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Review
. 2022 Feb 11;27(4):1210.
doi: 10.3390/molecules27041210.

Amyloidosis in Alzheimer's Disease: Pathogeny, Etiology, and Related Therapeutic Directions

Chen Ma  1   2 , Fenfang Hong  1 , Shulong Yang  3   4
Affiliations
Review

Amyloidosis in Alzheimer's Disease: Pathogeny, Etiology, and Related Therapeutic Directions

Chen Ma et al. Molecules. .

Abstract

The amyloid hypothesis of Alzheimer's disease has long been the predominant theory, suggesting that Alzheimer's disease is caused by the accumulation of amyloid beta protein (Aβ) in the brain, leading to neuronal toxicity in the central nervous system (CNS). Because of breakthroughs in molecular medicine, the amyloid pathway is thought to be central to the pathophysiology of Alzheimer's disease (AD). Currently, it is believed that altered biochemistry of the Aβ cycle remains a central biological feature of AD and is a promising target for treatment. This review provides an overview of the process of amyloid formation, explaining the transition from amyloid precursor protein to amyloid beta protein. Moreover, we also reveal the relationship between autophagy, cerebral blood flow, ACHE, expression of LRP1, and amyloidosis. In addition, we discuss the detailed pathogenesis of amyloidosis, including oxidative damage, tau protein, NFTs, and neuronal damage. Finally, we list some ways to treat AD in terms of decreasing the accumulation of Aβ in the brain.

Keywords: Alzheimer’s disease; amyloid beta protein; amyloid precursor protein; amyloidosis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The formation process of amyloid beta fibrils.
Figure 2
Figure 2
The mechanism of amyloid beta accumulation.
Figure 3
Figure 3
Transportation process of amyloid-beta by low-density lipoprotein receptor-related protein 1 and receptor for advanced glycation end products.
See this image and copyright information in PMC

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