The authors identify causality-enriched CpGs linked to aging using Mendelian randomization. They develop new epigenetic clocks, DamAge and AdaptAge, that more reliably track age-related changes, offering insights into aging mechanisms and interventions.
Posted in life extension
Here we have a deathist vid. This fellow does run a good channel, cool bloke. But he seems to think longer life means you’ll just never be motivated and only the knowledge of death with get you moving in life. I did leave a comment.
This story is part of a series on the current progression in Regenerative Medicine. This piece discusses advances in Alzheimer’s therapy.
In 1999, I defined regenerative medicine as the collection of interventions that restore normal function to tissues and organs damaged by disease, injured by trauma, or worn by time. I include a full spectrum of chemical, gene, and protein-based medicines, cell-based therapies, and biomechanical interventions that achieve that goal.
An emerging combination of focused ultrasound therapy with a recently approved medication could be our best treatment for Alzheimer’s disease to date. In the New England Journal of Medicine, Dr. Ali Rezai and colleagues from West Virginia University describe an approach to reduce cerebral amyloid-beta load, a biomarker for neurodegeneration, in patients with Alzheimer’s. While in its preliminary stages, the combination treatment can potentially help thousands, if not millions, suffering from the disease in the near future.
Research team stumble upon new discovery which potentially holds the key to aging in plants. Click here to find out what this means for the future.
Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhDDiscount Links: Telomere, Epigenetic Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7x…
Unlocking the secrets for living more years disease-free is increasingly the target for longevity researchers.
Data is written to the memory cell by changing the magnetization in the free layer (which acts as the ‘storage’ layer in the MRAM bit cell) by passing a current through the heavy metal layer, which generates a spin current and injects it into the adjacent magnetic layer, switching its orientation and thus changing its state. Reading data involves assessing the magnetoresistance of the MTJ by directing a current through the junction. The main difference between STT-and SOT-MRAM resides in the current injection geometry used for the write process, and apparently, the SOT method ensures lower power consumption and device longevity.
While SOT-MRAM offers lower standby power than SRAM, it needs high currents for write operations, so its dynamic power consumption is still quite high. Furthermore, SOT-SRAM cells are still larger than SRAM cells, and they are harder to make. As a result, while the SOT-SRAM technology looks promising, it is unlikely that it will replace SRAM any time soon. Yet, for in-memory computing applications, SOT-MRAM could make a lot of sense, if not now, but when TSMC learns how to make SOT-MRAM cost-efficiently.
In recent years, research has begun to reveal that the lines of communication between the body’s organs are key regulators of aging. When these lines are open, the body’s organs and systems work well together. But with age, communication lines deteriorate, and organs don’t get the molecular and electrical messages they need to function properly.
A new study from Washington University School of Medicine in St. Louis identifies, in mice, a critical communication pathway connecting the brain and the body’s fat tissue in a feedback loop that appears central to energy production throughout the body. The research suggests that the gradual deterioration of this feedback loop contributes to the increasing health problems that are typical of natural aging.
The study—published in the journal Cell Metabolism—has implications for developing future interventions that could maintain the feedback loop longer and slow the effects of advancing age.
A new Northwestern Medicine study shows that RNA interference may play a key role in Alzheimer’s. For the first time, scientists have identified short strands of toxic RNAs that contribute to brain cell death and DNA damage in Alzheimer’s and aged brains. Short strands of protective RNAs are decreased during aging, the scientists report, which may allow Alzheimer’s to develop.
The study also found that older individuals with a superior memory capacity (known as SuperAgers) have higher amounts of protective short RNA strands in their brain cells. SuperAgers are individuals aged 80 and older with a memory capacity of individuals 20 to 30 years younger.
“Nobody has ever connected the activities of RNAs to Alzheimer’s,” said corresponding study author Marcus Peter, the Tom D. Spies Professor of Cancer Metabolism at Northwestern University Feinberg School of Medicine. “We found that in aging brain cells, the balance between toxic and protective sRNAs shifts toward toxic ones.”
