Parkinson’s disease is a complex neurodegenerative disorder, mainly
characterized by the loss of dopaminergic neurons in the substantia nigra and their
projections to the striatum, causing several motor deficits. Neuronal cytoplasmic
inclusions, named Lewy Bodies, are found in the affected areas. Parkinson’s disease is
distributed worldwide, affecting all ethnic groups and socioeconomic classes. Protein
homeostasis is crucial for preventing neurodegeneration. Misfolding of proteins can
lead to loss or gain of function, resulting in protein dysfunction and causing various
types of diseases. Five genes containing pathogenic mutations were identified to
contribute for incorrect protein conformation in Parkinson’s disease. Mitochondrial
dysfunction and purinergic receptor signaling are also involved in the mechanism of
disorder. Several types of pharmacological intervention were developed. Dopamine
agonists are the most common therapeutic agents used currently. N-methyl-D-aspartate
type glutamate receptor antagonist, monoamine oxidases and anticholinergic drugs can
be therapeutic alternatives. New techniques and studies have contributed to the
discovery of new genes and genetic risk factors for Parkinson’s disease. Brain banks
and imaging analyses can also be very useful tools for understanding the mechanisms of
disease progression. Current studies on molecular aspects of Parkinson’s disease,
together with the development of new drugs, techniques and tests to improve diagnosis
accuracy will bring new perspectives for PD therapies.
Keywords: Parkinson’s disease, genetic mutations, pharmacology, protein
misfolding, oxidative stress, dopamine, L-DOPA, purinergic receptors, P2X7R,
PPAR, PGC-1α, α-synuclein, LRRK2, PARKIN, animal models, epidemiology,
diagnosis, therapy, ubiquitin-proteasome system, imaging.
