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In search of pathogenic amyloid β-peptide in familial Alzheimer's disease.
- Source :
-
Progress in molecular biology and translational science [Prog Mol Biol Transl Sci] 2019; Vol. 168, pp. 71-78. Date of Electronic Publication: 2019 Jul 13. - Publication Year :
- 2019
-
Abstract
- Early-onset familial Alzheimer's disease (FAD) is pathologically and clinically similar to the more common late-onset sporadic form of the disease. The study of rare genetic mutations that cause FAD should provide insight into the pathogenesis of sporadic Alzheimer's disease. FAD mutations have only been found in the substrate (amyloid precursor protein, APP) and protease (γ-secretase) that produces the amyloid-β peptide (Aβ). The secreted, aggregation-prone 42-residue Aβ peptide (Aβ42) has long been considered the pathogenic entity in Alzheimer's disease. However, recent understanding of the complexity of the processing of APP by γ-secretase and the effects of FAD mutations on this processing suggest other forms of Aβ as potentially pathogenic.<br /> (© 2019 Elsevier Inc. All rights reserved.)
Details
- Language :
- English
- ISSN :
- 1878-0814
- Volume :
- 168
- Database :
- MEDLINE
- Journal :
- Progress in molecular biology and translational science
- Publication Type :
- Academic Journal
- Accession number :
- 31699328
- Full Text :
- https://doi.org/10.1016/bs.pmbts.2019.07.002