Release date: 2007-11-05
Scientists have long struggled to understand and treat neurodegenerative diseases like Alzheimer’s, multiple sclerosis, and sporadic Creutzfeldt-Jakob disease. These conditions cause the gradual breakdown of nerve cells, leading to severe cognitive and physical impairments. However, a recent breakthrough by researchers at the University of Michigan has shed new light on the underlying mechanisms behind this cellular degeneration.
The study, published in the *Journal of the National Academy of Sciences*, focused on a previously unknown signaling molecule called PI(3,5)P2, or phosphatidylinositol-3,5-diphosphate. This lipid is found in all cells but exists in very low concentrations. It plays a crucial role in cellular communication, helping cells respond to changes in their environment and maintain internal balance.
Professor Louis Eisman and his team discovered that PI(3,5)P2 is essential for the health and survival of nerve cells. They found that when the levels of this molecule drop, it leads to significant neuronal damage. This discovery was made possible through research on genes involved in the production of PI(3,5)P2, specifically the *FIG4* and *VAC14* genes, which are present not only in yeast but also in mammals, including humans.
In experiments with rats, the absence of the *VAC14* gene resulted in severe neurological damage. The brains of these animals developed spongy, hollow areas, resembling the degeneration seen in mice with mutations in the *FIG4* gene. These findings suggest that disruptions in PI(3,5)P2 signaling may be a key factor in various neurodegenerative disorders.
This research opens up new possibilities for developing treatments for diseases like Alzheimer’s. By understanding how PI(3,5)P2 functions and how its levels can be maintained, scientists may one day find ways to prevent or slow down the progression of these devastating conditions.
— China Medicine 123 Network
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