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X-ALD is the most prevalent of the approximately 50 rare diseases that affect the white matter of the brain, referred to as leukodystrophies. The genetic damage in X-ALD is due to a defect in the X chromosome. Men who are affected by X-ALD experience a progressive deterioration of their mobility, balance, and sensory abilities, leading to issues such as incontinence and sexual dysfunction.

Although X-ALD is inherited through the X chromosome, female carriers can also experience symptoms of the disease. Approximately 30% of male children and 60% of adult men develop encephalitis, which is a fatal form of the disease that leads to death within two to three years. X-ALD affects roughly one in every 20,000 births globally.

Now, for the first time, scientists from all relevant leukodystrophy centers in Europe and the US have jointly succeeded in obtaining controlled trial data for X-linked adrenoleukodystrophy. Of the 116 patients, 77 received the drug leriglitazone and 39 a placebo. The drug had already shown in preclinical studies that it can prevent neurodegeneration and offer protection against the life-threatening inflammation of the brain.

For species classified as “extinct in the wild”, the zoos and botanical gardens where their fates hang by a thread are as often anterooms to oblivion as gateways to recovery, new research has shown.

Re-wilding what are often single-digit populations faces the same challenges that pushed these to the cusp of in the first place, including a lack of genetic diversity. But without , experts say, chances of these species surviving would be even smaller.

Since 1950, nearly 100 animal and plant species vanquished from nature by hunting, pollution, deforestation, invasive lifeforms and other drivers of extinction have been put into by scientists and conservationists, according to the findings.

On December 18, 2019, Wuhan Central Hospital admitted a patient with symptoms common for the winter flu season: a 65-year-old man with fever and pneumonia. AI Fen, director of the emergency department, oversaw a typical treatment plan, including antibiotics and anti-influenza drugs.

Six days later, the patient was still sick, and AI was puzzled, according to news reports and a detailed reconstruction of this period by evolutionary biologist Michael Worobey. The respiratory department decided to try to identify the guilty pathogen by reading its genetic code, a process called sequencing. They rinsed part of the patient’s lungs with saline, collected the liquid, and sent the sample to a biotech company. On December 27, the hospital got the results: The man had contracted a new coronavirus closely related to the one that caused the SARS outbreak that began 17 years before.

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Substance use disorder (SUD) is an extremely difficult disorder to overcome, and many individuals with SUD return to regular use after repeated attempts to quit.

A return to regular can be caused by the body’s physical dependence on the drug as well as experiences associated with prior drug use. Exactly how these drug associations are formed in the brain and how they trigger a return to drug use remain unclear.

“Individuals make long-lasting associations between the euphoric experience of the drug and the people, places and things associated with drug use,” said Christopher Cowan, Ph.D. professor in the Department of Neuroscience at the Medical University of South Carolina (MUSC) and member of the Brain and Behavior Research Foundation Scientific Council.

Talking about E5.


Rats are also useful for aging research and for cooking ratatouille. But in all seriousness, take a look at this recent headline article — “We have the oldest living female Sprague Dawley rat,” said Dr Harold Katcher, a former biology professor at the University of Maryland, now chief scientific officer at Yuvan Research, a California-based startup.

So, Rejuvenation & rats. That’s what we’re talking about today, and how this rat has apparently become the longest living rat for its species following concentrated plasma injections from young blood plasma, and what this could mean for human therapeutics, along my perspectives. But, before we get there we must go back, back to the late 1950s and early 1960…to a time when The Sheekey Science Show did not exist, but when researchers, such as Clive McKay did, and these researchers were conducting a procedure called heterochronic parabiosis.

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Cancer is not a uniform disease. Rather, cancer is a disease of phenotypic plasticity, meaning tumor cells can change from one form or function to another. This includes reverting to less mature states and losing their normal function, which can result in treatment resistance, or changing their cell type altogether, which facilitates metastasis.

In addition to direct changes in your DNA in cancer, a key driver of cancer progression is where and when your DNA is activated. If your DNA contains the “words” that spell out individual genes, then epigenetics is the “grammar” of your genome, telling those genes whether they should be turned on or off in a given tissue. Even though all tissues in the body have almost exactly the same DNA sequence, they can all carry out different functions because of chemical and structural modifications that change which genes are activated and how. This “epigenome” can be influenced by environmental exposures such as diet, adding a dimension to how researchers understand drivers of health beyond the DNA code inherited from your parents.

I’m a cancer researcher, and my laboratory at Johns Hopkins University studies how the differences among normal tissues are controlled by an epigenetic code, and how this code is disrupted in cancer. In our recently published review, colleague Andre Levchenko at Yale University and I describe a new approach to understanding cancer plasticity by combining epigenetics with mathematics. Specifically, we propose how the concept of stochasticity can shed light on why cancers metastasize and become resistant to treatments.