Cell metabolism: scientists find new ways to diagnose and treat Parkinson's disease

September 26, 2019 / biourn / - recently, researchers at Stanford University School of medicine pointed out a molecular defect that seems to be common in Parkinson's disease patients and people who are most likely to have the disease This finding can provide a way to find neurodegenerative diseases (mainly Parkinson's disease) before symptoms begin to appear, and it can prevent the development of the disease "We have identified a molecular marker that enables doctors to diagnose Parkinson's disease accurately, early and in a clinically practical manner," said Dr Xinnan Wang, associate professor of neurosurgery "This marker can be used to assess the ability of candidate drugs to prevent disease progression." (image source: www Pixabay Com) scientists have also found a compound that appears to reverse defects in cells of Parkinson's patients The results of animal models show that the compound can effectively prevent the death of neurons The results were published in the journal Cell Metabolism on September 26 Parkinson's disease is the second most common neurodegenerative disease, affecting 35 million people worldwide Although 5% - 10% of the cases are familial (this is the genetic result of known genetic mutations), most of them involve complex interactions between multiple unknown genes and environmental factors Wang said it was encouraging that the new diagnostic markers and treatments were suitable for all types of Parkinson's patients Parkinson's disease is a kind of age-related neurodegenerative disease, which originates from the death of a group of nerve cells or neurons in the brain that regulate body movement When a patient begins to show symptoms of the disease, it is estimated that more than 50% of dopaminergic neurons have died The cause of death of these specific neurons is unclear One theory is that the special intensity of their duties disrupts the normal function of mitochondria Because the respiratory function of mitochondria inevitably produces toxic by-products called "free radicals", which not only lead to cell damage, but also extremely harmful to mitochondria themselves Parkinson's disease involves mitochondrial dysfunction The stronger the cells work, the more energy they consume and the more likely they are to be damaged Our cells have the technology to remove the old mitochondria and transfer them to the "recycling center" of cells through a series of proteins But first, the proteins have to remove what's called "Miro" from the mitochondria Wang's team previously found a mitochondrial clearance defect in cells from Parkinson's patients: they were unable to remove Miro from damaged mitochondria In the new study, Wang's team took skin samples from 83 Parkinson's patients, five close relatives who were considered at high risk, 22 patients diagnosed with other motor disorders and 52 healthy control subjects They took fibroblasts from the samples, cultured them in a dish, and then added specific pressure stimulation to disrupt mitochondrial function However, the researchers found Miro removal defects in 78 of 83 Parkinson's fibroblasts (94%) and in all five "high-risk" samples, but no Miro removal defects were found in the control group or in fibroblasts from other or other exercise patients Next, the researchers worked with atomwise Inc to screen 6835320 small molecules According to the software, 11 of them can promote the separation of mitochondria by combining with Miro In addition, the drug is reported to be non-toxic, oral and able to cross the blood-brain barrier In the experiment, the author fed these compounds to Drosophila for 7 days, and determined that four of them could significantly reduce the Miro level of Drosophila, without toxicity They tested one of the compounds on fibroblasts from patients with Parkinson's disease, demonstrating its specificity for targeting Miro Information source: scientists find potential diagnostic tool, treatment for Parkinson's disease original source: MIRO1 marks Parkinson's disease subset and MIRO1 reducer rescue neuron loss in Parkinson's models Cell metabolism 2019 Doi: https://doi.org/10.1016/j.cmet.2019.08.023