Modeling Alzheimer's disease in mouse without mutant protein overexpression: cooperative and independent effects of Aβ and tau.
Alzheimer's disease (AD), the most common cause of dementia in the elderly, has two pathological hallmarks: Aβ plaques and aggregation of hyperphosphorylated tau (p-tau). Aβ is a cleavage product of Amyloid Precursor Protein (APP). Presenilin 1 (PS1) and presenilin 2 (PS2) are the catalytic sub...
Main Authors: | Qinxi Guo, Hongmei Li, Allysa L Cole, Ji-Yeun Hur, Yueming Li, Hui Zheng |
---|---|
Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2013-01-01
|
Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC3835479?pdf=render |
Similar Items
-
Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau
by: Silvia Zampar, et al.
Published: (2021-05-01) -
BMP4 overexpression induces the upregulation of APP/Tau and memory deficits in Alzheimer’s disease
by: Xiaoqing Zhang, et al.
Published: (2021-03-01) -
The Chronic Effects of a Single Low-Intensity Blast Exposure on Phosphoproteome Networks and Cognitive Function Influenced by Mutant Tau Overexpression
by: Marcus Jackson, et al.
Published: (2024-03-01) -
Tau phosphorylation in cells transfected with wild-type or an Alzheimer's disease mutant Presenilin 1.
by: Irving, N, et al.
Published: (1997) -
Human tau-overexpressing mice recapitulate brainstem involvement and neuropsychiatric features of early Alzheimer’s disease
by: Kanza M. Khan, et al.
Published: (2023-04-01)