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<title>Immune response linked to Parkinsons disease | National Institutes of Health (NIH)</title>
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<p class="publishdate"><span property="dc:date" datatype="xsd:dateTime" content="2017-07-11T00:00:00-04:00" class="date-display-single">July 11, 2017</span></p><div class='syndicate'><h1>Immune response linked to Parkinsons disease </h1><div class="callout callout-with-border"><h3>At a Glance</h3>
<ul>
<li>Researchers found that immune cells recognize and react to alpha-synuclein, the protein that builds up in the brains of people with Parkinsons disease.</li>
<li>These findings suggest that the immune system may play a role in the start or progression of Parkinsons disease. </li>
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</picture><span class="caption">Researchers have been trying to understand why deposits of the protein alpha-synuclein form in the brain cells of people with Parkinsons disease and what role they play in the disease. </span><span class="credit">BananaStock/Thinkstock</span></div>
</div><p>Parkinsons disease is a degenerative brain disorder that develops when nerve cells in the brain become impaired and eventually die. As these brain cells die, people with Parkinsons disease may start experiencing involuntary shaking, muscle stiffness, slowed movements, problems with balance, and other symptoms. At first, only a tremor in one hand may be noticeable. As the disease advances, people may have trouble talking, getting dressed, and walking. Theres no cure for the disease, but medicines or surgery can help with managing symptoms.</p>
<p>The affected brain cells of people with Parkinsons disease contain Lewy bodies—deposits consisting mainly of an abnormal form of a protein called alpha-synuclein. Researchers dont yet know why Lewy bodies form or what role they play in the disease. Some animal studies suggest that abnormal alpha-synuclein can trigger an immune response from T cells. These cells help the immune system destroy and remove foreign matter, but become problematic when they mistakenly attack the bodys own cells. T cells have also been found in the brains of people with Parkinsons disease. These findings suggested a connection between alpha-synuclein and immune responses.</p>
<p>To explore this possible connection, a team of researchers led by Drs. David Sulzer of the Columbia University Medical Center and Alessandro Sette of the La Jolla Institute for Allergy and Immunology carried out a study comparing T cell responses to alpha-synuclein in people with Parkinsons disease and healthy volunteers. The study was supported in part by NIHs National Institute of Neurological Disorders and Stroke (NINDS). Results were published in <em>Nature</em> on June 29, 2017.</p>
<p>The scientists collected blood samples from 67 people with Parkinsons disease and 36 healthy adults. They exposed the samples to various synthetic alpha-synuclein peptides. Each peptide represented a different fragment of the alpha-synuclein molecule. This allowed the scientists to map which regions of the protein elicit immune responses.</p>
<p>Samples taken from people with Parkinsons disease were far more likely than samples taken from healthy adults to show strong immune responses to the alpha-synuclein fragments. Two fragments, containing the S129 and Y39 regions of the alpha-synuclein protein, provoked the highest T cell responses among people with Parkinsons disease. These findings suggest that people with Parkinsons disease have a heightened immune response to alpha-synuclein.</p>
<p>“The idea that a malfunctioning immune system contributes to Parkinsons dates back almost 100 years,” Sulzer says. “But until now, no one has been able to connect the dots. Our findings show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinsons, can activate the T cells involved in autoimmune attacks.”</p>
<p>“It remains to be seen whether the immune response to alpha-synuclein is an initial cause of Parkinsons or if it contributes to neuronal death and worsening symptoms after the onset of the disease,” Sette explains. “These findings, however, could provide a much-needed diagnostic test for Parkinsons disease and could help us to identify individuals at risk or in the early stages of the disease.”</p>
<p>—by Geri Piazza</p>
</div><h2 class="label-above">Related Links</h2><ul class="spaced print-urls"><li><a href="https://www.nih.gov/news-events/nih-research-matters/tracking-parkinsonian-disease-progression" target="_top">Tracking Parkinsonian Disease Progression</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/molecule-may-impact-gaucher-parkinsons-disease" target="_top">Molecule May Impact Gaucher, Parkinsons Disease</a></li><li><a href="https://newsinhealth.nih.gov/issue/nov2014/feature2" target="_top">Parkinsons Disease: Understanding a Complicated Condition</a></li><li><a href="https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Hope-Through-Research/Parkinsons-Disease-Hope-Through-Research" target="_top">Parkinsons Disease: Hope Through Research</a></li><li><a href="https://www.genome.gov/10001217/" target="_top">Learning About Parkinson's Disease</a></li></ul><p class="footnote"><strong class="label-inline">References:&nbsp;</strong><a href="https://www.ncbi.nlm.nih.gov/pubmed/28636593">T cells from patients with Parkinson's disease recognize α-synuclein peptides</a>. Sulzer D, Alcalay RN, Garretti F, Cote L, Kanter E, Agin-Liebes J, Liong C, McMurtrey C, Hildebrand WH, Mao X, Dawson VL, Dawson TM, Oseroff C, Pham J, Sidney J, Dillon MB, Carpenter C, Weiskopf D, Phillips E, Mallal S, Peters B, Frazier A, Lindestam Arlehamn CS, Sette A. <em>Nature</em>. 2017 Jun 29;546(7660):656-661. doi: 10.1038/nature22815. Epub 2017 Jun 21. PMID: 28636593.</p><p class="footnote"><strong class="label-inline">Funding:&nbsp;</strong>NIHs National Institute of Neurological Disorders and Stroke (NINDS) and National Institute on Aging (NIA); the JPB, William F. Richter, Michael J. Fox, and Parkinsons Foundations; and the AHMMRF, JHH, and JHUSOM Parkinsons disease program.</p>
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