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Study leads to potential for new treatment approach to Alzheimer’s

Research looking at a possible new therapeutic approach for Alzheimer’s disease was recently published in the Journal of Neuroinflammation. The paper out of the University of Kentucky’s Sanders-Brown Center on Aging (SBCoA) is titled “Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition”. The work looked at targeting inflammation by using an antibody. Alzheimer’s disease and related dementias have no disease-modifying treatments at this time and represent a looming public health crisis given the continually growing aging population.

The paper explains that current therapeutic approaches to the treatment of Alzheimer’s focus on the major pathological hallmarks of the disease which are and neurofibrillary tangles. They are the requirements for a diagnosis of Alzheimer’s disease. However, the authors say there has been an explosion of genetic data suggesting the risk for sporadic Alzheimer’s disease is driven by several other factors including neuroinflammation, membrane turnover and storage, and .

In this study the researchers focused on triggering receptor expressed on myeloid cell-2 (TREM2). “TREM2 was identified several years ago as a gene that, when there’s a mutation, significantly increases risk of Alzheimer’s disease. The field thinks that this mutation reduces the function of the receptor, so we hypothesized that targeting TREM2 to increase its function might be a valid treatment for Alzheimer’s,” explained Donna Wilcock, SBCoA associate director.

The US military is trying to read minds

Elon Musk’s Neuralink will likely show off its design for a brain-computer interface Friday evening. The concept it unveiled last summer involves surgically implanting it into the brain to detect the activity of neurons. The US military also wants to develop a brain-computer interface, as we explain in this story from October. But here’s the kicker: no surgery required—and the device could be put on and taken off like a helmet or headband.


In August, three graduate students at Carnegie Mellon University were crammed together in a small, windowless basement lab, using a jury-rigged 3D printer frame to zap a slice of mouse brain with electricity.

The brain fragment, cut from the hippocampus, looked like a piece of thinly sliced garlic. It rested on a platform near the center of the contraption. A narrow tube bathed the slice in a solution of salt, glucose, and amino acids. This kept it alive, after a fashion: neurons in the slice continued to fire, allowing the experimenters to gather data. An array of electrodes beneath the slice delivered the electric zaps, while a syringe-like metal probe measured how the neurons reacted. Bright LED lamps illuminated the dish. The setup, to use the lab members’ lingo, was kind of hacky.

Artificial Kidneys Are a Step Closer With This New Tech

Our kidneys are crucial for keeping us alive and healthy. A sort of chemical computer that keeps our blood chemistry stable—whether we’re eating a sugary birthday cake or a vitamin-filled salad—they prevent waste buildup, stabilize our electrolyte levels, and produce hormones to regulate our blood pressure and make red blood cells.

Kidneys clean our blood using nephrons, which are essentially filters that let fluid and waste products through while blocking blood cells, proteins, and minerals. The latter get reintegrated into the blood, and the former leave the body in urine.

Scientists have struggled to come up with viable treatments for kidney disease and renal failure, and their complexity means kidneys are incredibly hard to synthetically recreate; each kidney contains around one million intricately-structured nephrons.

Scientists find that Citriodiol, ingredient in insect repellent, can kill COVID-19

British scientists have discovered that an active ingredient found in insect repellent can kill COVID-19, according to a report.

Researchers at the UK’s Defense Science and Technology Laboratory determined that Citriodiol can help fight coronavirus in a preliminary study, Sky News reported.

Insect repellents containing Citriodiol are not believed to be enough alone to protect people from the virus but can be used as an additional layer of defense along with face masks, hand washing and other health recommendations, according to the report.

Japanese doctor who lived to 105—his spartan diet, views on retirement, and other rare longevity tips

Dr. Shigeaki Hinohara had an extraordinary life for many reasons. For starters, the Japanese physician and longevity expert lived until the age of 105.

When he died, in 2017, Hinohara was chairman emeritus of St. Luke’s International University and honorary president of St. Luke’s International Hospital, both in Tokyo.

Perhaps best known for his book, “Living Long, Living Good,” Hinohara offered advice that helped make Japan the world leader in longevity. Some were fairly intuitive points, while others were less obvious:

Body fat transformed by CRISPR gene editing helps mice keep weight off

White fat cells can be turned into energy-burning brown fat using CRISPR gene-editing technology. These engineered cells have helped mice avoid weight gain and diabetes when on a high-fat diet, and could eventually be used to treat obesity-related disorders, say the researchers behind the work.

Human adults have plenty of white fat, the cells filled with lipid that make up fatty deposits. But we have much smaller reserves of brown fat cells, which burn energy as well as storing it. People typically lose brown fat as they age or put on weight. While brown fat seems to be stimulated when we are exposed to cold temperatures, there are no established methods of building up brown fat in the body.

Progress towards a cure for herpes

Researchers at the Fred Hutchinson Cancer Research Center in Seattle, USA, have used gene editing to remove latent herpes simplex virus 1 (HSV-1), also known as oral herpes.

In mice, the technique showed a 92% decrease in the latent virus – enough to keep the infection from coming back, according to the scientists. The study used two sets of “genetic scissors” to damage the virus’s DNA, fine-tune a delivery vehicle to the infected cells, and target the nerve pathways connecting the neck with the face, reaching the tissue where the virus lies dormant. The findings are published in Nature Communications.

“This is the first time that scientists have been able to go in and actually eliminate most of the herpes in a body,” said senior author Dr. Keith Jerome, Professor in the Vaccine and Infectious Disease Division at Fred Hutch. “We are targeting the root cause of the infection: the infected cells where the virus lies dormant and are the seeds that give rise to repeat infections.”

A ‘Kill Switch’ for Rogue Microbes

Biologists often speak of switching genes on and off to give microbes new abilities–like producing biofuels or drugs, or gobbling up environmental toxins. For the most part, though, it’s nearly impossible to turn off a gene without deleting it (which means you can’t turn it on again). This limits biologists’ ability to control how much of a particular protein a microbe produces. It also restricts bioengineers’ ability to design new microbes.

Now researchers at Boston University, led by biomedical engineering professor James Collins, have developed a highly tunable genetic “switch” that offers a greater degree of control over microbes. It makes it possible to stop the production of a protein and restart it again. The switch, which could be used to control any gene, can also act as a “dimmer switch” to finely tune how much protein a microbe would produce over time.

The researchers made a highly effective microbe “kill switch” to demonstrate the precision of the approach. For years, researchers have been trying to develop these self-destruction mechanisms to allay concerns that genetically engineered microbes might prove impossible to eradicate once they’ve outlived their usefulness. But previous kill switches haven’t offered tight enough control to pass governmental regulatory muster because it was difficult to make it turn on in all the cells in a population at the same time.