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The workshop is designed to be a combination of theoretical and hands-on sessions, providing students the… Read More

A new study has uncovered a critical mechanism that drives the inflammatory bowel disease (IBD), shedding light on… Read More

A workshop to understand the concept and practice of research uptake which ensures research findings are… Read More

Aberrant cell cycle activation in terminally differentiated neurons leads to apoptosis and contributes to neuronal loss in neurodegenerative diseases like Alzheimer's Disease (AD). However, the mechanisms underlying cell cycle-related neuronal apoptosis remain poorly understood.

In a transgenic APP/PS1 mouse model of AD (TgAD), researchers identified several dysregulated miRNAs, many of which target cell cycle-related genes. Notably, miR-449a plays a key role in neuronal function by: (a) promoting neuronal differentiation through cell cycle suppression, (b) showing impaired expression in cortical neurons exposed to amyloid-β (Aβ42), and (c) preventing aberrant cell cycle activation and apoptosis. miR-449a likely exerts its protective effect by targeting cyclin D1 and CDC25A, key regulators of the G1-S transition.

Importantly, lentiviral delivery of miR-449a in TgAD mouse brains significantly restored learning and memory deficits associated with AD, highlighting its therapeutic potential.

Reference:
Chauhan, M., Singh, K., Chongtham, C., A G, A., & Sharma, P. (2024). miR-449a mediated repression of the cell cycle machinery prevents neuronal apoptosis. The Journal of biological chemistry, 300(9), 107698. https://doi.org/10.1016/j.jbc.2024.107698
 

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