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An aging/longevity/junk dna link.

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The human body is essentially made up of trillions of living cells. It ages as its cells age, which happens when those cells eventually stop replicating and dividing. Scientists have long known that genes influence how cells age and how long humans live, but how that works exactly remains unclear. Findings from a new study led by researchers at Washington State University have solved a small piece of that puzzle, bringing scientists one step closer to solving the mystery of aging.

A research team headed by Jiyue Zhu, a professor in the College of Pharmacy and Pharmaceutical Sciences, recently identified a DNA region known as VNTR2-1 that appears to drive the activity of the telomerase gene, which has been shown to prevent aging in certain types of . The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).

Scientists at Cambridge and Leeds have successfully reversed age-related memory loss in mice and say their discovery could lead to the development of treatments to prevent memory loss in people as they age.

In a study published today in Molecular Psychiatry, the team show that changes in the extracellular matrix of the brain — ‘scaffolding’ around nerve cells—lead to loss of with aging, but that it is possible to reverse these using genetic treatments.

Recent evidence has emerged of the role of perineuronal nets (PNNs) in neuroplasticity—the ability of the brain to learn and adapt—and to make memories. PNNs are cartilage-like structures that mostly surround inhibitory neurons in the brain. Their main function is to control the level of plasticity in the brain. They appear at around five years old in humans, and turn off the period of enhanced plasticity during which the connections in the brain are optimized. Then, plasticity is partially turned off, making the brain more efficient but less plastic.

For decades, scientists have been trying to build a long-lasting replacement for the human heart. Now, an Australian inventor believes he’s cracked one of the hardest problems in medicine.

#Prognosis #Science #BloombergQuicktake.
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In March 2017, Read and his Penn State colleague David Kennedy published a paper in the Proceedings of the Royal Society B in which they outlined several strategies that vaccine developers could use to ensure that future vaccines don’t get punked by evolutionary forces. One overarching recommendation is that vaccines should induce immune responses against multiple targets. A number of successful, seemingly evolution-proof vaccines already work this way: After people get inoculated with a tetanus shot, for example, their blood contains 100 types of unique antibodies, all of which fight the bacteria in different ways. In such a situation, it becomes much harder for a pathogen to accumulate all the changes needed to survive. It also helps if vaccines target all the known subpopulations of a particular pathogen, not just the most common or dangerous ones. Richard Malley and other researchers at Boston Children’s Hospital are, for instance, trying to develop a universal pneumococcal vaccine that is not serotype-specific.

Vaccines should also bar pathogens from replicating and transmitting inside inoculated hosts. One of the reasons that vaccine resistance is less of a problem than antibiotic resistance, Read and Kennedy posit, is that antibiotics tend to be given after an infection has already taken hold — when the pathogen population inside the host is already large and genetically diverse and might include mutants that can resist the drug’s effects. Most vaccines, on the other hand, are administered before infection and limit replication, which minimizes evolutionary opportunities.

But the most crucial need right now is for vaccine scientists to recognize the relevance of evolutionary biology to their field. Last month, when more than 1000 vaccine scientists gathered in Washington, D.C., at the World Vaccine Congress, the issue of vaccine-induced evolution was not the focus of any scientific sessions. Part of the problem, Read says, is that researchers are afraid: They’re nervous to talk about and call attention to potential evolutionary effects because they fear that doing so might fuel more fear and distrust of vaccines by the public — even though the goal is, of course, to ensure long-term vaccine success. Still, he and Kennedy feel researchers are starting to recognize the need to include evolution in the conversation. “I think the scientific community is becoming increasingly aware that vaccine resistance is a real risk,” Kennedy said.

Summary: A new study found a person’s math ability was linked to levels of GABA and glutamate in the brain. In children, greater math fluency was associated with higher GABA levels in the left intraparietal sulcus, while lower levels of GABA were linked to math ability in adults. The reverse was true for glutamate in both children and adults.

Source: PLOS

The neurotransmitters GABA and glutamate have complementary roles — GABA inhibits neurons, while glutamate makes them more active.

“What is exciting about this is that although our study was only in mice, the same mechanism should operate in humans – the molecules and structures in the human brain are the same as those in rodents,” says Fawcett. “This suggests that it may be possible to prevent humans from developing memory loss in old age.”


An intriguing new study from researchers in the United Kingdom is proposing an innovative method to treat age-related memory loss. The preclinical research shows memory decline in aging mice can be reversed by manipulating the composition of structures in the brain known as perineuronal nets.

Perineuronal nets (PNNs) are structures in the brain that envelop certain subsets of neurons, helping stabilize synaptic activity. They essentially put the brakes on the neuroplasticity seen in the first few years of life.

Although PNNs are vital to the effective functioning of a mature adult brain, by their very nature they also limit future neural plasticity and adaptability. A new wave of research is beginning to investigate ways to modulate PNNs in adult brains in the hope of treating a variety of diseases from diabetes to post-traumatic stress disorder (PTSD).