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I am not sure what you mean by "naked advocacy" and "nihilistic disruption" but I suppose it means that I advocate conventional, traditional, mainstream academic standards, and I think the library at Los Alamos is a better place to find scientific information than Wikipedia.

In summary, using high-throughput screening followed by medicinal chemistry optimization, in-cell assays, biochemical assessment of target engagement, and tumour models in mice and fish, we have developed a novel class of inhibitors for a hitherto unexplored category of epigenetic regulators. These inhibitors engage the MYST family of lysine acetyltransferases in primary cells, specifically induce cell cycle exit and senescence, and are effective in preventing the progression of lymphoma in mice.

A sizable amount of effort is devoted to the comparative biology of aging, and in particular mapping the noteworthy differences between naked mole-rats and other similar-sized rodent species. Naked mole-rats live nearly ten times longer than mice and are near immune to cancer. It is possible that a sufficiently comprehensive understanding of why this is the case could result in therapies for humans, though I believe the odds of this coming to pass in the near future of the next couple of decades are much larger for cancer than aging. Research into calorie restriction mimetic drugs has demonstrated that safely inducing even small shifts in the operation of metabolism, even when aiming to mimic states that occur naturally and are very well studied, is very expensive and very slow work. While naked mole-rat resistance to cancer may boil down to just a couple of mechanisms, any one of which might be exploited alone, their longevity most likely has many contributing factors, and will be much harder to map and understand.

The open access papers noted here report on what are fairly standard fishing expeditions into the cellular biochemistry of the naked mole-rat, comparing it with that of the guinea pig. This sort of work takes place throughout the research community, and in many contexts. Researchers pick likely tissues and processes to examine, and then compare as much genetic, epigenetic, and proteomic data as they have the capacity to produce and process. Differences are pulled up from the depths for examination, and theories advanced based on what is presently known. Of the findings in these papers, some reinforce earlier theories on the damage resistance of specific cellular components in naked mole-rats, particularly mitochondria, while the most interesting item is the presence of raised levels of enzymes that are protective against oxidative damage. Past research has shown that older naked mole-rats appear to have all the signs of high levels of oxidative stress, but are largely unaffected by it.

The cytosolic protein alpha-synuclein (α-syn) is associated with a range of neurodegenerative diseases, including Parkinson's disease (PD). In PD there has been discussion of the possible involvement of microglia and experiments with rodent PD models have shown that microglial activation can cause PD-like symptoms. In the current work, we establish iron overload as a mechanism to switch microglial phenotype to one that has many of the characteristics of senescent microglia. Iron overload was achieved by growing microglia in high concentrations of iron. We also show that iron overloaded (iron-fed) microglia release factors, including increased levels of the cytokine TNFα that caused an increased expression of α-syn, altered its activity, and increased its aggregation.

Founded by Reason and Bill Cherman in April 2018, Repair Biotechnologies will use these new funds to expand its foundational gene therapy development work with the addition of a recombinant protein engineering program, as it proceeds towards proof of concept results in animal models.

Pathological forms of tau can impair mitochondrial function, including mitochondrial morphology, transport, and bioenergetics. Interestingly, we found that the expression of pathological tau species, in particular truncated tau, induces mitochondrial fragmentation and bioenergetics failure in neurons. Similarly, phosphorylated tau induces mitochondrial fragmentation and affects the bioenergetics function of mature neurons. Thus, the absence of tau protein in neural cells could prevent the effects on mitochondrial structure and function produced by post-translationally-modified tau.

Considering that limited research has used tau-deficient mouse models and the role of tau on the regulation of mitochondrial function and the resulting implications on cellular and cognitive processes are not entirely clear, a study examining the impact of tau ablation will contribute to the understanding of the physiological function of tau protein in vivo. The present study was conducted in litters of young mice (3 months old) to investigate the effects of tau reduction in hippocampal tissue, to identify the implications of tau on mitochondrial function and behavior during youth.

You might recall that Juvenescence invested in AgeX Therapeutics not so long ago. AgeX aims to build out an platform that is intended as an incremental advance over present approaches to regenerative medicine, mixing in telomerase upregulation with the production and deployment of cell therapies. Juvenescence has now expanded their support of AgeX Therapeutics. It will be interesting to see how this line of work matures, and whether the AgeX staff choose to explore some of the surprising outcomes that are emerging from the induced pluripotency field these days, particularly those resulting from inducing pluripotency in vivo - something that sounds like a terrible idea, but has in fact produced initially intriguing results in mice.

The majority of mammals show adult hippocampal neurogenesis to some extent, with exceptions in dolphins, humans, and some bats. Neurogenesis seems to be under selective pressure. Under an evolutionary profile, humans have it during the youngest ages that likely had the greatest phylogenetic importance in the past. Open questions about adult human neurogenesis include: (i) are low levels of neurogenesis functionally relevant? (ii) are there vestigial/quiescent remnants of stem cell niches and can these be reactivated in some way? Some authors, considering that the new neurons within the dentate gyrus, even a low number, can be highly functional (at least in animal models), argue that "there has been evolution toward neurogenesis-based plasticity rather than away from it". At present, no systematic, fully comparable studies are available on a wide range of mammalian species to support this view.

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