Abstract
Alzheimer’s disease (AD) is chronic neurodegenerative dementia representing the most common cause of dementia in the elderly population. It is a major source of morbidity, mortality, and healthcare expenditure worldwide. Although the molecular and cellular properties related to AD have been demonstrated decades before the onset of clinical symptoms, AD’s pathogenesis is still unknown as a combination of risk factors causes it. Today, pathogenesis theories focused on senile plaques (SP) formed by the extracellular accumulation and deposition of Aβ peptides and neurofibrillary tangles (NFTs), which are composed of the hyperphosphorylated tau protein. Furthermore, growing evidence points out that toxic Aβ plays a primary causal role in the induction and transmission of pathology and neuronal dysfunction and loss. Therefore, Aβ is crucial to the development of AD and is a noteworthy issue in AD research. This review shows the formation of Aβ and the differences of cytotoxicity of its various isoforms and aggregation states. It also summarizes the mechanisms by which Aβ induce AD through its neurotoxicity and state how these mechanisms interact and reinforce each other.
Highlights
Alzheimer’s Disease(AD) is one of the most well-known neurodegenerative diseases, and it is currently the fourth most common cause of death in the United State [1]
It is known that Alzheimer's disease (AD) is the most prevalent neurodegenerative disease, especially in the elderly population
The pathogenesis of AD is mainly studied in the following aspects: amyloid cascade hypothesis, tau hyperphosphatation, effect of GSK-3β, and cholinergic injury hypothesis
Summary
Alzheimer’s Disease(AD) is one of the most well-known neurodegenerative diseases, and it is currently the fourth most common cause of death in the United State [1]. It is possible to slow the disease's progression, there are presently no cures for AD because the mystery behind the understanding of its cellular, molecular, and pathological initiation and development is not clear [3]. It is generally accepted in the scientific community that AD has three characteristic pathological changes: senile plaques(SP), neurofibrillary tangles (NFTs), and the loss of neurons. Substantial data indicate that the solubility of Aβ, and the quantity of Aβ in different pools, maybe more closely related to the disease state The composition of these pools of Aβ reflects different amyloid deposits and has definite correlates with the patient's clinical status. This review suggests how abnormalities in the AD brain form Aβ, highlight the importance of differentiating between various species of Aβ, and summarize the many mechanisms by which Aβ triggers AD in cellular and molecular levels
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