Cognito Therapeutics, founded by Prof. Ed Boyden and Prof. Li-Huei Tsai, is using a 40 Hzlight-flickering and auditory headset to help slow the progression of Alzheimer’s and restore cognition, reports William A. Haseltine for Forbes. “A recent pilot clinical trial found that this technology is not only safe and tolerable for home use, but also has a positive impact on reducing symptoms associated with age-related neurodegeneration,” writes Haseltine.
Researchers at MIT and elsewhere have identified key cell types that may protect the brain against Alzheimer’s symptoms, reports Sara Reardon for Nature. “Most Alzheimer’s research has focused on excitatory neurons, which relay electrical signals to activate other neurons,” explains Reardon. “But the authors found that the cells with reelin or somatostatin were inhibitory neurons, which halt neuronal communication. These inhibitory cells might therefore have a previously unknown role in the types of cognitive function that are lost during Alzheimer’s.”
MIT scientists have developed a new brain “atlas” and computer model that sheds insight into the brain-body connections in C. elegans worms, reports Lauren Leffer for Scientific American. “Through establishing those brain-behavior links in a humble roundworm,” writes Leffer, “neuroscientists are one step closer to understanding how all sorts of animal brains, even potentially human ones, encode action.”
In a new study, researchers at MIT showed that they “were able to interfere with an enzyme typically found to be overactive in the brains of Alzheimer’s patients,” reports Alex Mitchell for The New York Post. After using a peptide to treat the overactive enzyme, they found that “the peptide shows protective effects against loss of neurons and also appears to be able to rescue some of the behavior deficits,” says Prof. Li-Huei Tsai.
Prof. Li-Huei Tsai and Prof. Ed Boyden co-founded Cognito Therapeutics after their research found that gamma waves could help clear amyloid plaques, which are known to appear in Alzheimer’s patients, reports Ryan Cross for The Boston Globe. “It was the most surprising result I’ve ever got in my life,” says Tsai. “When we published our first paper, most people said, ‘I don’t believe it. This is too good to be true. How can something this simple have this kind of effect?’”
In an excerpt from “Your Brain on Art” published in Fast Company, Susan Magsamen and Ivy Ross spotlight Prof. Li-Huei Tsai research exploring whether gamma oscillations from light and sound could help ease Alzheimer’s symptoms. “Li-Huei believes that increased gamma oscillations in the brain engage many different systems and cell types,” write Magsamen and Ross. “Because of this, the gamma waves may help with amyloid removal.”
Researchers at MIT have found that those with an E4 variant display abnormalities in cholesterol metabolism, reports William A. Haseltine for Forbes. “The MIT team suggest that the disruption of cholesterol metabolism could be a fundamental reason why those with the E4 variant are more likely to develop Alzheimer’s disease symptoms,” writes Haseltine.
An MIT research study suggests that those with the E4 variant of the APOE gene are more likely to develop Alzheimer’s symptoms, reports William A. Haseltine for Forbes. The variant “disrupts how fat molecules are processed in the brain,” writes Haseltine. “It appears that the disruption of these fat molecules could be the fundamental reason why those that contain the E4 variant are more likely to develop Alzheimer’s symptoms.”
Researchers at MIT have found “the brain is not wired to transmit a sharp ‘stop’ command in the most direct or intuitive way,” reports Kevin Hartnett for Quanta Magazine. The brain “employs a more complicated signaling system based on principles of calculus,” writes Hartnett.
Nature reporter Elie Dolgin writes that a new study by MIT researchers explores the role of the gene variant APOE4 in Alzheimer’s, and finds that the gene is linked with faulty cholesterol processing in the brain, impacting the insulation around nerve cells and potentially causing memory and learning deficits. “The work suggests that drugs that restore the brain’s cholesterol processing could treat the disease,” writes Dolgin.
A study by Prof. Emery Brown suggests that the combination of Covid-19 and anesthesia could prompt the human brain into a state of quiet that can last weeks or months, similar to how turtles quiet their neurons to survive winter, reports Carl Zimmer for The New York Times. The findings “might point to new ways to save people from brain damage: by intentionally putting people into this state, rather than doing so by accident.”
Prof. Edward Boyden has developed a new imaging technique called expansion-revealing microscopy that can reveal tiny protein structures in tissues, reports The Economist. “Already his team at MIT has used it to reveal detail in synapses, the nanometer-sized junctions between nerve cells, and also to shed light on the mechanisms at play in Alzheimer’s disease, revealing occasional spirals of amyloid-beta protein around axons, which are the threadlike parts of nerve cells that carry electrical impulses.”
Researchers at MIT have found that the brain can send a burst of noradrenaline when it requires you to pay attention to something crucial, reports Juandre for Popular Mechanics. “The MIT team discovered that one important function of noradrenaline, commonly known as norepinephrine, is to assist the brain in learning from unexpected results,” explains Juandre.
USA Today reporter Karen Weintraub spotlights Prof. Li-Huei Tsai’s work studying a potential new approach to treating Alzheimer's disease and “whether certain tones of sound and frequencies of light can help regulate brain waves and help clear our cellular trash, including toxic proteins.” Tsai explains that: “The major difference between this approach and all other approaches is that this approach doesn’t just target one molecule or one pathway or one cell type. This is a holistic approach to take care of the whole system.”
STAT reporter Megan Molteni writes that a new study by MIT researchers finds that senescent cells, which are linked to aging, may potentially be a cause of Down syndrome. “We hope it opens up new avenues for how we look at Down syndrome — that there seems to be this whole other element that plays on a different timeline that we really need to explore more.”