Abstract

This article will summarize the results of recent years of exploration into deeper causes of Alzheimers disease with possible therapeutic strategies. The most popular pathological hypothesis for the causation of Alzheimers is the A cascade hypothesis. A has a dominant role in the pathophysiology of Alzheimers disease, according to genetic and pathological data. Another significant histological characteristic of Alzheimers disease brains is the presence of neurofibrillary tangles made of the protein tau, which is related with microtubules. In the brain, neuronal loss, neuroinflammation, and oxidative stress can result from the cascade consequences of tau toxicity. But as research has progressed, it has been found the A. The accumulation of protein and neurofibrillary tangles composed of phosphorylated tau are only manifestations of AD, not the result. This is also the reason why many drugs fail the phase III clinic. So people began to look for a way out of the problem, starting in the direction of the gene. How to diagnose AD early in the MCI stage, how to find markers for early diagnosis and how to inhibit the progression from the MCI stage to the dementia stage are all questions that need to be investigated in the future.

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