scholarly journals Gliosis Precedes Amyloid-β Deposition and Pathological Tau Accumulation in the Neuronal Cell Cycle Re-Entry Mouse Model of Alzheimer’s Disease

2020 ◽  
Vol 4 (1) ◽  
pp. 243-253 ◽  
Author(s):  
Kevin H.J. Park ◽  
Tomás Barrett
Keyword(s):  
Alzheimer’S Disease ◽  
Cell Cycle ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Β ◽  
Neuronal Cell ◽  
Model Of Alzheimer’S Disease

scholarly journals Effects of γ-Secretase Inhibition on the Amyloid β Isoform Pattern in a Mouse Model of Alzheimer’s Disease

2009 ◽  
Vol 6 (5-6) ◽  
pp. 258-262 ◽  
Author(s):  
Erik Portelius ◽  
Bin Zhang ◽  
Mikael K. Gustavsson ◽  
Gunnar Brinkmalm ◽  
Ann Westman-Brinkmalm ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Β ◽  
Model Of Alzheimer’S Disease

scholarly journals Neurogenesis, Neurodegeneration, Interneuron Vulnerability, and Amyloid-β in the Olfactory Bulb of APP/PS1 Mouse Model of Alzheimer's Disease

2016 ◽  
Vol 10 ◽  
Author(s):  
Carlos De la Rosa-Prieto ◽  
Daniel Saiz-Sanchez ◽  
Isabel Ubeda-Banon ◽  
Alicia Flores-Cuadrado ◽  
Alino Martinez-Marcos
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Olfactory Bulb ◽  
Amyloid Β ◽  
Model Of Alzheimer’S Disease

scholarly journals Impact of CRFR1 Ablation on Amyloid-β Production and Accumulation in a Mouse Model of Alzheimer's Disease

2015 ◽  
Vol 45 (4) ◽  
pp. 1175-1184 ◽  
Author(s):  
Shannon N. Campbell ◽  
Cheng Zhang ◽  
Allyson D. Roe ◽  
Nickey Lee ◽  
Kathleen U. Lao ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Β ◽  
Model Of Alzheimer’S Disease

scholarly journals Klotho overexpression improves amyloid‐β clearance and cognition in the APP/PS1 mouse model of Alzheimer's disease

Aging Cell ◽  
2020 ◽  
Vol 19 (10) ◽  
Author(s):  
Yue Zhao ◽  
Chen‐Ye Zeng ◽  
Xiao‐Hong Li ◽  
Ting‐Ting Yang ◽  
Xi Kuang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Β ◽  
Model Of Alzheimer’S Disease

scholarly journals Increased levels of Stress-inducible phosphoprotein-1 accelerates amyloid-β deposition in a mouse model of Alzheimer’s disease

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Rachel E. Lackie ◽  
Jose Marques-Lopes ◽  
Valeriy G. Ostapchenko ◽  
Sarah Good ◽  
Wing-Yiu Choy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Protein Quality ◽  
Amyloid Β ◽  
Amyloid Burden ◽  
C Elegans ◽  
Model Of Alzheimer’S Disease

Abstract Molecular chaperones and co-chaperones, which are part of the protein quality control machinery, have been shown to regulate distinct aspects of Alzheimer’s Disease (AD) pathology in multiple ways. Notably, the co-chaperone STI1, which presents increased levels in AD, can protect mammalian neurons from amyloid-β toxicity in vitro and reduced STI1 levels worsen Aβ toxicity in C. elegans. However, whether increased STI1 levels can protect neurons in vivo remains unknown. We determined that overexpression of STI1 and/or Hsp90 protected C. elegans expressing Aβ(3–42) against Aβ-mediated paralysis. Mammalian neurons were also protected by elevated levels of endogenous STI1 in vitro, and this effect was mainly due to extracellular STI1. Surprisingly, in the 5xFAD mouse model of AD, by overexpressing STI1, we find increased amyloid burden, which amplifies neurotoxicity and worsens spatial memory deficits in these mutants. Increased levels of STI1 disturbed the expression of Aβ-regulating enzymes (BACE1 and MMP-2), suggesting potential mechanisms by which amyloid burden is increased in mice. Notably, we observed that STI1 accumulates in dense-core AD plaques in both 5xFAD mice and human brain tissue. Our findings suggest that elevated levels of STI1 contribute to Aβ accumulation, and that STI1 is deposited in AD plaques in mice and humans. We conclude that despite the protective effects of STI1 in C. elegans and in mammalian cultured neurons, in vivo, the predominant effect of elevated STI1 is deleterious in AD.

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