precursor gene mutations on chromosome 21, and the risk of development is associated with mutations in progerin 1 and progerin 2 on chromosome 14 and the number of apolipoprotein E-4 alleles on chromosome 19. Additional epidemiological studies suggest that the onset of AD is influenced by environmental factors and is associated with low literacy, smoking, vascular risk factors such as hypertension, diabetes, hyperhomocysteine, vitamin B1 vitamin B12 deficiency, traumatic brain injury and history of heavy metal exposure. Atrophy of the temporal, parietal and frontal lobes can be seen, especially hippocampal atrophy with high specificity. pick disease and frontotemporal dementia are dominated by temporal frontal lobe atrophy, and the weaving pathology is characterized mainly by senile plaques and neurogenic fiber tangles. The senile plaques contain extracellular deposits of amyloid, progerin 1, progerin 2, apolipoprotein E and ubiquitin, which are 50-200um spherical structures. Immunoinflammatory reactions such as massive glial cell proliferation and activated microglia can be seen around the senile plaques. Neurogenic fibrillary tangles are intracellular deposits containing hyperphosphorylated proteins and ubiquitin, intra-neuronal structures composed of abnormal cytoskeletons, and are a major component of microtubule-associated proteins that are found throughout the brain in patients, commonly in the hippocampus and internal olfactory cortex, in significantly greater numbers than in normal older adults. Patients also have neuronal loss, granular vacuolar degeneration, and vascular amyloidosis.