Energy changes exchange

Changes in energy metabolism affect the process of neurodegeneration in parkinsonism. Patients were found to have impaired mitochondrial enzyme activity and mitochondrial DNA damage, leading to a marked energy deficit. Mitochondrial damage occurs as a result of an increase in free radical oxidation (GN Kryzhanovsky et al., 1995). Methylphenyl tetrahydropyridine neurotoxin (MPTP), which reproduces Parkinson’s syndrome in animals, causes free radical damage to mitochondria, a decrease in mitochondrial respiration, and eventually the death of dopaminergic neurons (Y. Mizuno et al., 1994). In patients with parkinsonism, a defect in the respiratory chain enzyme NADH- ubiquinone oxidoreductase was detected, which interferes with the passage of electrons through the respiratory chain,increases the formation of oxygen free radicals and increases the level of oxidative stress (WD Parker et al., 1989).

According to most researchers, in parkinsonism, local cerebral blood flow and glucose metabolism in the caudate nucleus, ventral striatum and lower thalamus are increased (A. Antonini et al., 1995; M. Dogali et al., 1995; M. Hirato et al., 1995 ; V. Molina Rodríguez et al., 1997; S. Dethy et al., 1998). The prevalence of glucose metabolism on the contralateral side of the more pronounced symptoms of parkinsonism is also shown. It is assumed that increased blood flow is associated with hyperactivity of striatal cholinergic neurons (S. Dethy et al., 1998). Only in individual works with parkinsonism was a decrease in cerebral blood flow in the basal ganglia or its compliance with its glucose metabolism and norm (M. Otsuka et al., 1991; M. Oishi et al., 1996).

In the cerebral cortex, a decrease in cerebral blood flow and glucose metabolism was detected in the frontal, prefrontal, and premotor areas receiving major ascending projections from the striopallidary system (M. Hirato et al., 1995; L. Defebvre et al., 1995; M. Oishi et al. , 1996). These changes in energy metabolism are obviously due to dopamine deficiency and impaired neurodynamics, since l-dopa preparations restore normal glucose metabolism (M. Hirato et al., 1995). It was the studies of cerebral blood flow using HO-assisted PET that established that akinesia in Parkinson’s disease is associated with impaired activation of the posterior prefrontal and additional motor areas involved in decision making and preparation of the motor act (DJ Brooks, 1997).

local_offerevent_note August 4, 2019

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