Partial cellular reprogramming via miR-10a-5p-γCaMKII axis linked to cognitive decline in female midlife in preclinical models.

This preclinical study investigated senescence-associated features in middle-aged female mice and human tissues, identifying an epigenetic upregulation of RBMX that increases splenic miR-10a-5p levels. The researchers found that miR-10a-5p can cross from the periphery to the brain, where it represses γCaMKII, influencing mitochondrial function, cellular senescence, and memory performance. In neurons from Alzheimer's disease patients and in model mice, inhibition of miR-10a-5p attenuated disease-associated phenotypes.