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Category: life extension – Page 80

Aging is a common phenomenon among organisms, however, lifespan tends to vary across different species to a significant extent among vertebrates themselves. Aging occurs due to the gradual increase in DNA damage, disruption of cellular organelles, deregulation of protein function, disrupted metabolism and oxidative stress [1].

Longevity. Technology: The differences in lifespan are driven by trade-offs and evolutionary trajectories in the genomes of organisms. Age-specific selection also impacts allele (variations of a gene) frequencies in a population. This in turn impacts environment-specific mortality risk and disease susceptibility. Moreover, mutational processes are influenced by life history and age in both somatic and germline cells.

Now, a new review published in Trends in Genetics discusses recent advances in the evolution of aging at population, organismal and cellular scales.

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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.

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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.

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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.

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