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The hallmark symptom of LATE is a progressive memory loss that predominantly affects short-term and episodic memory. [1] This impairment is often severe enough to interfere with daily functioning and usually remains the chief neurologic deficit, unlike other types of dementia in which non-memory cognitive domains and behavioral changes might be noted earlier or more prominently. [1]
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] Amyloid beta is a short peptide that is an abnormal proteolytic byproduct of the transmembrane protein amyloid-beta precursor protein (APP), whose function is ...
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]
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]
Alpha secretases are a family of proteolytic enzymes that cleave amyloid precursor protein (APP) in its transmembrane region.Specifically, alpha secretases cleave within the fragment that gives rise to the Alzheimer's disease-associated peptide amyloid beta when APP is instead processed by beta secretase and gamma secretase.
Lymphedema is most frequently a complication of cancer treatment or parasitic infections, but it can also be seen in a number of genetic disorders. Tissues with lymphedema are at high risk of infection because the lymphatic system has been compromised. [3] Though incurable and progressive, a number of treatments may improve symptoms. [2]
Alzheimer's disease (AD) is clinically characterized by a progressive decline in memory and cognitive functions, leading to severe dementia. Microscopically, AD is identified by the presence of two types of insoluble fibrous materials: (1) extracellular amyloid (Aβ) protein forming senile plaques and (2) intracellular neurofibrillary lesions ...
To date, 37 human proteins have been found to form amyloid in pathology and be associated with well-defined diseases. [2] The International Society of Amyloidosis classifies amyloid fibrils and their associated diseases based upon associated proteins (for example ATTR is the group of diseases and associated fibrils formed by TTR). [3]
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