Glutamatergic brainstem neurons drive motor and respiratory deficits, and GABAergic basal ganglia neurons cause hypothermia and fatal epileptic events, in a model of mitochondrial disease.

Rapamycin treatment inhibits mTOR activity and preserves ATP levels in neurons derived from induced pluripotent stem cells from a maternally inherited Leigh syndrome patient.

A revertible Leigh Syndrome French Canadian Type (LSFC) disease model recapitulates the clinical phenotypes which can be rescued using a liver-specific genetic model therapy.

Mitochondrial functional and structural defects caused by PARL deficiency lead to arrested spermatogenesis and germ cell ferroptosis.

In vivo studies reveal that mitochondrial Complex I deficiencies induce iron misregulation and liver iron overload that may contribute to neurodegeneration in mitochondrial disease mice, and that iron restriction is effective in reducing disease progression.

The discovery of three distinct and independent trans-regulating genomic loci influencing heart mass using a well-characterized mouse reference population provides evidence in support of the hypothesis that genetic diversity in the mitochondrial proteome plays a critical role in heart pathophysiology.

Structural analysis of translating human mitoribosome illustrates elemental steps of translation in mitochondria.

Reflective practice can help postgraduate students to navigate work environments, deal with difficult supervisory relationships, and improve their work-life balance.

New computer algorithms have allowed people with paralysis to achieve the highest reported typing performance using a brain-computer interface.

Cryo-EM reveals atomic details of two membrane half-channels for translocation of protons that drive rotary catalysis in ATP synthase.