Paricalcitol Accelerates BACE1 Lysosomal Degradation and Inhibits Calpain-1 Dependent Neuronal Loss in APP/PS1 Transgenic Mice

2019 ◽  
Author(s):  
Yong-Gang Fan ◽  
Tian Guo ◽  
Xiao-Ran Han ◽  
Jun-Lin Liu ◽  
Yu-Ting Cai ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Neuronal Loss ◽  
Lysosomal Degradation

scholarly journals Paricalcitol accelerates BACE1 lysosomal degradation and inhibits calpain-1 dependent neuronal loss in APP/PS1 transgenic mice

EBioMedicine ◽  
2019 ◽  
Vol 45 ◽  
pp. 393-407 ◽  
Author(s):  
Yong-Gang Fan ◽  
Tian Guo ◽  
Xiao-Ran Han ◽  
Jun-Lin Liu ◽  
Yu-Ting Cai ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Neuronal Loss ◽  
Lysosomal Degradation

Dopaminergic neuronal loss in transgenic mice expressing the Parkinson's disease-associated UCH-L1 I93M mutant

2007 ◽  
Vol 50 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Rieko Setsuie ◽  
Yu-Lai Wang ◽  
Hideki Mochizuki ◽  
Hitoshi Osaka ◽  
Hideki Hayakawa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Transgenic Mice ◽  
Neuronal Loss ◽  
Dopaminergic Neuronal Loss

scholarly journals DL0410 ameliorates cognitive deficits in APP/PS1 transgenic mice by promoting synaptic transmission and reducing neuronal loss

2019 ◽  
Vol 41 (5) ◽  
pp. 599-611 ◽  
Author(s):  
Wei Zhou ◽  
Wen-wen Lian ◽  
Rong Yan ◽  
Hao Jia ◽  
Lv-jie Xu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Synaptic Transmission ◽  
Cognitive Deficits ◽  
Neuronal Loss

184 Cre/LoxP-Mediated Constitutive Activation of IKK2 in GFAP-Positive Cells Induces Enteric Gliosis and Neuronal Loss in Transgenic Mice

2012 ◽  
Vol 142 (5) ◽  
pp. S-45
Author(s):  
Daniel Bitner ◽  
Yonggang Zhang ◽  
Nomble F. Lee ◽  
Fang Li ◽  
Wenhui Hu
Keyword(s):  
Transgenic Mice ◽  
Neuronal Loss ◽  
Constitutive Activation

scholarly journals APPSW Transgenic Mice Develop Age-related Aβ Deposits and Neuropil Abnormalities, but no Neuronal Loss in CA1

1997 ◽  
Vol 56 (9) ◽  
pp. 965-973 ◽  
Author(s):  
MICHAEL C. IRIZARRY ◽  
MEGAN MCNAMARA ◽  
KERRI FEDORCHAK ◽  
KAREN HSIAO ◽  
BRADLEY T. HYMAN
Keyword(s):  
Transgenic Mice ◽  
Neuronal Loss ◽  
Age Related

scholarly journals Small Heat Shock Protein 22 Improves Cognition and Learning in the Tauopathic Brain

2022 ◽  
Vol 23 (2) ◽  
pp. 851
Author(s):  
Santiago Rodriguez Ospina ◽  
Danielle Blazier ◽  
Marangelie Criado-Marrero ◽  
Lauren Gould ◽  
Niat Gebru ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Heat Shock ◽  
Transgenic Mice ◽  
Neuronal Loss ◽  
Small Heat Shock Protein ◽  
Functional Benefit ◽  
Canonical Pathways ◽  
Cognition And Learning ◽  
Shock Proteins ◽  
Heat Shock Protein 22

The microtubule-associated protein tau pathologically accumulates and aggregates in Alzheimer’s disease (AD) and other tauopathies, leading to cognitive dysfunction and neuronal loss. Molecular chaperones, like small heat-shock proteins (sHsps), can help deter the accumulation of misfolded proteins, such as tau. Here, we tested the hypothesis that the overexpression of wild-type Hsp22 (wtHsp22) and its phosphomimetic (S24,57D) Hsp22 mutant (mtHsp22) could slow tau accumulation and preserve memory in a murine model of tauopathy, rTg4510. Our results show that Hsp22 protected against deficits in synaptic plasticity and cognition in the tauopathic brain. However, we did not detect a significant change in tau phosphorylation or levels in these mice. This led us to hypothesize that the functional benefit was realized through the restoration of dysfunctional pathways in hippocampi of tau transgenic mice since no significant benefit was measured in non-transgenic mice expressing wtHsp22 or mtHsp22. To identify these pathways, we performed mass spectrometry of tissue lysates from the injection site. Overall, our data reveal that Hsp22 overexpression in neurons promotes synaptic plasticity by regulating canonical pathways and upstream regulators that have been characterized as potential AD markers and synaptogenesis regulators, like EIF4E and NFKBIA.

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