Could there really be a magic pill for immortality?

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.

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.

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.

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 methylation^3,5. 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.