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At 92 He is Testing a Mitochondrial Transplant That Could Rewrite Aging | Dr John Cramer

Dr. John Cramer, 92-year-old nuclear physicist, discusses participating in the first mitochondrial transplant trial for aging and his longevity theory.
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Dr. John Cramer is a 92-year-old emeritus professor at the University of Washington who has spent decades researching nuclear physics and quantum mechanics. Now, he’s turned his attention to longevity, and he’s not just theorizing. Dr. Cramer is participating in Mitrix’s groundbreaking mitochondrial transplantation trial, which aims to replace damaged mitochondrial DNA with healthy versions grown in bioreactors.

In this conversation, Dr. Cramer explains why he believes mitochondrial dysfunction is the root cause of aging, not just another hallmark. He discusses how energy depletion cascades into all other aging symptoms, why previous interventions like telomere extension haven’t delivered, and what markers will be tracked throughout his trial. He also shares his personal longevity protocol, including rapamycin, senolytics, and hyperbaric oxygen therapy.

This is one of the first detailed discussions of autologous mitochondrial transplantation for aging in humans.

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NDR2 regulates non-small cell lung cancer cell migration under starvation by supporting autophagosome biogenesis through LC3 and ATG9A regulation

Biojout, T., Bergot, E., Taylor, J. et al. Cell Death Discov. (2025). https://doi.org/10.1038/s41420-025-02889-9

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Ex.50.T aptamer impairs tumor–stroma cross-talk in breast cancer by targeting gremlin-1

Quintavalle, C., Ingenito, F., Roscigno, G. et al. Ex.50.T aptamer impairs tumor–stroma cross-talk in breast cancer by targeting gremlin-1. Cell Death Discov. 11, 94 (2025). https://doi.org/10.1038/s41420-025-02363-6

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Reversing aging in blood stem cells by targeting lysosomal dysfunction

As people age, these cells become defective and lose their ability to renew and repair the blood system, decreasing the body’s ability to fight infections as seen in older adults. Another example is a condition called clonal hematopoiesis; this asymptomatic condition is considered a premalignant state that increases the risk of developing blood cancers and other inflammatory disorders. Its prevalence increases significantly with age.

The team discovered that lysosomes in aged HSCs become hyper-acidic, depleted, damaged, and abnormally activated, disrupting the cells’ metabolic and epigenetic stability. Using single-cell transcriptomics and stringent functional assays, the researchers found that suppressing this hyperactivation with a specific vacuolar ATPase inhibitor restored lysosomal integrity and blood-forming stem cell function.

The old stem cells started acting young and healthy once more. Old stem cells regained their regenerative potential and ability to be transplanted and to produce more healthy stem cells and blood that is balanced in immune cells; they renewed their metabolism and mitochondrial function, improved their epigenome, reduced their inflammation, and stopped sending out “inflammation” signals that can cause damage in the body.

Remarkably, ex vivo treatment (when cells are removed from the body, modified in a laboratory, and returned to the body) of old stem cells with the lysosomal inhibitor boosted their in vivo blood-forming capacity more than eightfold, demonstrating that correcting lysosomal dysfunction can restore regenerative potential.

This restoration also dampened harmful inflammatory and interferon-driven pathways by improving lysosomal processing of mitochondrial DNA and reducing activation of the cGAS-STING immune signaling pathway, which they find to be a key driver of inflammation and aging of stem cells.

Researchers have discovered how to reverse aging in blood-forming stem cells in mice by correcting defects in the stem cell’s lysosomes. The breakthrough, published in Cell Stem Cell, identifies lysosomal hyperactivation and dysfunction as key drivers of stem cell aging and shows that restoring lysosomal slow degradation can revitalize aged stem cells and enhance their regenerative capacity.

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Zap-and-freeze’ technique used to watch human brain cell communication

For the new study, the researchers used samples from the brains of normal mice as well as living cortical brain tissue sampled with permission from six individuals undergoing surgical treatment for epilepsy. The surgical procedures were medically necessary to remove lesions from the brain’s hippocampus.

The researchers first validated the zap-and-freeze approach by observing calcium signaling, a process that triggers neurons to release neurotransmitters in living mouse brain tissues.

Next, the scientists stimulated neurons in mouse brain tissue with the zap-and-freeze approach and observed where synaptic vesicles fuse with brain cell membranes and then release chemicals called neurotransmitters that reach other brain cells. The scientists then observed how mouse brain cells recycle synaptic vesicles after they are used for neuronal communication, a process known as endocytosis that allows material to be taken up by neurons.

The researchers then applied the zap-and-freeze technique to brain tissue samples from people with epilepsy, and observed the same synaptic vesicle recycling pathway operating in human neurons.

In both mouse and human brain samples, the protein Dynamin1xA, which is essential for ultrafast synaptic membrane recycling, was present where endocytosis is thought to occur on the membrane of the synapse.

“Our findings indicate that the molecular mechanism of ultrafast endocytosis is conserved between mice and human brain tissues,” the author says, suggesting that the investigations in these models are valuable for understanding human biology.

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Researchers Identify People That Are Missing a Critical Cell Process — Unique Insight Into Human Physiology

Patients with a unique cellular disorder are helping researchers understand a series of health complications better. For the first time, researchers led by Newcastle University, UK have identified a group of patients with neurological disease who lack a critical cell process called autophagy. The

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