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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 ]
The study found that increased levels of both amyloid-beta and tau proteins in the brain may lead to changed brain activity before the cognitive symptoms of Alzheimer’s disease appear. Focusing ...
The biomarkers can be used to diagnose Alzheimer's disease (AD) in a very early stage, but they also provide objective and reliable measures of disease progress. It is imperative to diagnose AD disease as soon as possible, because neuropathologic changes of AD precede the symptoms by years. [ 1 ]
Alternatively, diseases exhibiting tau pathologies attributed to different and varied underlying causes are termed 'secondary tauopathies'. Some neuropathologic phenotypes involving tau protein are Alzheimer's disease, frontotemporal dementia, progressive supranuclear palsy, and corticobasal degeneration. [1]
“A study from 2019 reported that a woman carrying the presenilin 1 (PSEN1) mutation, a genetic cause of early-onset Alzheimer’s disease, did not develop dementia in her 40s as others with the ...
The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold. [6] [7] A study has suggested that APP and its amyloid potential is of ancient origins, dating as far back as early deuterostomes. [8]
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