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Overexpression of MTMR14 induced learning and memory impairments in 2-month-old C57 mice
Qiong Feng1, Xiao Li2, Ruijuan Liu3
1Department of Pathology, Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 43001, China.
Abstract:
Multiple biological functions of MTMR14 including regulation of autophagy, inflammation and Ca2+ homeostasis have been reported. However, its functional contribution to learning and memory remains unclear. In this study, we investigated whether upregulation of MTMR14 induced cognitive impairment and the underlying mechanisms. MTMR14 level was significantly increased in cells or brain tissues that overexpressed P301S-tau. The fusion of autophagosome and lysosome was significantly inhibited by overexpression of MTMR14 or P301S-tau. Upregulation of MTMR14 led to cognitive impairments in 2-month-old mice by inhibiting synaptic protein expression. These findings suggest that MTMR14 may be a key risk factor for cognitive ability.
Insights
Myotubularin-related protein 14 (MTMR14) upregulation impairs cognitive function by inhibiting synaptic protein expression. This suggests MTMR14 is a potential risk factor for cognitive decline.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Myotubularin-related protein 14 (MTMR14) is involved in autophagy, inflammation, and calcium homeostasis.
- The role of MTMR14 in learning and memory remains largely unknown.
Purpose of the Study:
- To investigate the impact of MTMR14 upregulation on cognitive function.
- To elucidate the underlying molecular mechanisms of MTMR14-induced cognitive impairment.
Main Methods:
- Assessed MTMR14 levels in cells and brain tissues overexpressing P301S-tau.
- Examined the effect of MTMR14 and P301S-tau on autophagosome-lysosome fusion.
- Evaluated cognitive function and synaptic protein expression in mice with MTMR14 upregulation.
Main Results:
- MTMR14 levels were elevated in P301S-tau overexpressing cells and tissues.
- Overexpression of MTMR14 or P301S-tau inhibited autophagosome-lysosome fusion.
- Upregulated MTMR14 caused cognitive deficits in mice by reducing synaptic protein expression.
Conclusions:
- MTMR14 upregulation is linked to cognitive impairment.
- Inhibition of synaptic protein expression and autophagosome-lysosome fusion are potential mechanisms.
- MTMR14 may represent a significant risk factor for cognitive ability.
