**Anastasiia Bohush, Grazyna Niewiadomska and Anna Filipek \***

Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur Street, 02-093 Warsaw, Poland; a.bohush@nencki.gov.pl (A.B.); g.niewiadomska@nencki.gov.pl (G.N.)

**\*** Correspondence: a.filipek@nencki.gov.pl; Tel.: +48-22-5892-332; Fax: +48-22-822-53-42

Received: 30 August 2018; Accepted: 26 September 2018; Published: 29 September 2018

**Abstract:** Parkinson's disease (PD) is a neurodegenerative disorder caused by insufficient dopamine production due to the loss of 50% to 70% of dopaminergic neurons. A shortage of dopamine, which is predominantly produced by the dopaminergic neurons within the substantia nigra, causes clinical symptoms such as reduction of muscle mass, impaired body balance, akinesia, bradykinesia, tremors, postural instability, etc. Lastly, this can lead to a total loss of physical movement and death. Since no cure for PD has been developed up to now, researchers using cell cultures and animal models focus their work on searching for potential therapeutic targets in order to develop effective treatments. In recent years, genetic studies have prominently advocated for the role of improper protein phosphorylation caused by a dysfunction in kinases and/or phosphatases as an important player in progression and pathogenesis of PD. Thus, in this review, we focus on the role of selected MAP kinases such as JNKs, ERK1/2, and p38 MAP kinases in PD pathology.

**Keywords:** apoptosis; ERK1/2; JNKs; mitochondrial dysfunction; neurodegeneration; neuro-inflammation; oxidative stress; p38 MAPKs; Parkinson's disease
