Pharmacological Modulation of GSAP Reduces Amyloid-β Levels and Tau Phosphorylation in a Mouse Model of Alzheimer's Disease with Plaques and Tangles

2014 ◽  
Vol 41 (3) ◽  
pp. 729-737 ◽  
Author(s):  
Jin Chu ◽  
Elisabetta Lauretti ◽  
Caryne P. Craige ◽  
Domenico Praticò
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Β ◽  
Tau Phosphorylation ◽  
Pharmacological Modulation ◽  
Model Of Alzheimer’S Disease

scholarly journals Characterization of a Mouse Model of Alzheimer’s Disease Expressing Aβ4-42 and Human Mutant Tau

2021 ◽  
Vol 22 (10) ◽  
pp. 5191
Author(s):  
Silvia Zampar ◽  
Oliver Wirths
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Pyramidal Neurons ◽  
Behavioral Assessment ◽  
Large Body ◽  
Amyloid Β ◽  
Tau Phosphorylation ◽  
Model Of Alzheimer’S Disease

The relationship between the two most prominent neuropathological hallmarks of Alzheimer’s Disease (AD), extracellular amyloid-β (Aβ) deposits and intracellular accumulation of hyperphosphorylated tau in neurofibrillary tangles (NFT), remains at present not fully understood. A large body of evidence places Aβ upstream in the cascade of pathological events, triggering NFTs formation and the subsequent neuron loss. Extracellular Aβ deposits were indeed causative of an increased tau phosphorylation and accumulation in several transgenic models but the contribution of soluble Aβ peptides is still controversial. Among the different Aβ variants, the N-terminally truncated peptide Aβ4–42 is among the most abundant. To understand whether soluble Aβ4–42 peptides impact the onset or extent of tau pathology, we have crossed the homozygous Tg4–42 mouse model of AD, exclusively expressing Aβ4–42 peptides, with the PS19 (P301S) tau transgenic model. Behavioral assessment showed that the resulting double-transgenic line presented a partial worsening of motor performance and spatial memory deficits in the aged group. While an increased loss of distal CA1 pyramidal neurons was detected in young mice, no significant alterations in hippocampal tau phosphorylation were observed in immunohistochemical analyses.

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 Repeated cold exposures protect a mouse model of Alzheimer's disease against cold-induced tau phosphorylation

2019 ◽  
Vol 22 ◽  
pp. 110-120 ◽  
Author(s):  
Marine Tournissac ◽  
Philippe Bourassa ◽  
Ruben D. Martinez-Cano ◽  
Tra-My Vu ◽  
Sébastien S. Hébert ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Tau Phosphorylation ◽  
Model Of Alzheimer’S Disease
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