huntington's disease vs parkinson's

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Huntington's Disease vs. Parkinson's Disease by Haley ByrnesHealth news Is there a link between Alzheimer's, Parkinson and Huntington's diseases? Researchers focus on abnormal proteins that might be causing brain damage associated with these three neurological diseases. Is an abnormal protein the cause of Alzheimer's, Parkinson and Huntington's diseases? A group of researchers is investigating that question. If successful, your research could lead to diagnostic tools and new treatments that could be used in all three of these deadly neurological ailments. The scientists at the University of Loyola Chicago were published in the journal Acta Neuropathologica at the end of the month. "A possible therapy would involve increasing the capacity of a brain cell to degrade a group of damaged proteins and gallbladders," explained Edward Campbell, PhD, chief author of study, and associate professor at Loyola in a statement. "If we could do this in a disease, it is a good bet that therapy would be effective in the other two diseases." Neurodegenerative diseases are basically caused by the death of cells in the brain. In Alzheimer's, this destruction mainly destroys memory. In Parkinson and Huntington's, it mainly affects the movement. Despite these effective differences, Loyola researchers say they may have discovered a common thread between the trio of diseases. In the three evils, the previous research has suggested that proteins that are abnormally folded are grouped into brain cells. Different proteins have been involved in each of the three diseases. In Alzheimer's, it's tau. In Parkinson, it's alpha-synucleine. At Huntington's, it's Hunttin. Loyola researchers concluded that these different proteins behave the same way when they enter the brain cells. They said these proteins invaded gallbladders, small compartments that fit into the membranes. Proteins damage these membranes, allowing them to invade a cell's cytoplasm and cause even more destruction. Researchers said that damaged cells try to gather broken vesicles and protein groupings to destroy them. However, proteins are resistant to degradation. "The cell's attempt to degrade proteins is something like a stomach trying to digest a nail package," Campbell said. Experts in these fields told Healthline that this particular research provides some encouragement. James Hendrix, director of global scientific initiatives of the Alzheimer's Association, said that although the three diseases involve different proteins and have different effects on the brain, there is still some coincidence. He liked to study the engines of cars, planes and boats. Although they are different modes of transport, they still have similar engines. "It is valuable to have this cross-conversation. You don't want to work on a silo," Hendrix told Healthline. "A discovery in an area can revolutionize another field." George Yohrling, PhD, the senior mission director and scientific affairs of the Huntington Disease Society, agrees." They're seeing what's happening on a cellular level. What cellular machinery is being disrupted," he told Healthline. "It is reduced to cellular level," Hendrix added. "If you can understand what is going on wrong, you can prevent that mechanism from happening. " A huge breakthrough is needed for all these diseases. At the end of the month, the Centers for Disease Control and Prevention (CDC) that the Alzheimer's mortality rate in the United States increased by 55 percent between 1999 and 2014. Also, around the United States is diagnosed with Parkinson each year. It is estimated that 500,000 Americans live with the disease. Huntington's usually in his 30s and 40s. Most people die from 15 to 20 years after diagnosis. Yohrling and Hendrix both said finding a treatment that worked for the three diseases would be a truly fantastic thing. That would be wonderful," Yohrling said. That would be amazing," Hendrix added. Read this now.

12Alzheimer's, Parkinson's and Huntington share a common crucial feature Finding suggests that treatment for a disease could work for the other study at the University of Loyola Chicago has found that abnormal proteins found in Alzheimer's disease, Parkinson's disease, and Huntington's disease share a similar ability to cause damage when they invade brain cells. The finding could potentially explain the mechanism by which Alzheimer's, Parkinson, Huntington and other neurodegenerative diseases spread within the brain and alter normal brain functions. The finding also suggests that effective treatment for neurodegenerative disease could also work for other neurodegenerative diseases. The study of senior author Edward Campbell, PhD, first author William Flavin, PhD and colleagues is published in the journal Acta Neuropathologica. "A possible therapy would involve increasing the capacity of a brain cell to degrade a group of damaged proteins and gallbladders," Campbell said. "If we could do this in a disease, it is a good bet that therapy would be effective in the other two diseases. " Neurodegenerative diseases are caused by the death of neurons and other brain cells, with different diseases affecting different regions of the brain. Alzheimer's destroys memory, while Parkinson and Huntington affect movement. The three diseases are progressive, debilitating and incurable. The previous research has suggested that in the three diseases, the proteins that are abnormally folded form the lumps within the brain cells. These groups spread from cell to cell, with the time they caused cell deaths. Different proteins are involved in each disease: tau in Alzheimer's, alpha-synuclein in Parkinson's and huntin in Huntington's disease. The Loyola study focused on how these lumps of proteins invade a healthy brain cell. The authors noted that once the proteins enter into the cell, they enter into vesicles (small compartments that fit into the membranes). Proteins damage or break the vesicles membranes, allowing proteins to invade cytoplasm and cause additional dysfunction. (cytoplasm is the part of the cell that is outside the nucleus). The Loyola study also showed how a cell responds when protein groupings invade vesicles: The cell gathers the broken gallbladders and protein groupings together so that the gallbladders and proteins can be destroyed. However, proteins are resistant to degradation. "The cell's attempt to degrade proteins is something like a stomach trying to digest a nail package," Campbell said. Flavin said the finding that protein pumps associated with the three diseases cause the same type of bladder damage was unexpected. Loyola researchers initially focused on alpha-synuclein proteins associated with Parkinson's disease. So they asked the collaborator Ronald Melki, PhD, to send them samples of different types of alpha-synuclein. (To do the experiment blindly and impartially, Loyola researchers did not know what types of alpha-synuclein were which). Melki, a protein researcher at the Paris-Saclay Institute of Neuroscience, is known for its ability to generate different types of alpha-synuclein. Without telling Loyola researchers, Melki also sent other types of proteins. This led to surprise finding that tau and Hunttin proteins can also damage the gallbladders. Campbell stressed that the findings of the study should be followed and confirmed in future studies. Loyola's study is entitled: "Endoutic vesicle breakup is a preserved cellular invasion mechanism by amyloid proteins." He was supported by grants from the Michael J. Fox Foundation, Parkinson's Disease Foundation, Illinois chapter of the ARCS Foundation, Arthur J. Schmitt Foundation and other sources. Campbell is an associate professor at the Department of Microbiology and Immunology at Loyola University, Chicago Stritch School of Medicine. Flavin is a student at the University of Chicago MD/PhD Loyola. Other co-authors are Zachary Green, Stratos Skarpathiotis, and Michael Chaney from Loyola University Chicago; Luc Bousset and Ronald Melki from Paris-Saclay Institute of Neuroscience; and Yaping Chu and Jeffrey Kordower from the Rush University Medical Center. Source of history:Materials provided by . Note: Content can be edited for style and length. Journal Reference: Cite This page: Get the latest scientific news with ScienceDaily's free email newsletters, updated daily and weekly. Or see the news updated per hour in your RSS reader: Stay up to date with ScienceDaily's latest news through social media: Tell us what ScienceDaily thinks -- we welcome both positive and negative feedback. Do you have a problem with the site? Questions?

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