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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.

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Continue reading “Dasatinib + Quercetin: Longevity Biohacker Kenneth Scott’s Experience” »

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.”

Wang, Z., Zhang, Z., Li, P. et al. Multi-omics analysis reveals the genetic aging landscape of Parkinson’s disease. Sci Rep 14, 31,167 (2024). https://doi.org/10.1038/s41598-024-82470-z.

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From indestructible tardigrades to body-merging comb jellies, animals can teach humans so much about medicine, robotics, aging and survival.

Background and objectives: Aging clocks are computational models designed to measure biological age and aging rate based on age-related markers including epigenetic, proteomic, and immunomic changes, gut and skin microbiota, among others. In this narrative review, we aim to discuss the currently available aging clocks, ranging from epigenetic aging clocks to visual skin aging clocks.

Methods: We performed a literature search on PubMed/MEDLINE databases with keywords including: “aging clock,” “aging,” “biological age,” “chronological age,” “epigenetic,” “proteomic,” “microbiome,” “telomere,” “metabolic,” “inflammation,” “glycomic,” “lifestyle,” “nutrition,” “diet,” “exercise,” “psychosocial,” and “technology.”

Results: Notably, several CpG regions, plasma proteins, inflammatory and immune biomarkers, microbiome shifts, neuroimaging changes, and visual skin aging parameters demonstrated roles in aging and aging clock predictions. Further analysis on the most predictive CpGs and biomarkers is warranted. Limitations of aging clocks include technical noise which may be corrected with additional statistical techniques, and the diversity and applicability of samples utilized.

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.

Surprisingly, the organoids were still healthy when they returned from orbit a month later, but the cells had matured faster compared to identical organoids grown on Earth—they were closer to becoming adult neurons and were beginning to show signs of specialization. The results, which could shed light on potential neurological effects of space travel, were published on October 23, 2024, in Stem Cells Translational Medicine.

“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.”

On Earth, the team used stem cells to create organoids consisting of either cortical or dopaminergic neurons, which are the neuronal populations impacted in multiple sclerosis and Parkinson’s disease—diseases that Loring has studied for decades. Some organoids also included microglia, a type of immune cell that is resident within the brain, to examine the impact of microgravity on inflammation.

Continue reading “Effects of microgravity on human iPSC-derived neural organoids on the International Space Station” »