Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer’s disease, affecting 7 to 10 million people worldwide. Patients with the illness have reduced levels of dopamine in the brain, causing them to have difficulty controlling motor movements, with symptoms such as tremor and rigidity of muscles in hands, arms, and legs. They can also develop some non-motor symptoms, like sleep disturbance, depression, and loss of smell. Through laboratory investigations and in vivo experiments, a team led by Professor Yoon HoSup, PhD, from the Nanyang Technological University (NTU) School of Biological Sciences in Singapore, and Professor Kwang-Soo Kim, PhD, from McLean Hospital and Harvard Medical School in the United States found that the “molecular pair,” prostaglandin E1 (PGE1), a type of hormone, and prostaglandin A1 (PGA1), can be the key to boosting dopamine levels and slowing Parkinson’s disease. PGE1 and PGA1 do this by binding to Nurr1, a class of proteins crucial to the development and maintenance of dopamine in the brain. [Editor’s Note: The nuclear receptor related 1 protein (Nurr1), also known as NR4A2 (nuclear receptor subfamily 4, group A, member 2) is a protein that in humans is encoded by the NR4A2 gene. Nurr1 is a member of the nuclear receptor family of intracellular transcription factors. Image shows Nurr1 interacting with DNA.] The binding of these prostaglandins causes Nurr1 to be activated, resulting in a marked increase in dopamine production, while preventing dopamine-producing brain cells from dying. After activation of Nurr1, mice with a model of Parkinson’s disease showed significant improvements in their motor functions.
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