The Mutation of Amyloid Precursor Protein and the Development of Alzheimer's Disease
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Authors
Parks-Medina, Ericka
Redman, Rachel
Reed, Sandra
Brabetz, Barbara
Issue Date
2016-04-04
Type
Learning Object
Presentation
Presentation
Language
en_US
Keywords
Alzheimer's disease , Amyloid beta-protein precursor , Cerebral Amyloid Angiopathy , Β-amyloid
Alternative Title
Abstract
Alzheimer's Disease is a build of problematic plaques in the brain. These plaques are caused by the mutation of the amyloid precursor protein (APP). It is expressed in a wide range of different cell types including neurons. It can be proteolytically processed by beta and y-secretase. It has a copper binding domain and a central role in the development of Alzheimer's Disease. Amyloid precursor protein is cleaved by helper proteins which leads to the release of the Aβpeptide. If there is a single amino acid mutation in the Aβpeptide the material tangles, accumulates and creates plaques in the brain of Alzheimer's patients. APP is produced in large quantities and is metabolized quickly. APP is sorted in the endoplasmic reticulum and the Golgi, after sorting the protein is then shipped to the axons.