Analysis and comparison of biomarkers for Alzheimer's disease

Abstract. Alzheimer's disease (AD), commonly known as dementia, is a neurodegenerative disease that causes memory and cognitive decline. Alzheimer's disease is a neurodegenerative disease that causes memory and cognitive deterioration in patients. 70% of the world's more than 50 million elderly patients suffer from Alzheimer's disease. Currently, scholars around the world mainly classify Alzheimer's disease (AD) patients into seven stages from onset to death. The pathogenesis of Alzheimer's disease (AD) has not yet been clarified by studies on different stages, and the main theories include the A- amyloid hypothesis and other theories such as abnormal phosphorylation of Tau protein. The A- amyloid hypothesis proposes that a type of A42 forms a large number of oligomers in the patient's brain due to misfolding and accumulation, which then develop into mature fibres and protofibrils, eventually accumulating into plaques that impede signalling between the patient's nerves and neurons to cause problems in the brain. The Tau protein theory proposes that it is due to over phosphorylation of pTau protein that disrupts the neuronal skeleton and forms neuronal fibre tangles (NFTS) causing impaired axonal transport to affect signalling. fibre tangles (NFTS) causing impaired axonal transport to affect signalling. This review provides an overview of the A amyloid hypothesis and the abnormal phosphorylation of Tau protein hypothesis, and compares their pathogenic mechanisms and proposes ideas to address the different mechanisms. This thesis finds that Alzheimer's disease (AD) can be treated using targeted approaches for different pathogenic mechanisms.