Tackling the inflammation cycle in Parkinson’s Disease

According to scientists familiar with the biology of the phenomenon and recent studies, the next therapeutic frontier in treating Parkinson's disease may involve preventing or reversing neuroinflammation.

A number of biopharmaceutical firms, including Olatec, Halia Therapeutics, Gain Therapeutics, and NodThera, are working to break the neuroinflammatory loop that is a contributing factor to Parkinson's disease. Researchers studying Alzheimer's disease have also been interested in neuroinflammation; firms like Vigil Neuroscience and Cerevance are focusing on the TREM2 protein and the KCNK13 gene, respectively.

Regarding Parkinson's disease, most people believe that inflammation is the body's defensive reaction to an infection or trauma. He clarified that long-term low-grade inflammation can harm brain neurons and result in cell death, and that NodThera aims to intervene and prevent this with medication.

According to David Bearss, CEO of Halia Therapeutics, chronic inflammation contributes to practically every chronic illness that can be thought of. Among the businesses investigating treatment options that target the inflammasome NLRP3, a factor in numerous neurodegenerative illnesses, are NodThera and Halia. According to Bearss, NLRP3 functions as a kind of first responder, alerting microglia to initiate the inflammatory response in order to resolve brain problems and alerting the rest of the body. Still, an issue doesn't always arise.

Halia is looking into a NEP7/NLRP3 inhibitor that may be able to stop the cycle of chronic inflammation. A protein called NEK7 is implicated in the formation of the chronic inflammation-causing NLRP3 inflammasome. According to phase I trials, this medication candidate may help deconstruct fully formed inflammasome complexes in Parkinson's disease and prevent the inflammasome from assembling.

NodThera, which released Phase II data for its NLRP3 inhibitor in March, likewise wants to stop NLRP3 and microglial dysfunction. The medication was administered to patients with Parkinson's disease at all stages for 28 days; blood and cerebrospinal fluid samples obtained on day 28 revealed inflammatory chemical levels that were significantly lower than those on day 1 and almost identical to those of healthy older persons without Parkinson's disease. Decreases were also observed in the neurodegenerative indicators soluble TREM2 and neurofilament light chain.