New research identifies E-TCmito as a key link between neuronal activity and mitochondrial function, highlighting its potential to address cognitive decline in aging and diseases like Alzheimer’s.

New research in mice has identified a critical mechanism that connects neuronal activity with mitochondrial function, offering insight into potential strategies to address age-related cognitive decline. Mitochondria, essential for meeting the energy needs of active neurons, generate adenosine triphosphate (ATP) primarily through oxidative phosphorylation (OXPHOS).

As mammals age, the efficiency of mitochondrial metabolism in the brain declines, significantly impacting neuronal and network function. The disruption of the OXPHOS pathway contributes to oxidative stress and mitochondrial dysfunction, exacerbating these challenges.

Microgravity is known to affect muscles, bones, the immune system, and cognition, but its specific effects on the brain remain largely unexplored. To investigate this, scientists from Scripps Research partnered with the New York Stem Cell Foundation to send tiny clusters of brain cells, known as “organoids,” to the International Space Station (ISS). These organoids were derived from stem cells and designed to mimic certain aspects of brain development.

Remarkably, the organoids returned from their month-long stay in orbit still healthy. However, they exhibited accelerated maturation compared to identical organoids grown on Earth. The space-exposed cells progressed closer to becoming fully developed neurons and showed early signs of specialization. These findings, recently published in Stem Cells Translational Medicine, offer new insights into how space travel might influence neurological development and brain function.

“The fact that these cells survived in space was a big surprise,” says co-senior author Jeanne Loring, PhD, professor emeritus in the Department of Molecular Medicine and founding director of the Center for Regenerative Medicine at Scripps Research. “This lays the groundwork for future experiments in space, in which we can include other parts of the brain that are affected by neurodegenerative disease.”

The secret to cellular youth may lie in maintaining a small nucleolus—a dense structure within the cell nucleus—according to investigators at Weill Cornell Medicine. These findings were uncovered in yeast, a model organism renowned for its role in making bread and beer, yet surprisingly similar to humans at the cellular level.

The study, published Nov. 25 in Nature Aging, may lead to new longevity treatments that could extend human lifespan. It also establishes a mortality timer that reveals how long a cell has left before it dies.

As people get older, they are more likely to develop health conditions, such as cancer, cardiovascular disease and neurodegenerative diseases.