Exercise promotes the hypothalamus to release MOTS-c. Mitochondrial encoded MOTS-c interacts with the nuclear genome and regulates both cell metabolism and the stress response.
Expressing neuron enriched mitochondrial proteins, researchers achieved a four times higher glial cell conversion rate and simultaneously increased the speed of neural reprogramming.
MP-Pt(IV), a second generation prodrug appears to have curative properties against glioblastoma when coupled with chemotherapy in mouse models.
The retrieval of mitochondria via a feedback loop is vital to sustaining synaptic transmission.
Mitochondria regulate how neural stem cells become neurons during brain development. The findings may help explain how humans developed larger brains during evolution and how mitochondrial defects lead to some neurodevelopmental disorders.
In both human cell and mouse models of Huntington's disease, RNA from mitochondria was misplaced within spiny projection neurons. The stray RNAs, which looked different to cells than RNA derived from the cell nucleus, trigger an immune reaction that can lead to striatal cell type vulnerability.
Exposing mice to THC, researchers noted persistent activation of mitochondrial cannabinoid receptors located within astrocytes resulted in a cascade of molecular processing that led to dysfunctional glucose metabolism. The ability of astrocytes to transform glucose into "food" for neurons was reduced. The reduction resulted in a compromise in neural function, with a harmful impact on behavior. Specifically, social interactions were reduced for 24 hours post cannabis exposure.
Humanin, a peptide encoded in mitochondria, appears to have a beneficial impact on both health and longevity in both humans and animals. Higher levels of humanin in the body are associated with longer life spans and a reduced risk of neurodegenerative disorders, like Alzheimer's disease.
Enhancing mitochondrial transportation and cellular energetics could help promote regeneration and function following spinal cord injury.