Lifeboat Foundation: Safeguarding Humanity
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Category: life extension – Page 608

(Phys.org) —Tufts University biologists using new, automated training and testing techniques have found that planarian flatworms store memory outside their brains and, if their heads are removed, can apparently imprint these memories on their new brains during regeneration.

The work, published online in the Journal of Experimental Biology, can help unlock the secrets of how memories can be encoded in living tissues, noted Michael Levin, Ph.D., Vannevar Bush professor of biology at Tufts and senior author on the paper.

“As and biomedicine advance, there’s a great need to better understand the dynamics of memory and the brain-body interface. For example, what will happen to stored memory if we replace big portions of aging brains with the progeny of fresh ?” said Levin, who directs the Center for Regenerative and Developmental Biology in Tufts’ School of Arts and Sciences.

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The quest for the fountain of youth is as ancient as humanity itself. Now, it appears scientists may have found the source.

Using a process designed to “reprogram” normal adult cells into pluripotent stem cells—cells that can transform into many different kinds of cells—researchers have managed to boost the life spans of mice by up to 30% and rejuvenate some of their tissues.

The treatment did not change the cell’s genetic code, but rather chemical attachments on their DNA called epigenetic marks, responsible for regulating the genome and determining how active certain genes are.

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Senolytics to remove senescent cells will deliver the first “repair” based approach to treat the aging process. This is the arrival of true rejuvenation biotechnology in the SENS model of damage repair.

Senescent cell removal with companies such as Unity, entering human clinical trials in the next 18 months will deliver the first true damage repair rejuevenation biotechnology. This will be the first “repair” approach to the aging process and one the SENS Research Foundation has been advocating for over a decade.

#aging #crowdfundthecure

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This is probably important.

Scientists at The Scripps Research Institute (TSRI) have discovered a protein that fine-tunes the cellular clock involved in aging.

This novel , named TZAP, binds the ends of chromosomes and determines how long , the segments of DNA that protect chromosome ends, can be. Understanding telomere length is crucial because telomeres set the lifespan of cells in the body, dictating critical processes such as aging and the incidence of cancer.

“Telomeres represent the clock of a cell,” said TSRI Associate Professor Eros Lazzerini Denchi, corresponding author of the new study, published online today in the journal Science. “You are born with telomeres of a certain length, and every time a cell divides, it loses a little bit of the telomere. Once the telomere is too short, the cell cannot divide anymore.”

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Once again the figures show that young to old disparity in the population is the problem not overpopulation. We really need to develop rejvenation biotechnology with all haste.

Once again overpopulation isnt the problem it is the disparity between young and old in the workforce. This makes rejuvenation biotechnology a suitable solution to avoid economic collapse.

“The world is experiencing unparalleled population aging. This poses problems for productivity and growth, unless we do something about it”

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The microglia are central to aging in the brain and science is already finding ways to reverse it like introducing young microglia to the brain to remove plaques associated with Alzheimers. Brain aging is not a one way process!

The difference between an old brain and a young brain isn’t so much the number of neurons but the presence and function of supporting cells called glia. In Cell Reports on January 10, researchers who examined postmortem brain samples from 480 individuals ranging in age from 16 to 106 found that the state of someone’s glia is so consistent through the years that it can be used to predict someone’s age. The work lays the foundation to better understand glia’s role in late-in-life brain disease.

“We extensively characterized aging-altered changes across 10 human and found that, in fact, glial cells experience bigger changes than ,” says Jernej Ule, a neurobiologist at the Francis Crick Institute and the University College London, who led the study with departmental colleague Rickie Patani (@PataniLab) and first author Lilach Soreq. “There’s quite a bit of regional information that will be of interest to different people—for example some will notice a very unique pattern of astrocyte-specific changes in the substantia nigra—and we provide a lot of data that still needs to be analyzed.”

There are three types of glia cells, each providing different kinds of support to neurons: oligodendrocytes insulate, microglia act as immune cells, and astrocytes help with neuron metabolism, detoxification, among many functions. Based on analysis of human tissue samples, primarily from the UK Brain Expression Consortium, the researchers show that astrocytes and oligodendrocytes shift their regional gene expression patterns upon aging, (e.g., which genes are turned on or off) particularly in the hippocampus and substantia nigra—important brain regions for memory and movement, respectively—while the expression of microglia-specific genes increases in all brain regions.

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