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The biochemistry of Alzheimer's disease, the most common cause of dementia, is not yet very well understood. Alzheimer's disease (AD) has been identified as a proteopathy: a protein misfolding disease due to the accumulation of abnormally folded amyloid beta (Aβ) protein in the brain. [1]
[4] [7] Structural modeling of Aβ channels, however, suggests that the channels are highly polymorphic, with the ability to move and change size and shape within the lipid membrane. The broad range of conformations adopted by the Aβ channel makes design of a specific, highly effective Aβ channel blocker difficult. [4]
Vascular dementia; The misfolding of proteins is a common component of the proposed pathophysiology of many aging-related diseases. However, there is insufficient evidence to prove this. For example, the tau hypothesis for Alzheimer's proposes that tau protein accumulation results in the breakdown of neuron cytoskeletons, leading to Alzheimer's ...
Brain Aβ is elevated in people with sporadic Alzheimer's disease. Aβ is the main constituent of brain parenchymal and vascular amyloid; it contributes to cerebrovascular lesions and is neurotoxic. [33] [34] [35] It is unresolved how Aβ accumulates in the central nervous system and subsequently initiates the disease of cells. Significant ...
People who die of severe COVID-19 have brain abnormalities that resemble changes seen in Alzheimer's disease - accumulation of a protein called tau inside brain cells, and abnormal amounts of the ...
The diagnosis of Alzheimer's disease typically requires a microscopic analysis of plaques and tangles in brain tissue, usually at autopsy. [40] However, Aβ plaques (along with cerebral Aβ-amyloid angiopathy ) can be detected in the brains of living subjects by preparing radiolabeled agents that bind selectively to Aβ deposits in the brain ...
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