Parkinson's disease (PD) is a long-term disorder of the central nervous system that mainly occurs in older people. In most cases, the cause is unknown, while only a small portions of cases can be attributed to known genetic factors. One pathogenic feature of the disease is accumulation of α-synuclein in the brain, which causes damage to brain cells that produce dopamine, an important chemical that helps regulate movement and emotional responses. Some studies indicates that inflammation in the brain is implicated in PD. New research in Acta Neuropathologica has shown how inflammation drives the development of PD. It reveals that a toll-like receptor, called TLR2, is increased in nerve cells in the brain tissues of PD patients, and activating the receptor induces inflammatory response that elevates the levels of α-synuclein, indicating that TLR2 may be a useful target for PD. Toll-like receptors (TLRs) are a class of proteins that play key roles in both the the innate and adaptive immune responses. They can detect pathogens and molecules that indicate tissue damage. The TLR signaling pathway plays a key role in inflammation. Furthermore, growing evidence shows that TLR2 is implicated in PD. In this study, the researchers examined the expression of TLR2 in the brain tissues from PD patients, and discovered that TLR2 was elevated. When the researchers activated TLR2 in stem cells, they found it stimulated a inflammatory response, leading to increased α-synuclein concentrations. Besides, a drug that inhibited TLR2 suppressed α-synuclein accumulation in neurons. The results were encouraging because they provide a new treatment strategy for HD. Flarebio provides TLR2, α-synuclein related proteins and antibodies like HRP conjugated antibody.
