Parkinson’s disease (PD) is a relatively common disorder of the Central Nervous System (CNS), whose
etiology is characterized by a selective and progressive degeneration of dopaminergic neurons, and the presence of
Lewy bodies in the pars compacta of the substantia nigra, and gaping dopamine depletion in the striatum. Patients
with this disease suffer from tremors, slowness of movements, gait instability, and rigidity. These patients may also
present functional disability, reduced quality of life, and rapid cognitive decline. It has been shown that nicotine
exerts beneficial effects in patients with PD and in in-vitro and in-vivo models of this disease. Astrocytes are an important component in
the immune response associated with PD, and that nicotine might be able to inhibit the inflammation-related apoptosis of these cells, being
this a potential strategy for PD treatment. This action of nicotine could be due mainly to activation of α7 nicotinic acetylcholine receptors
(α7-nAChRs) expressed in glial cells. However, nicotine administration can protect dopaminergic neurons against degeneration
by inhibiting astrocytes activation in the substantia nigra pars compacta (SNpc) and therefore reduce inflammation. Owing to the toxicity
and capacity of nicotine to induce addiction, analogues of this substance have been designed and tested in various experimental paradigms,
and targeting α7-nAChRs expressed in glial cells may be a novel therapeutic strategy for PD treatment.
Keywords: Parkinson disease, nicotine, astrocytes, nAChRs, neuroinflammation, neuroprotection, apoptosis.
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