Mount Sinai study Maps Sienny production of the washed pathogeans Alzheimer

The new study conducted by the ICAHN School of Medicine on Mount Sinai offers one of the most comprehensive views on the interaction of brain cells in Alzheimer’s disease, mapping protein networks that reveal communication failures and indicate new therapeutic possibilities.

The study published online on September 25 analyzed protein activity in brain tissue from almost 200 people. Scientists have found that disturbances in communication between neurons and supporting cerebral cells called astrocytes and microgle-are closely related to the progression of Alzheimer’s disease. In particular, one protein, called Ahnak, was identified as the highest factor of these harmful interactions.

Alzheimer does not only apply to the accumulation of tiles or dying neurons; It’s about how the entire brain ecosystem breaks down. Our study shows that the loss of healthy communication between neurons and glial cells It can be the main cause of the disease. “

Bin Zhang, dr.

Most Alzheimer’s research focused on the accumulation of amyloid tiles and Tau’s tangles. But these accumulation of proteins themselves do not explain the full history, and some treatments focused on tiles only bring little benefits. In this study, the team adopted the so -called “without supervision” approach, which does not start with the assumptions that proteins are important in the most by examining brain tissue samples with almost 200 people with Alzheimer’s disease.

“This study brought a broader view, examining how over 12,000 proteins interact in the brain,” said the author, Dr. Junmin Peng, a member and professor of structural biology and development neurobiology in a research hospital for children of St. Jude. “Using the latest protein profiling technology, the protein expression in the brain was quantitatively determined, enabling a comprehensive view of proteomical changes and interactions in Alzheimer.”

Using advanced computing modeling, they built a large -scale networks that reproduced how these proteins interact and indicate where communication is distributed in the disease, enabling the identification of entire systems that are not so instead of focusing on one molecule. The most critical among these systems is Glej-Neuron communication, which lies at the center of Alzheimer’s Proteomic Network. In healthy brains, neurons send and receive signals, while glial cells support and protect them. But in Alzheimer’s disease, this balance seems lost: glial cells become overactive, neurons become less functional and inflammation rises. This change was consistent in many independent data sets.

Analyzing how the proteomic networks moved in Alzheimer’s disease, scientists identified a number of “key drivers” protein molecules that seem to play an exceeded role in releasing or accelerating the disease.

Ahnak, protein found mainly in astrocytes, was one of the best -rated drivers. The team said that Ahnak levels grow as Alzheimer’s progress and are associated with a higher level of toxic proteins in the brain, such as beta amyloid and tau. To test its influence, they used models of human brain cells from stem cells. The reduction of Ahnak in these cells led to a decrease in Tau levels and improving the neuron function after the laboratory factor.

“These results suggest that Ahnak can be a promising therapeutic goal,” said the author, author of MD, author, Dongming Cai, neurology professor and director of the Grossman Center for Memory Research and Care at the University of Minnesota. “By lowering its activity, we saw both less toxicity and greater neuronal activity, two encouraging signs that we can be able to restore a healthier brain function.”

While Ahnak is a strong candidate for the future development of drugs, studies are also a wider framework for understanding and treating Alzheimer’s disease. The study identified over 300 proteins, which were rarely studied in the context of the disease, offering new tests.

It also showed that various biological factors, such as genetic genetic and background, can affect the behavior of these protein networks. For example, people with a gene, a well -known genetic risk factor for Alzheimer’s disease, showed clear patterns of network disturbances compared to people without a gene.

While more work is needed to study Ahnak and other key proteins in live systems, comprehensive data from this study is publicly available to scientists around the world, accelerating progress throughout the field.

“This study opens a new way of thinking about Alzheimer’s disease, not only as the accumulation of toxic proteins, but as a breakdown in how brain cells talk to each other,” added Dr. Zhang. “Understanding these conversations and where they are wrong, we can start developing treatments that will restore the system to balance.”