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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 ]
An advance in 1984 and 1985 was the identification of Aβ as the protein that forms the cores of plaques. [20] This discovery led to the generation of new tools to study plaques, particularly antibodies to Aβ, and presented a molecular target for the development of potential therapies for Alzheimer's disease. [4] [21] [22] [23]
A main theory behind the cause of Alzheimer’s disease is the build-up of the protein amyloid-beta in the brain. Researchers from the University of Cincinnati provide evidence suggesting it’s ...
It is currently unclear as to whether or not primary age-related tauopathy (PART), a term in which includes some cases formerly referred to as neurofibrillary tangle-predominant dementia (NFTPD) or tangle-only dementia, is a variant of the traditional Alzheimer's disease, or a distinct entity.
One of the leading theories behind Alzheimer’s disease is that the toxic accumulation of the proteins beta-amyloid and tau in the brain can cause many of the symptoms related to this condition.
p3 peptide also known as amyloid β- peptide (Aβ) 17–40/42 is the peptide resulting from the α-and γ-secretase cleavage from the amyloid precursor protein . It is known to be the major constituent of diffuse plaques observed in Alzheimer's disease (AD) brains and pre-amyloid plaques in people affected by Down syndrome. However, p3 peptide ...
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