Accumulation of α-synuclein in the brain is a pathological hallmark of Parkinson's disease (PD), a long-term movement disorder. This accumulation causes damage to brain cells that produce dopamine, an important chemical that helps regulate movement and emotional responses. But what causes PD is not completely understood. Some studies have shown that inflammation in the brain is a key contributor to the disease.
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TLR2 is involved in Parkinson's disease
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Posted 05 December 2016 - 12:45 AM
Now, a study appearing in the journal Acta Neuropathologica has demonstrated how inflammation drives the development of PD. The new study, led by Glenda M. Halliday from Neuroscience Research Australia, shows that a toll-like receptor, called TLR2, is increased in nerve cells in the brain tissues of PD patients.
Toll-like receptors (TLRs) are a class of proteins that play key roles in the immune response. They can detect pathogens and molecules that indicate tissue damage. TLR signaling is a major pathway mediating inflammation. Moreover, growing evidence shows that TLR2 is implicated in PD.
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