Tokyo, Japan – Researchers from Tokyo Metropolitan University have discovered that impaired glucose metabolism in glial cells, a type of cell in our nervous system, plays a key role in the degeneration caused by Alzheimer’s disease. Using fruit fly retinas, they showed that promoting glucose metabolism in glial cells with tau protein build-up, like in Alzheimer’s patients, helps relieve inflammation and photoreceptor degeneration. Their findings present an exciting new therapeutic target for treating neurodegenerative conditions.

A specialized model used by researchers is becoming a valuable tool for studying human brain development, diseases and potential treatments, according to a team of scientists at Rutgers University-New Brunswick.  Known as chimeric brain models, these laboratory tools provide a unique way to understand human brain functions in a living environment, which may lead to new and better therapies for brain disorders, researchers said in a review article in Neuron.

A team of researchers at Cornell University have made a discovery in fruit flies that could change the way we understand brain diseases like Alzheimer’s and Parkinson’s in humans. The scientists found that Eato—a fruit-fly protein whose counterparts in mammals were already known for helping brain cells get rid of harmful fats—actually has a much bigger job. It not only protects neurons (brain cells), from being destroyed, but also increases the efficiency by which other cells, called phagocytes, clean up damaged neurons. 

A new 3D "atlas" of the mouse brain, developed by Duke University School of Medicine and collaborators, promises to sharpen scientists' ability to measure brain changes and share findings across studies of diseases like Alzheimer's. The Duke Mouse Brain Atlas combines microscopic detail from multiple imaging techniques into a living, distortion-free map—offering a powerful new tool for research and discovery. The open-source atlas, reported April 30 in Science Advances, is already helping scientists track neurodegeneration in mouse models.

Researchers have developed a new protocol to transplant immune cells called microglia into the brain – and show the strategy can protect neurons and combat hallmarks of neurological disorders in mice. Their therapy stands out from traditional microglia replacement methods because it doesn’t rely on risky conditioning regimens, making it a safer and more practical approach for microglia replacement. Studies have established a firm link between some neurological disorders and defects in microglia, which are immune cells that maintain and clean up the central nervous system. Scientists theorize that correcting or replacing these dysfunctional microglia could help treat neurological conditions such as Alzheimer’s disease. However, traditional methods to replenish microglia rely on bone marrow transplantation, which is arduous and inefficient. Furthermore, these transplants require strict preconditioning regimens that use radiation or chemotherapy, which can damage the brain, and the microglia that result from the transplanted bone barrow aren’t faithful copies of the originals. To avoid the need for preconditioning, Dadian Chen and colleagues developed a new approach named tricyclic microglial depletion for transplantation (TCMDT). This strategy uses three cycles of an experimental compound that inhibits the CSF1R receptor, which microglia require to proliferate. The treatments deplete the native, dysfunctional microglia and provide an optimal window to transplant cultured, healthy microglia. Chen et al. found that TCMDT given before symptoms replaced defective microglia and slowed the degeneration of neurons in mouse models of Alzheimer’s disease and Sandhoff disease, an inherited neurodegenerative disorder. The team calls for further research into the mechanisms at play, and to test whether human induced pluripotent stem cells could be used as a more clinically relevant source for microglia.