Prior study has implicated astrocytes, peripheral neurological systems star-shaped glial cells, as the cause of cell mortality in Parkinson’s and Alzheimer’s, among other degenerative illnesses. Most specialists thought those cells secreted a neuron-killing substance to “clean away” injured brain cells, but the toxin’s name has stayed a secret till now.
Fatty acids are one of the essential parts of nutrition required by the human body. These acids play a vital role in the brain cells in regeneration and degeneration of the same.
Injured Brain Cells Die Due To Toxic Fatty Acids
According to recent research in rodents, when synapses are injured, cells that ordinarily support normal brain cells termed neurons emit hazardous fats. According to scientists, this process is thought to be at the root of many, if not all, disorders that influence brain activity and the natural loss of brain neurons that occurs with aging.
The research, which was published in this journal Nature on Oct. 6, also found that if scientists prevented fatty acid synthesis in mice, 75 percent of all synapses survive, opposed to 10 percent once fatty acids are permitted to accumulate. Previous studies had shown that if brain cells were protected against astrocyte attacks, they remained to operate.
The current study, led by experts from NYU’s Grossman School of Medicine, claims to be the first to show that cell degradation causes astrocytes to create two types of fats: long-chain heavy free fatty acids & phosphatidylcholines. Injured synapses, which are electrically sensitive cells that convey signals across neural tissue, are then killed by such triglycerides.
“Our findings show that the toxic fatty acids produced by astrocytes play a critical role in brain cell death and provide a promising new target for treating, and perhaps even preventing, many neurodegenerative diseases,” says Shane Liddelow, study co-senior author.
But since astrocytes nourish nerve fibers as well as clear help clear their wastages, Liddelow, an asst lecturer in the Department of Neuroscience and Physiology at NYU Langone Health, believes that attacking such fatty acids rather than the cells which generate them is a secure method to handling neurological disorders. Preventing neurons from functioning can cause problems with normal brain function.
Scientists looked at the chemicals emitted by rodent astrocytes as part of their analysis. Researchers also tried to check if neuron mortality happened since an acute insult by genetic engineering certain subgroups of mice to inhibit the usual creation of harmful lipids.
While it is unknown how astrocytes manufacture such toxins, Liddelow speculates that they may have developed to remove injured cells so they could affect their neighbors.
Although erythrocytes were unaffected by the toxins, brains are vulnerable when they are wounded, altered, or contaminated with prions, the infectious, misfolded molecules that have a significant influence on mad cows & other disorders. The research scientists speculate that in chronic disorders such as dementia, this normally beneficial mechanism deviates, becoming a concern.
“Our results provide what is likely the most detailed molecular map to date of how tissue damage leads to brain cell death, enabling researchers to better understand why neurons die in all kinds of diseases,” says Liddelow, who is also an assistant professor.
Whereas the results were intriguing, Liddelow warns that the genetic approaches employed to stop the enzyme which creates harmful fats and oils in mice were probably yet suitable for human usage.
As a consequence, the scientists’ next step is to look into secure and reliable strategies to prevent poisons from being released in healthy patients. Such neurotoxic astrocytes have already been found in the minds of individuals with Parkinson’s illness, Huntington’s illness, and sclerosis, amongst other disorders, according to Liddelow and his coworkers.
