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Signal transduction molecules may prevent Alzheimer’s disease – Harvard Gazette

 


New studies in humans and mice identify specific signaling molecules that can help alter inflammation and the immune system to protect against Alzheimer’s disease. The study, led by researchers at the Massachusetts General Hospital (MGH) at Harvard University, It was published in Nature.

The cognitive decline associated with Alzheimer’s disease occurs when neurons begin to die. “Neuron death can be caused by inadequate immune response and excessive neuroinflammation, or brain inflammation caused by high levels of amyloid beta deposits and tau tangles, which are two hallmarks of Alzheimer’s disease. “, Explains Philip Swarski, co-author of the paper. The work was done by a senior researcher at MGH’s Systems Biology Center.

“As neurons begin to die more and more, brain cells called microglia and astrocytes (which usually grow cells that clean up debris) are activated, causing neuroinflammation in an attempt to protect the brain. It is evolutionarily programmed to wipe out areas of the brain that have excessive neuronal cell death because it may be the cause. Brain health at MGH.

In Alzheimer’s disease, neuronal cell death caused by amyloid beta deposition and tau entanglement activates this response. “If neuroinflammation continues, the amount of cell death is at least 10 times higher than that caused by stains and tangles,” says Tanzi. “In fact, without the induction of neuroinflammation, there are no symptoms of dementia. It has many plaques and tangles in the individual’s brain, but is asymptomatic at death due to minimal or no neuroinflammation.” You can tell from the “elastic” brain. Tanji provides an analogy, noting that amyloid beta is a “match” that illuminates a tangled “wildfire,” which is “forested” by neuroinflammation activated by microglia and astrocytes. Only if it leads to an increase in the number of “fires” will one be fully lost neurons suffering from cognitive decline and dementia.

With this new study in Nature, a subset of astrocytes actually try to extinguish the fire by releasing a molecule called interleukin 3 (IL-3), which is a growing cell that does not wipe out killer microglia cells. It became clear that it was returned to protected cells. Instead, focus on clearing amyloid beta deposits and tau tangles.

“It may have important clinical implications to know that astrocytes talk to microglia via IL-3, educate them, and help reduce the severity of Alzheimer’s disease.” Swirski says. “Think about how to use IL-3 to not only suppress neuroinflammation, which performs most of the neuronal cell death in Alzheimer’s disease, but also invite microglia to take on the beneficial task of removing deposits again. Can be the first medical condition of Alzheimer’s disease, entanglement. “

“I was surprised to find IL-3 in my brain,” said lead author Cameron McCarpine, followed by an instructor at the Center for Systems Biology. “Our findings suggest that IL-3-mediated communication between astrocytes and microglia is an important mechanism for preventing Alzheimer’s disease by adapting protective functions to microglia. Studies show that IL-3 signaling may offer new therapeutic opportunities to combat neurological disorders. “

Tanji is Vice-Chair of Neurology and Director of the Genetics and Aging Research Unit of MGH. Swirski is the director of the Cardiovascular Institute and a professor of medicine (cardiology) and diagnostic molecules and interventional radiology at Mount Sinai School of Medicine in New York City. McCarpine is an assistant professor of medicine (cardiology) and neuroscience at Mount Sinai School of Medicine. Co-authors of the study include Joseph Park, Ana Griciuc, Eunhee Kim, Se Hoon Choi, PhD, Yoshiko Iwamoto, and Máté G. Includes Kiss, Kathleen A. Christie, Claudio Vinegoni, Wolfram C. Poller, John E. Mindur, Christopher T. Chan. , Shun He, Henrike Janssen, Lai Ping Wong, Jeffrey Downey, Sumnima Singh, Atsushi Anzai, Florian Kahles, Mehdi Jorfi, Paolo Fumene Feruglio, Ruslan I. Sadreyev, Ralph Weissleder, Benjamin P. Kleinstiveah, Matt

This study was funded by the Cure Alzheimer’s Fund, the National Institutes of Health, the Patricia and Scott Eston MGH Research Scholar, the Canadian Institutes of Health Research Banting Fellowship, and the Kirschstein National Research Service Award’s Individual Predoctoral Fellowship.

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