Possible extrapyramidal system degradation in Parkinson’s disease

• Published in: Brain research bulletin Vol. 53; no. 4; pp. 425 - 430
• Main Authors: DROBNY, Michal, KURCA, Egon
• Format: Journal Article Conference Proceeding
• Language: English
• Published: New York, NY Elsevier Inc 01-11-2000; Elsevier Science
• Subjects: Aged; Animals; Apoptosis; Biological and medical sciences; Cerebral Cortex - pathology; Cerebral Cortex - physiopathology; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Dopamine agonists; Excitotoxicity; Humans; Medical sciences; Neuroglia - pathology; Neuroglia - physiology; Neurology; Neurons - pathology; Neurons - physiology; Oxidative Stress; Parkinson Disease - genetics; Parkinson Disease - pathology; Parkinson Disease - physiopathology; Programmed cell death; Oxidative stress; Dopamine agonists; Programmed cell death; Excitotoxicity; Apoptosis; Nervous system diseases; Agonist; Extrapyramidal motor pathway; Dopamine receptor; Toxicity; Parkinson disease; Cerebral disorder; Cell death; Central nervous system disease; Neurotransmitter; Excitatory aminoacid; Degenerative disease; Extrapyramidal syndrome
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/S0361-9230(00)00367-1

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.