scholarly journals Amyloid Oligomers Exacerbate Tau Pathology in a Mouse Model of Tauopathy

2012 ◽  
Vol 11 (4) ◽  
pp. 165-181 ◽  
Author(s):  
Maj-Linda B. Selenica ◽  
Milene Brownlow ◽  
Jeffy P. Jimenez ◽  
Daniel C. Lee ◽  
Gabriela Pena ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tau Pathology ◽  
Amyloid Oligomers

Zinc Exacerbates Tau Pathology in a Tau Mouse Model

2018 ◽  
Vol 64 (2) ◽  
pp. 617-630 ◽  
Author(s):  
Kristen M. Craven ◽  
William R. Kochen ◽  
Carlos M. Hernandez ◽  
Jane M. Flinn
Keyword(s):  
Mouse Model ◽  
Tau Pathology ◽  
Tau Mouse Model

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 Obesity, diabetes, and leptin resistance promote tau pathology in a mouse model of disease

Neuroscience ◽  
2016 ◽  
Vol 315 ◽  
pp. 162-174 ◽  
Author(s):  
T.L. Platt ◽  
T.L. Beckett ◽  
K. Kohler ◽  
D.M. Niedowicz ◽  
M.P. Murphy
Keyword(s):  
Mouse Model ◽  
Leptin Resistance ◽  
Tau Pathology

scholarly journals Anti-Aβ antibodies bound to neuritic plaques enhance microglia activity and mitigate tau pathology

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Vanessa Laversenne ◽  
Sameer Nazeeruddin ◽  
Emma C. Källstig ◽  
Philippe Colin ◽  
Christel Voize ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tau Protein ◽  
Hippocampal Formation ◽  
Dystrophic Neurites ◽  
Neuritic Plaques ◽  
Tau Pathology ◽  
Continuous Administration ◽  
Plaque Deposition ◽  
5Xfad Mice

AbstractThe brain pathology of Alzheimer’s disease (AD) is characterized by the misfolding and aggregation of both the amyloid beta (Aβ) peptide and hyperphosphorylated forms of the tau protein. Initial Aβ deposition is considered to trigger a sequence of deleterious events contributing to tau pathology, neuroinflammation and ultimately causing the loss of synapses and neurons. To assess the effect of anti-Aβ immunization in this context, we generated a mouse model by overexpressing the human tau protein in the hippocampus of 5xFAD mice. Aβ plaque deposition combined with human tau overexpression leads to an array of pathological manifestations including the formation of tau-positive dystrophic neurites and accumulation of hyperphosphorylated tau at the level of neuritic plaques. Remarkably, the presence of human tau reduces microglial clustering in proximity to the Aβ plaques, which may affect the barrier role of microglia. In this mouse model, continuous administration of anti-Aβ antibodies enhances the clustering of microglial cells even in the presence of tau. Anti-Aβ immunization increases plaque compaction, reduces the spread of tau in the hippocampal formation and prevents the formation of tau-positive dystrophic neurites. However, the treatment does not significantly reduce tau-induced neurodegeneration in the dentate gyrus. These results highlight that anti-Aβ immunization is able to enhance microglial activity around neuritic plaques, mitigating part of the tau-induced pathological manifestations.

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