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Neuron-Specific Menin Deletion Leads to Synaptic Dysfunction and Cognitive Impairment by Modulating p35 Expression.
Kai Zhuang1, Changquan Huang1, Lige Leng1
1Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Cell Reports
|July 19, 2018
Summary
Menin protein (MEN1) is vital for brain function. Deleting it in neurons impairs learning and memory by affecting synaptic connections through the p35-Cdk5 pathway.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Menin (MEN1) is crucial for tissue development and linked to MEN1 syndrome.
- Menin is abundant in the nervous system, but its adult brain function is unclear.
Purpose of the Study:
- To investigate the role of menin in the adult brain, specifically its impact on neuronal structure and cognitive functions.
- To elucidate the molecular mechanisms by which menin influences synaptic function and learning.
Main Methods:
- Generated neuron-specific Men1 conditional knockout (CcKO) mice.
- Assessed dendritic branching, spine formation, synaptic function, learning, and memory in CcKO mice.
- Investigated menin's interaction with the p35 promoter and its effect on p35 transcription.
Main Results:
- Neuron-specific deletion of Men1 (CcKO) led to defects in dendritic branching and spine formation.
- CcKO mice exhibited impaired synaptic function, learning, and memory.
- Menin was found to bind the p35 promoter, enhancing p35 transcription.
- Restoring p35 expression in CcKO mice rescued synaptic and cognitive deficits.
Conclusions:
- Menin plays a critical role in maintaining synaptic and cognitive function in the adult brain.
- Menin modulates the p35-Cdk5 pathway, which is essential for synaptic plasticity and cognitive processes.
- Targeting the menin-p35-Cdk5 pathway may offer therapeutic strategies for cognitive impairments.
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