Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson's Disease.
Érica Novaes SoaresAna Carla Dos Santos CostaGabriel de Jesus FerrolhoRodrigo Portes UreshinoBruk GetachewSilvia Lima CostaVictor Diógenes Amaral SilvaYousef TizabiPublished in: Cells (2024)
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.
Keyphrases
- induced apoptosis
- cell cycle arrest
- neuropathic pain
- randomized controlled trial
- stem cells
- traumatic brain injury
- spinal cord injury
- cell therapy
- endoplasmic reticulum stress
- bipolar disorder
- depressive symptoms
- signaling pathway
- spinal cord
- cognitive impairment
- metabolic syndrome
- parkinson disease
- blood pressure
- subarachnoid hemorrhage
- single cell
- uric acid
- cell proliferation
- single molecule