Cargando…
Switched Aβ43 generation in familial Alzheimer’s disease with presenilin 1 mutation
Presenilin (PS) with a genetic mutation generates abundant β-amyloid protein (Aβ) 43. Senile plaques are formed by Aβ43 in the cerebral parenchyma together with Aβ42 at middle ages. These brains cause the early onset of Alzheimer’s disease (AD), which is known as familial Alzheimer’s disease (FAD)....
Autores principales: | Kakuda, Nobuto, Takami, Mako, Okochi, Masayasu, Kasuga, Kensaku, Ihara, Yasuo, Ikeuchi, Takeshi |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8564532/ https://www.ncbi.nlm.nih.gov/pubmed/34728605 http://dx.doi.org/10.1038/s41398-021-01684-1 |
Ejemplares similares
-
Altered γ-secretase activity in mild cognitive impairment and Alzheimer's disease
por: Kakuda, Nobuto, et al.
Publicado: (2012) -
Generation and deposition of Aβ43 by the virtually inactive presenilin‐1 L435F mutant contradicts the presenilin loss‐of‐function hypothesis of Alzheimer's disease
por: Kretner, Benedikt, et al.
Publicado: (2016) -
Selective ferroptosis vulnerability due to familial Alzheimer’s disease presenilin mutations
por: Greenough, Mark A., et al.
Publicado: (2022) -
Distinct deposition of amyloid-β species in brains with Alzheimer’s disease pathology visualized with MALDI imaging mass spectrometry
por: Kakuda, Nobuto, et al.
Publicado: (2017) -
Modeling Presenilin-Dependent Familial Alzheimer's Disease: Emphasis on Presenilin Substrate-Mediated Signaling and Synaptic Function
por: Parent, Angèle T., et al.
Publicado: (2010)