Stanford Medicine researchers have developed a blood test that measures organ biological aging, revealing that younger brains correlate with increased longevity and reduced disease risk.

Some patients with highly drug-resistant tuberculosis could benefit from a shorter treatment with fewer drugs, while others may warrant more aggressive therapy, according to the findings of a new study led by an international group of researchers, including scientists from Harvard Medical School, and conducted across six countries in Asia, Africa, and South America.
The study is the first-ever clinical trial to focus exclusively on people with pre-extensively drug-resistant tuberculosis (pre-XDR-TB), a hard-to-treat form of the disease that is more challenging to cure than multi-drug resistant TB but not as extremely impervious to medicines as the most dreaded form of the infection known as extensively drug-resistant TB.
Pre-XDR-TB is resistant to rifampin—the most potent first-line drug used against TB—and fluoroquinolone, which thus far has been the most potent second-line TB drug.
“Artificial conversion of carbon dioxide into food and chemicals offers a promising strategy to address both environmental and population-related challenges while contributing to carbon neutrality,” the team said in a paper published in the peer-reviewed journal Science Bulletin in May.
Reducing carbon dioxide to less complex molecules has proven successful, though the researchers said that generating long-chain carbohydrates – the most abundant substances in nature – has proven to be a challenge for scientists.
“In vitro biotransformation (ivBT) has emerged as a highly promising platform for sustainable biomanufacturing,” the team from the Chinese Academy of Sciences’ Tianjin Institute of Industrial Biotechnology wrote.
A recent study led by Paul DeCaen, Ph.D., associate professor of Pharmacology, has identified novel molecular mechanisms by which genetic mutations in the PKD2 gene cause the most common form of polycystic kidney disease, according to findings published in the Proceedings of the National Academy of Sciences.
PKD2 encodes an ion channel localized to the primary cilia of cells lining the kidney collecting ducts, a series of tubules and ducts that helps achieve electrolyte and fluid balance in the body. Both inherited and acquired mutations in PKD2 are known to cause autosomal dominant polycystic kidney disease (ADPKD), a condition characterized by the growth of fluid-filled cysts in the kidneys that can lead to kidney failure and other serious complications.
According to the National Institute of Diabetes and Digestive and Kidney Diseases, one in 1000 individuals will develop ADPKD and more than 95% of patients carry disease-causing genetic variants in PKD1 or PKD2. However, there are no available therapies that target these disease-causing variants.
A new Yale study has found a promising target for treating the brain fog that can follow COVID-19 and offers new insight into a hypothesis about the origin of Alzheimer’s disease.
One of the hallmarks of Alzheimer’s disease is the presence of plaque formed by the buildup of amyloid beta peptides (short chains of amino acids) in and around brain cells. Some researchers suspect that amyloid beta, which is structurally similar to antimicrobial peptides, protects the brain against bacteria, viruses, parasites, and fungal infections. Because the blood-brain barrier tends to lose its integrity in Alzheimer’s disease patients, the accumulation of amyloid beta might be a signal that pathogens are infiltrating the brain.
In a new study published in Science Advances, Yale researchers investigated whether infection by SARS-CoV-2—the virus that causes COVID-19—can trigger Alzheimer’s disease-like amyloid beta buildup, leading to neurological impairments like brain fog.