Effect of treadmill exercise on PI3K/AKT/mTOR, autophagy, and Tau hyperphosphorylation in the cerebral cortex of NSE/htau23 transgenic mice

2015 ◽  
Vol 6 (1) ◽  
pp. 199-209
Author(s):  
Eun-Bum Kang ◽  
Joon-Yong Cho
Keyword(s):  
Cerebral Cortex ◽  
Transgenic Mice ◽  
Treadmill Exercise ◽  
Tau Hyperphosphorylation

scholarly journals Glutamate Metabolism is Impaired in Transgenic Mice with Tau Hyperphosphorylation

2013 ◽  
Vol 33 (5) ◽  
pp. 684-691 ◽  
Author(s):  
Linn Hege Nilsen ◽  
Caroline Rae ◽  
Lars M Ittner ◽  
Jürgen Götz ◽  
Ursula Sonnewald
Keyword(s):  
Cerebral Cortex ◽  
Transgenic Mice ◽  
High Performance ◽  
Pathogenic Mutation ◽  
Relative Increase ◽  
Gas Chromatography Mass Spectrometry ◽  
Resonance Spectroscopy ◽  
Tau Hyperphosphorylation ◽  
Hypermetabolic State ◽  
Carboxylation Pathway

In neurodegenerative diseases including Alzheimer's disease and frontotemporal dementia, the protein tau is hyperphosphorylated and eventually aggregates to develop neurofibrillary tangles. Here, the consequences of tau hyperphosphorylation on both neuronal and astrocytic metabolism and amino-acid neurotransmitter homeostasis were assessed in transgenic mice expressing the pathogenic mutation P301L in the human tau gene (pR5 mice) compared with nontransgenic littermate controls. Mice were injected with the neuronal and astrocytic substrate [1-13C]glucose and the astrocytic substrate [1,2-13C]acetate. Hippocampus and cerebral cortex extracts were analyzed using 1H and 13C nuclear magnetic resonance spectroscopy, gas chromatography–mass spectrometry and high-performance liquid chromatography. The glutamate level was reduced in the hippocampus of pR5 mice, accompanied by reduced incorporation of 13C label derived from [1-13C]glucose in glutamate. In the cerebral cortex, glucose utilization as well as turnover of glutamate, glutamine, and GABA, were increased. This was accompanied by a relative increase in production of glutamate via the pyruvate carboxylation pathway in cortex. Overall, we revealed that astrocytes as well as glutamatergic and GABAergic neurons in the cortex of pR5 mice were in a hypermetabolic state, whereas in the hippocampus, where expression levels of mutant human tau are the highest, glutamate homeostasis was impaired.

Pattern of tau hyperphosphorylation and neurotransmitter markers in the brainstem of senescent tau filament forming transgenic mice

2013 ◽  
Vol 1497 ◽  
pp. 73-84 ◽  
Author(s):  
Kerstin Morcinek ◽  
Christoph Köhler ◽  
Jürgen Götz ◽  
Hannsjörg Schröder
Keyword(s):  
Transgenic Mice ◽  
Tau Hyperphosphorylation

Treadmill exercise inhibits amyloid-β generation in the hippocampus of APP/PS1 transgenic mice by reducing cholesterol-mediated lipid raft formation

Neuroreport ◽  
2019 ◽  
Vol 30 (7) ◽  
pp. 498-503 ◽  
Author(s):  
Xian-Liang Zhang ◽  
Na Zhao ◽  
Bo Xu ◽  
Xiang-He Chen ◽  
Tuo-Jian Li
Keyword(s):  
Transgenic Mice ◽  
Lipid Raft ◽  
Treadmill Exercise ◽  
Amyloid Β

Treadmill Exercise Attenuates Aβ-Induced Mitochondrial Dysfunction and Enhances Mitophagy Activity in APP/PS1 Transgenic Mice

2020 ◽  
Vol 45 (5) ◽  
pp. 1202-1214 ◽  
Author(s):  
Na Zhao ◽  
Qing-Wei Yan ◽  
Jie Xia ◽  
Xian-Liang Zhang ◽  
Bai-Xia Li ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Mitochondrial Dysfunction ◽  
Treadmill Exercise

P1-046: Melatonin attenuates Tau hyperphosphorylation in Tg2576 transgenic mice

2008 ◽  
Vol 4 ◽  
pp. T219-T219
Author(s):  
Caixia Peng ◽  
Juan Hu ◽  
Jianzhi Wang
Keyword(s):  
Transgenic Mice ◽  
Tau Hyperphosphorylation

Decreased expression of calretinin in the cerebral cortex and hippocampus of SOD1G93A transgenic mice

2005 ◽  
Vol 1035 (1) ◽  
pp. 105-109 ◽  
Author(s):  
Yoon Hee Chung ◽  
Kyeung Min Joo ◽  
Ryoung Hee Nam ◽  
Mi Haeng Cho ◽  
Dae Jin Kim ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Transgenic Mice

scholarly journals Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical Trauma in Appswe/PS1dE9 Mice

2018 ◽  
Vol 46 (4) ◽  
pp. 1398-1411 ◽  
Author(s):  
Yanhua Jiang ◽  
Zhe Li ◽  
Hong Ma ◽  
Xuezhao Cao ◽  
Fang Liu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits ◽  
Calcium Binding ◽  
Glycogen Synthase ◽  
Morris Water Maze Test ◽  
Surgical Trauma ◽  
Tau Hyperphosphorylation ◽  
Particle Injection ◽  
Model Of Alzheimer’S Disease ◽  
Gsk 3Β

Background/Aims: TREM2 plays a crucial role in modulating microglial function through interaction with DAP12, the adapter for TREM2. Emerging evidence has demonstrated that TREM2 could suppress neuroinflammatory responses by repression of microglia-mediated cytokine production. This study investigated the potential role of TREM2 in surgery-induced cognitive deficits and neuroinflammatory responses in wild-type (WT) and APPswe/PS1dE9 mice. Methods: Adult APPswe/PS1dE9 transgenic male mice (a classic transgenic model of Alzheimer’s disease, 3 months old) and their age-matched WT mice received intracerebral lentiviral particles encoding the mouse TREM2 gene and then were subjected to partial hepatectomy at 1 month after the lentiviral particle injection. The behavioral changes were evaluated with an open-field test and Morris water maze test on postoperative days 3, 7, and 14. Hippocampal TREM2, DAP12, and interleukin (IL)-1β were measured at each time point. Ionized calcium-binding adapter molecule 1 (Iba-1), microglial M2 phenotype marker Arg1, synaptophysin, tau hyperphosphorylation (T396), and glycogen synthase kinase-3β (GSK-3β) were also examined in the hippocampus. Results: Surgical trauma induced an exacerbated cognitive impairment and enhanced hippocampal IL-1β expression in the transgenic mice on postoperative days 3 and 7. A corresponding decline in the levels of TREM2 was also found on postoperative days 3, 7, and 14. Overexpression of TREM2 downregulated the levels of IL-1β, ameliorated T396 expression, inhibited the activity of GSK-3β, and improved sickness behavior. Increased Arg1 expression and a high level of synaptophysin were also observed in the transgenic mice following TREM2 overexpression. Conclusion: The downregulation of TREM2 exacerbated surgery-induced cognitive deficits and exaggerated neuroinflammatory responses in this rodent model. Overexpression of TREM2 potentially attenuated these effects by decreasing the associated production of proinflammatory cytokines, inhibiting tau hyperphosphorylation, and enhancing synaptophysin expression.

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