Ceramide exposure impairs the ability for neurons to make energy by directly damaging mitochondria. Additionally, ceramides force neurons to rapidly uptake glucose in order to provide cellular energy.
Mouse models of DiGeorge/22q1 Deletion Syndrome reveal a connection between mitochondrial dysfunction, deficits in cortical connectivity and cognitive impairments. Function was restored through antioxidant therapy.
Mitochondrial function may help explain the link between intelligence, general health and aging.
Two different parts to the BAX protein can bind to BH3-only, and these sites function at different stages of BAX activation. When BH3-only binds to one of the regions, BAX becomes able to damage mitochondria.
Increasing levels of the MFN1 protein counterbalances mutated MFN2, reducing symptoms associated with Charcot-Marie-Tooth disease and neurodegeneration in mouse models.
Researchers have developed a new model of mitochondrial epilepsy which captures specific features observed in patients. The new model may help provide better therapies and treatments for the condition.
Researchers report dysfunctional mitophagy may contribute to the development of Alzheimer's disease. When mitophagy is improved, symptoms of Alzheimer's almost disappeared in animal models of the disease.