Neuroinflammation-induced neurodegeneration and associated microglia activation in Parkinson’s disease: a novel neurotherapeutic avenue

Abstract

Parkinson’s disease (PD) is classified as one type of neurodegenerative disorder. Movement disorder, which includes resting tremors and slowness of movement, is a common clinical symptom in PD patients. Neuroinflammation is one of the most important processes involved in the pathogenesis of PD. An inflammatory response in the brain can induce neuronal cell death. Microglia, a type of immune cell, plays a crucial role in neuroinflammation. In this review, we discussed the information on microglia-activated neuroinflammation, its relationship with PD, and therapeutic approaches for neuroinflammation in PD. Under normal conditions, microglia in their inactive state (M0) act as surveillance agents in the brain to investigate potential invasions. They regulate neuron production, remodel synapses, and secrete growth factors to protect the neurons. Under pathological conditions, the M0 transforms into active phenotypes, dividing into pro-inflammatory (M1) and anti-inflammatory (M2) microglia. The M1 and M2 microglia exhibit opposite functions, where M1 microglia promote pro-inflammatory responses, and M2 microglia promote anti-inflammatory responses. This dichotomy of functions is essential for maintaining a healthy level of inflammation in the brain. Presently, multiple therapeutic strategies are available for PD, encompassing anti-inflammatory drugs, neuroprotective compounds, antioxidants, nanoparticles targeting neuroinflammation, stem cell interventions, lifestyle adjustments, and microglia-focused treatments. These treatments improve patients' movement, allowing them to have lifestyles like others, consequently benefiting their mental and emotional well-being. Preventing microglia from polarising into the M1 phenotype and promoting their polarisation into the M2 phenotype could be a challenging and promising approach for treating PD.