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Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease

2024; Multidisciplinary Digital Publishing Institute; Volume: 13; Issue: 6 Linguagem: Inglês

10.3390/cells13060474

2073-4409

Érica Novaes Soares, Ana Carla dos Santos Costa, Gabriel de Jesus Ferrolho, Rodrigo Portes Ureshino, Bruk Getachew, Sílvia Lima Costa, Víctor Diógenes Amaral da Silva, Yousef Tizabi,

Adenosine and Purinergic Signaling

Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, and postural instability that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) is the primary neurotransmitter involved in this disease, but cholinergic imbalance has also been implicated. Current intervention in PD is focused on replenishing central DA, which provides remarkable temporary symptomatic relief but does not address neuronal loss and the progression of the disease. It has been well established that neuronal nicotinic cholinergic receptors (nAChRs) can regulate DA release and that nicotine itself may have neuroprotective effects. Recent studies identified nAChRs in nonneuronal cell types, including glial cells, where they may regulate inflammatory responses. Given the crucial role of neuroinflammation in dopaminergic degeneration and the involvement of microglia and astrocytes in this response, glial nAChRs may provide a novel therapeutic target in the prevention and/or treatment of PD. In this review, following a brief discussion of PD, we focus on the role of glial cells and, specifically, their nAChRs in PD pathology and/or treatment.