Cargando…
Modeling Alzheimer’s Disease in Mouse without Mutant Protein Overexpression: Cooperative and Independent Effects of Aβ and Tau
BACKGROUND: 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 cataly...
Autores principales: | Guo, Qinxi, Li, Hongmei, Cole, Allysa L., Hur, Ji-Yeun, Li, Yueming, Zheng, Hui |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835479/ https://www.ncbi.nlm.nih.gov/pubmed/24278307 http://dx.doi.org/10.1371/journal.pone.0080706 |
Ejemplares similares
-
Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau
por: Zampar, Silvia, et al.
Publicado: (2021) -
Brainstem tau pathology in Alzheimer’s disease is characterized by increase of three repeat tau and independent of amyloid β
por: Uematsu, Miho, et al.
Publicado: (2018) -
BMP4 overexpression induces the upregulation of APP/Tau and memory deficits in Alzheimer’s disease
por: Zhang, Xiaoqing, et al.
Publicado: (2021) -
Vascular and parenchymal amyloid pathology in an Alzheimer disease knock-in mouse model: interplay with cerebral blood flow
por: Li, Hongmei, et al.
Publicado: (2014) -
TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading
por: Martini-Stoica, Heidi, et al.
Publicado: (2018)