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At 81, however, Scott maintains that he does not have time to wait for the FDA to approve the age-reversal treatments needed to achieve his goal of immorality.

“My concern is me, not the regulations which have been created,” he said.


Kenneth Scott travels internationally for experimental treatments, doesn’t use soap, and spends hundreds of thousands of dollars on his quest for immortality.

One prevailing hypothesis is that physical fitness mitigates structural brain changes that contribute to cognitive decline. Recent evidence points to a potential role involving myelin —the insulating sheath surrounding neurons that is crucial for efficient neural signaling and overall cognitive health. Myelination facilitates rapid signal transmission and supports neural network integrity.

The degeneration of myelin in the brain is increasingly recognized as a critical factor contributing to disruptions in neural communication, which may play a significant role in the cognitive decline observed in Alzheimer’s disease and other neurodegenerative disorders. Emerging research suggests that myelin breakdown may even precede the formation of amyloid-beta plaques and neurofibrillary tangles—the hallmark pathological features of Alzheimer’s disease. Advanced imaging studies have detected early myelin degeneration in individuals who later develop Alzheimer’s, indicating that myelin damage could be an initial event in the disease’s progression.

Age-related deterioration of myelin is closely associated with cognitive decline. Reduced white matter integrity—often resulting from myelin damage—is correlated with declines in memory, executive function, and processing speed in older adults. As myelin degradation leads to the slowing of cognitive processes and disrupts the synchronization of neural networks, preserving myelin integrity is essential for sustaining cognitive health across the lifespan.

What keeps some immune systems youthful and effective in warding off age-related diseases? In a new paper published in Cellular & Molecular Immunology, USC Stem Cell scientist Rong Lu and her collaborators point the finger at a small subset of blood stem cells, which make an outsized contribution to maintaining either a youthful balance or an age-related imbalance of the two main types of immune cells: innate and adaptive.

Innate immune cells serve as the body’s first line of defense, mobilizing a quick and general attack against invading germs. For germs that evade the body’s innate immune defenses, the second line of attack consists of , such as B cells and T cells that rely on their memory of past infections to craft a specific and targeted response. A healthy balance between innate and adaptive immune cells is the hallmark of a youthful immune system—and a key to longevity.

“Our study provides compelling evidence that when a small subset of overproduces innate immune cells, this drives the aging of the immune system, contributes to disease, and ultimately shortens the lifespan,” said Lu, who is an associate professor of stem cell biology and , , medicine, and gerontology at USC, and a Leukemia & Lymphoma Society Scholar. Lu is also a member of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, and the USC Norris Comprehensive Cancer Center at the Keck School of Medicine of USC.

The generation and maintenance of protective immunity is a dynamic interplay between host and environment that is impacted by age. Understanding fundamental changes in the healthy immune system that occur over a lifespan is critical in developing interventions for age-related susceptibility to infections and diseases. Here, we use multi-omic profiling (scRNA-seq, proteomics, flow cytometry) to examined human peripheral immunity in over 300 healthy adults, with 96 young and older adults followed over two years with yearly vaccination. The resulting resource includes scRNA-seq datasets of 16 million PBMCs, interrogating 71 immune cell subsets from our new Immune Health Atlas. This study allows unique insights into the composition and transcriptional state of immune cells at homeostasis, with vaccine perturbation, and across age. We find that T cells specifically accumulate age-related transcriptional changes more than other immune cells, independent from inflammation and chronic perturbation. Moreover, impaired memory B cell responses to vaccination are linked to a Th2-like state shift in older adults’ memory CD4 T cells, revealing possible mechanisms of immune dysregulation during healthy human aging. This extensive resource is provided with a suite of exploration tools at https://apps.allenimmunology.org/aifi/insights/dynamics-imm-health-age/ to enhance data accessibility and further the understanding of immune health across age.

A.W.G. serves on the scientific advisory boards of ArsenalBio and Foundery Innovations.

Haven’t heard from Bill Andrews in awhile.


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Here we talk with Dr Bill Andrews all about telomeres, why they are on the critical path of aging and finding a way to lengthen them is required in an complete longevity solution.
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00:00 Why telomeres.
07:10 Telomeres and aging.
14:36 Telomerase in stem cells.
20:15 BiOptimizers.
21:44 Telomere shortening.
23:25 Measuring telomere length.
25:30 Biological age.
30:30 Slowing telomere shortening.
39:30 Supplements to help.
41:30 Sierra Science Chemicals \& Gene therapy.
49:30 How is telomerase repressed.
56:10 Liz Parrish \& Gene therapy.
1:01:40 Gene therapy delivery.
1:09:20 Telomerase \& cancer.
1:17:00 Why aging.
1:20:30 Telomeres \& senescence.
1:24:30 More information.

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It is well-established that chronic MSK pain is the key factor for physical disability in the adult population. 19 The World Health Organization (WHO) estimates that 20–33% (over 1.71 billion individuals) of the global population suffers from chronic MSK pain. 20 This type of disorder is characterized by acute or chronic pain in MSK structures, which involve muscles, tendons, ligaments, bones, and nerves. 21 The most common conditions responsible for visits to a physician’s office are OA, rheumatoid arthritis, myofascial pain syndrome (MPS), and low back and neck pain. 22 Less common incidents are generally accompanying with injuries like of tendon sprains, ligament tears, muscle tears, fractures, and similar damage during sports. 20

If left untreated, these conditions progressively increase suffering, disability, and drug consumption, which subsequently diminish an individual’s quality of life. 23 This also translates to a main community health problem due to significant high expenses for health-care systems and insurance for disability. Advanced age may remain the top variable associated with the increased risk of musculoskeletal disorders (MSDs) and MSK pain; however, these conditions may still unfold at any given age for various reasons. Therefore, every individual is at risk of experiencing MSK pain throughout an entire lifetime. 24 Acute pain can become chronic due to numerous factors. The level of intensity, site, and time of noxious stimuli are dictated by the interplay between mechanical, chemical, and thermal receptors and immune cells. 25 Under standard conditions, noxious stimuli and painful sensations gradually decrease with the progression of healing.

Aging senescent cells do not become hypometabolic.

Instead they become HYPERmetabolic, burning energy faster than their younger selves.

This likely steals energy for other useful cellular functions, possibly accounting for their aberrant behaviors.

As we…


The authors offer a new energy-focused perspective on aging by introducing a brain–body model that positions the brain’s response to cytokine signals of hypermetabolism as a mechanistic link between the cellular hallmarks and organismal manifestations of aging.