title: Possible extrapyramidal system degradation in Parkinson's disease.
abstract: Extrapyramidal system, a rich network of nerve and glial cells consists of subcortical and cortical grey matter. The system serves as an integrator of unaware, automatic, repeated, spontaneous, complicated and purposeful motor samples. Muscle tone regulation and its distribution is another decisive extrapyramidal function. This review article concerns to some degradation mechanisms in extrapyramidal system, as either the programmed cell death or apoptosis. The physiologic extracellular decreasing signals creating apoptosis (nerve growth factor--fall) are either genetically expressed or there are neuropathophysiologic processes that may activate pathways leading to apoptosis, namely oxidative stress, glutamate toxicity and calcium homeostasis disruption. The level of dopamine transporter expression (mRNA, methyl-phenyl-pyridinium) might determine the vulnerability of the nigral neurons to the Parkinsonian insult. The most common clinical picture of extrapyramidal disorder-Parkinson's disease-consists of an active dopamine cell death-apoptosis, which is partially programmed like as programmed cell death and partially accidentally installed chain of events. Without morphological criteria, biochemical indicators such as laddered DNA fragmentation pattern and/or the requirement for macromolecular synthesis merely suggest but do not provide unequivocal evidence for apoptosis. There are either genetic or acquired conditions creating unbalance of Bax/Bcl-2 families-proapoptotic and prooncogenic factors, respectively. The first Bax gene cooperates with other genes coding the new transmembrane proteins into the mitochondrial megapores determinating transition by means of death receptors. Bcl-2 codes prooncogenic mitoses and tissue proliferation. The neuroprotective hypothesis of the dopamine agonist action is a very attractive working hypothesis and some of its tenets are derived from the oxidative stress hypothesis for neurodegeneration, but this hypothesis is still controversial.
authors.affiliation: Clinic of Neurology, Jessenius Faculty of Medicine, Comenius University, Martin, Slovak Republic.
authors.forename: M
authors.initials: M
authors.lastname: Drobný
authors.forename: E
authors.initials: E
authors.lastname: Kurca
mesh_terms: D000368:Aged; D000818:Animals; D017209:Apoptosis; D002540:Cerebral Cortex / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D009457:Neuroglia / Q000473:pathology / Q000502:physiology; D009474:Neurons / Q000473:pathology / Q000502:physiology; D018384:Oxidative Stress; D010300:Parkinson Disease / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*