A study by the Queensland Institute of technology in Australia found that the risk of migraine was associated with abnormal levels of five proteins in the blood, one of which was also associated with Alzheimer's disease. This discovery is expected to bring new ideas to the development of treatment methods for migraine. Relevant papers have been published in the British journal Nature communication recently. Using data from six studies published between March 2016 and October 2020, the researchers analyzed the levels of 4625 proteins in patients' blood samples and found that when the levels of proteins fars2, GSTA4 and chic2 were low, or when the levels of proteins DKK1 and PDGFB were high, they were likely to increase the risk of migraine. Among them, the symptoms caused by the increased level of protein DKK1 are similar to the pathological changes observed in the brain of patients with Alzheimer's disease. Dale nieholt, a professor at Queensland Polytechnic University and one of the authors of the paper, said that when the levels of fars2, GSTA4 and chic2 are low, migraine related inflammation may occur. When the levels of DKK1 and PDGFB are high, it will inhibit Wnt signaling pathway and cause calcification in the brain. Wnt signal plays an important role in early embryonic development, organ formation, tissue regeneration and other physiological processes. Because the increase of DKK1 level has been confirmed to be associated with Alzheimer's disease and cerebral amyloid angiopathy, and migraine is also an early symptom of cerebral amyloid angiopathy, researchers believe that the current Wnt activator for Alzheimer's disease may also become a new method for the treatment of migraine. Nieholt points out that people with migraines do not necessarily develop Alzheimer's disease. Understanding the common pathogenesis of these two diseases will help to develop targeted diagnosis and treatment methods, alleviate migraine and prevent the deterioration of the disease. (Xinhua News Agency)
Edit：Huang Huiqun Responsible editor：Huang Tianxin
Source：gmw.cn
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