scholarly journals Analysis of Tau Phosphorylation and Truncation in a Mouse Model of Human Tauopathy

2008 ◽  
Vol 172 (1) ◽  
pp. 123-131 ◽  
Author(s):  
Patrice Delobel ◽  
Isabelle Lavenir ◽  
Graham Fraser ◽  
Esther Ingram ◽  
Max Holzer ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tau Phosphorylation

A mouse model to study tau pathology related with tau phosphorylation and assembly

2007 ◽  
Vol 257 (1-2) ◽  
pp. 250-254 ◽  
Author(s):  
Tobias Engel ◽  
José J. Lucas ◽  
Félix Hernández ◽  
Jesús Avila
Keyword(s):  
Mouse Model ◽  
Tau Phosphorylation ◽  
Tau Pathology

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

scholarly journals Tau Phosphorylation in a Mouse Model of Temporal Lobe Epilepsy

2019 ◽  
Vol 11 ◽  
Author(s):  
Marianna Alves ◽  
Aidan Kenny ◽  
Gioacchino de Leo ◽  
Edward H. Beamer ◽  
Tobias Engel
Keyword(s):  
Mouse Model ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Tau Phosphorylation

scholarly journals Haloperidol inactivates AMPK and reduces tau phosphorylation in a tau mouse model of Alzheimer's disease

2016 ◽  
Vol 2 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Jeremy Koppel ◽  
Heidy Jimenez ◽  
Leslie Adrien ◽  
Blaine S. Greenwald ◽  
Philippe Marambaud ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Tau Phosphorylation ◽  
Model Of Alzheimer’S Disease ◽  
Tau Mouse Model

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.

Cognitive enhancement, TAU phosphorylation reduction, and neuronal protection by the treatment of an LRRK2 inhibitor in a tauopathy mouse model

2020 ◽  
Vol 96 ◽  
pp. 148-154 ◽  
Author(s):  
Sara Castro-Sánchez ◽  
Josefa Zaldivar-Diez ◽  
Enrique Luengo ◽  
Manuela G. López ◽  
Carmen Gil ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cognitive Enhancement ◽  
Tau Phosphorylation ◽  
Neuronal Protection
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