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EN
This study examined verbal and nonverbal aspects of explicit and implicit memory in a sample of 19 Parkinson's disease (PD) patients and 21 control subjects. For implicit memory evaluation, we used a Mirror Reading (MR) task employing verbal material as well as a nonverbal Serial Reaction Time (SRT) task. For explicit memory measurement we applied a word pairs task (verbal) and pairs of a Japanese ideograms task (nonverbal). The PD patients displayed impairments in the nonverbal tasks only, namely, in the SRT task and the pairs of Japanese ideograms task. No correlation between Wisconsin Card Sorting Test (WCST) scores and the results of tasks in which PD patients displayed deficits (SRT and pairs of Japanese ideograms) were discovered. Interestingly, such a correlation was found in the case of MR and words pairs tasks, which did not distinguish PD patients from control group.
EN
The inflammatory reaction and oxidative stress has been linked with PD. Proinflammatory cytokines promote neurodegeneration or neuroprotection in different animal models. In addition, these cytokines have been reported to increase iNOS expression. With the RT-PCR method we evaluated mRNA levels for IL1beta, IL6, TNF, IFN gamma, IL-10 and iNOS in the striatum of C57BL/6 mice after MPTP intoxication. The IL1beta mRNA expression rapidly increased, nad peaked at 6 h. The first increase of mRNA for TNFalpha and INFgamma was noticed at 6-24 h and the second at the 7th day after MPTP intoxication. Two peaks of IL10 mRNA were seen, immediately (6 h) and at the 3rd day post MPTP injection. The peak of mRNA level for IL6 was observed at the 7th day. Expression of mRNA for iNOS peaked at 24 h, started decreasing on the 3rd day, but was still present till the 14th day Those findings suggest that cytokine network and iNOS may be involved in the development of immune changes accompanying degeneration of the nigrostriatal system.
EN
According to the oxidative stress theory iron may play an important role in the pathogenesis of neurodegenerative diseases, as e.g. Parkinson's disease (PD). This review presents the results of studies, obtained by various methods, of iron in substantia nigra (SN) - a cerebral structure which degenerates in PD - and shows controversies concerning the amount of iron, its redox state, and the iron binding compounds. Taking into account all published experimental results, the increase in the concentration of iron in parkinsonian SN vs. control may be estimated as (3 + - 5)%. The presence of large amounts of divalent iron in post mortem SN can be unequivocally negated. It is, however, still possible that iron is involved in the pathogenesis of PD, as even minor changes in the amount and form of iron may initiate processes leading to cells death.
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Motor deficiency in Parkinson's disease

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EN
The basal ganglia comprise a group of gray matter structures beneath the cerebral cortex, that surrounds the thalamus and hypothalamus. The basal ganglia play an important role in controlling movement. The motor circuits within the striato-pallidal complex are thought to facilitate desired movement and inhibit unwanted movement through their influence, via the thalamus, mainly on cortical precentral motor regions. Localized damage to parts of the basal ganglia occurs in certain diseases such as Parkinson's disease. Parkinsonism is a common neurological disorder that affects about one person in every 1,000 of the general population and about 2% in the elderly. The diagnosis of Parkinson's disease is based on the presence of two or more of the major symptoms: tremor, rigidity, postural instability, and bradykinesia. The pathological process behind the motor disabilities of Parkinsonism is a progressive degeneration of dopaminergic neurons of the substantia nigra, that results in dopamine depletion in the striatum. Brain dopamine deficiency is sufficient to explain all of the major symptoms of Parkinson's disease.
EN
Alpha-Synuclein is a neuronal protein implicated both in synaptic transmission and in neurodegenerative diseases. Although it is evident that this protein is enriched in the presynaptic terminals of neurons, localization in synaptic vesicles has not been conclusively determined. Here, we show that alpha-synuclein is present, but not enriched, in synaptic vesicles using highly purified synaptic vesicle preparations from rat brain homogenate. Immunoisolation of vesicles using antibodies against synaptophysin or synaptobrevin confirmed the presence of alpha-synuclein in synaptic vesicles. Additional separation of synaptic vesicles by sucrose velocity centrifugation showed that there are different subpopulations of synaptic vesicles and that alpha-synuclein is present only in a specific subpopulation, whereas synaptophysin and synaptobrevin were found in all the synaptic vesicles. Presence of alpha-synuclein only in a subset of synaptic vesicles suggests that this protein may have a specific function in synaptic vesicle cycling, hence in synaptic transmission.
EN
Neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are accompanied by increased levels of 8-oxo-2'-deoxyguanosine (8-oxo2dG) and alterations in levels of homocysteine (Hcy), methionine (Met), and cysteine (Cys). Hcy may undergo remethylation due to involvement of MTHFR, MTR and MTHFD1 proteins. Present studies are aimed at determination of 8-oxo2dG, Hcy, Met, and Cys in AD and PD patients as well as in control groups, using HPLC/EC/UV, as well as estimation, by restriction analysis, frequency of following gene polymorphisms: MTHFR (C677T, A1298C, G1793A), MTHFD1 (G1958A), and MTR (A2756G). In AD there were significant differences of the levels of only Cys (GG, MTHFR, G1793A) and Met/Hcy (AA, MTHFD1, G1958A) whereas in PD there were more significant differences of the levels of thiols: Hcy [MTHFR: CT (C677T) and GG (G1793A); MTR, AG (A2756G)], Met [MTR, AA (A2756G)], Cys [MTR, AG (A2756G)], and Met/Hcy [MTHFR: CC, CT (C677T) and AA (A1298C), and GG (G1793A); MTHFD1 AA(G1958A); MTR AA(A2756G)]. Significant differences in the levels of Cys/Hcy, MTHFD1 GA (G1958) were varied between AD and PD groups. The results indicate that of the enzymes studied only polymorphisms of folate-dependent enzyme MTHFD1 have pointed to significant differences in intensity of turnover of circulating thiols between AD and PD patients.
EN
This paper reviews the changes in dopaminergic, cholinergic and glutamatergic neurotransmission, which occur in the aging of central nervous system CNS and in age-related diseases: Parkinson's disease (PD) and Alzheimer's disease (AD).
EN
A critical role of mitochondrial dysfunction and oxidative damage has been implicated in etiopathology of many neurodegenerative disorders, as well as in normal aging. Alzheimer's and Parkinson's diseases are common devastating late-onset neurodegenerative disorders, associated with mitochondrial DNA variations, which are suggested to affect mitochondrial functions. This paper reviews the current knowledge on the inherited and somatic mtDNA variations in both conditions.
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