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Category: life extension – Page 325

Well, they don’t.

Thousands are currently engaged in solving the problem of death. Maybe they’ll succeed, and out of sheer boredom I’ll reread this sentence when I’m 900 years old, reflecting fondly on the first wasted century of my life. In the meantime, billions are going to die—some from disease, some in freak accidents, and a substantial number from what we generally call “old age.” That last sounds like a pleasant way to go, comparatively—a peaceful winding-down. But what exactly does it look like? What does it really mean to die from old age? For this week’s Giz Asks, we reached out to a number of experts to find out.

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A study from researchers at KAIST (Korea Advanced Institute of Science and Technology) is providing new insights into a cellular energy pathway that has been linked to longer lifespan. The research, conducted in human cells and roundworms, raises the prospect of anti-aging therapeutics that can extend lifespan by activating this pathway.

AMPK (adenosine monophosphate-activated protein kinase) is an enzyme that acts as a metabolic master switch. It has been described as a “magic bullet” protein, conferring broad beneficial health effects, from improving cardiovascular health to extending lifespan. It is activated in response to low cellular energy levels, as is often seen during exercise or periods of caloric restriction.

An increasing volume of study has found activating AMPK in animal models leads to notable increases in lifespan, prompting a surge in research investigating this enzyme.

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Ready for the latest recommended weekly reads in the world of stem cells and the regenerative medicine space including a bunch of important new FDA posts & changes?

This post has quite a lot on the FDA since it had a very big week with several new items of major importance to the cellular and regenerative medicine arena. I’ve linked to each announcement below with the agency’s title of the announcements. Underneath I provide some analysis and ask questions.

I’ve also included some other stem cell news and exciting papers too as usual, which I’ll start with here.

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In mammals, the acquisition of the germline from the soma provides the germline with an essential challenge, the necessity to erase and reset genomic methylation1. In the male germline, RNA-directed DNA methylation silences young active transposable elements (TEs)2–4. The PIWI protein MIWI2 (PIWIL4) and its associated PIWI-interacting RNAs (piRNAs) instruct TE DNA methylation3,5. piRNAs are proposed to tether MIWI2 to nascent TE transcripts; however, the mechanism by which MIWI2 directs de novo TE methylation is poorly understood but central to the immortality of the germline. Here we define the interactome of MIWI2 in foetal gonocytes that are undergoing de novo genome methylation and identify a novel MIWI2-associated factor, SPOCD1, that is essential for young TE methylation and silencing. The loss of Spocd1 in mice results in male-specific infertility but impacts neither piRNA biogenesis nor localization of MIWI2 to the nucleus. SPOCD1 is a nuclear protein and its expression is restricted to the period of de novo genome methylation. We found SPOCD1 co-purified in vivo with DNMT3L and DNMT3A, components of the de novo methylation machinery as well as constituents of the NURD and BAF chromatin remodelling complexes. We propose a model whereby tethering of MIWI2 to a nascent TE transcript recruits repressive chromatin remodelling activities and the de novo methylation apparatus through SPOCD1. In summary, we have identified a novel and essential executor of mammalian piRNA-directed DNA methylation.

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Even healthy brains become less efficient as they age, but they do so at different rates for different tasks in different people. Understanding what contributes to this decline, and the ways in which that decline varies, can provide significant insight into the function of the brain.

In a new study, researchers at The University of Texas at Dallas documented how some parts of the brain perform differently over time in response to various kinds of visual input.

A team from the Center for Vital Longevity (CVL) analyzed a phenomenon called neural dedifferentiation, in which regions of the brain that normally are specialized to perform distinct tasks become less selective in their responses to stimulus types.

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I hope they get funding.

SAN DIEGO — The average American lives to be around 75 or 80 years old; but if you had an opportunity to slow down the aging process and live an extra couple of decades would you take it? It’s a loaded question, strife with philosophical, religious, and societal considerations. Humans have pondered the possibilities of extended, or even immortal, life for as long as we’ve inhabited this planet. But at the end of the day it’s all just a daydream, right?

Not necessarily, according to new research out of the University of California, San Diego. The study, led by UCSD molecular biologists and bioengineers, produced a groundbreaking discovery regarding the intricacies of cellular aging. In light of their findings, researchers say the notion of “dramatically” extending human life isn’t so farfetched after all.

Each human’s lifespan and personal rate of aging is determined by the aging of their individual cells. Originally, the study’s authors just wanted to investigate if different types of cells age at different speeds based on different stimuli/causes. To that end, they studied aging in the budding yeast Saccharomyces cerevisiae. This provided a suitable model with which to track aging mechanisms of various cell types.

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While the issue of aging and DNA methylation is an area that is well-studied, modifications of DNA to reduce or reverse aging remains an area in need of exploration. Studies in mice utilizing interventions such as caloric restriction and the drug rapamycin have reversed and/or slowed age-related DNA methylation by up to 40%. Understanding the cross-species aging based on similar DNA behaviors may open more doors to investigating therapeutics to minimize lifetime risks of age-related illnesses such as Alzheimer’s disease and cancers.

A recent study published in Cell Systems sought to debunk one of the most common myths about dogs: much to our surprise, one “dog year” does not equal seven “human years.” As described in a recent Forbes piece by Sara Tabin, the relationship between dog years and human years is not linear, but is based on a logarithmic formula. The research group, based at the University of California, San Diego (UCSD), created the formula as follows:

Age in human years = 16 ln(age in dog years) +31. (ln means “natural logarithm).

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Japan boasts one of the longest life expectancies on earth, and it also a world leader in “healthy life expectancy”—the number of years of good health people can expect on average. Since diet is believed to play a key role in a population’s health and longevity, researchers around the world have been studying the benefits of the Japanese diet for some time now.

But what exactly is the Japanese diet? The people of Japan do not dine primarily on sushi, tempura, or other well-known Japanese specialties. Moreover, their eating habits have changed over the years. For our research, we used national surveys to compile weekly menus representative of the Japanese diet at various points in time over the past half century. In the following, we will take a look at the comparative health effects of these menus.

The health benefits of Japanese cooking are widely touted, but what exactly is a healthy Japanese diet? Food scientists in Japan have homed in on the nutritional keys to health and longevity, and their conclusions may bode ill for the younger generation.

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