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MHC class II positive microglia and lymphocytic infiltration are present in the substantia nigra and striatum in mouse model of Parkinson's disease

100%
Kurkowska-Jastrzebska I., Wronska A., Kohutnicka M., Czlonkowski A., Czlonkowska A.
Acta Neurobiologiae Experimentalis
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1999
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vol. 59
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issue 1
1-8
EN
We have studied MHC class II antigen expression and lymphocytic infiltration during dopaminergic neurone degeneration produced by intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridine (MPTP). Microglial activation was observed in the striatum and in the substantia nigra (SN) in this model. We noticed a marked increase of MHC class II antigen expression on microglia and T-cell recruitment in these regions after MPTP treatment. B-lymphocytes were not observed. T-cell infiltration predominantly consisted of CD8+ cells at every time point but CD4+ cells were present too. More than a half of the observed lymphocytes showed strong staining of CD44 antigen. Our findings suggest a possible immune system involvement in the pathological process following MPTP intoxication.
2

Molecular biology of polyglutamine diseases

100%
Owecki M., Kozubski W.
Postępy Higieny i Medycyny Doświadczalnej
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2002
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vol. 56
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issue 6
779-788
EN
Polyglutamine diseases include at least 9 neurodegenerative disorders: Huntigton?s disease (HD), dentatorubral pallidoluysian atrophy (DRPLA), spinobulbar muscular atrophy (SBMA), and spinocerebellar ataxia (SCA) type: 1-3, 6-7 and 17, each caused by a CAG-trinucleotide repeat expansion in a different gene. The poly-CAG sequence is translated into a polyglutamine stretch in the respective proteins. This review discusses mutual molecular features of polyglutamine diseases. The formation of intranuclear inclusions, recruitment of physiological polyglutamine proteins as well as a potential role of molecular chaperones, capsases, and inhibition of histone acetyltransferases-depended transcription in cellular pathogenesis are considered.
3
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Inducible cAMP early repressor (ICER) isoforms and neuronal apoptosis in cortical in vitro culture

80%
Klejman A., Kaczmarek L.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
267-272
EN
CREB activation and CREB-dependent signaling pathways are crucial for neuronal survival. The term ICER (inducible cAMP early repressor) refers to four protein isoforms that are all endogenous, inducible antagonists of CREB. Jaworski and others (2003) have previously shown that one of those isoforms, ICER II, is highly expressed in apoptotic neurons in vitro and its overexpression evokes neuronal death. In this study we investigated the role of all four ICER isoforms in cortical neuronal culture, comparing their expression level in serum-deprived/MK-801-treated neurons and their pro-apoptotic properties towards transfected cortical neurons. We have found that all four isoforms are induced upon pro-apoptotic treatment, and also that each of them separately evokes neuronal cell death following cortical culture transfection with the genes. The most efficiently induced, as well as the most effective in evoking neuronal cell death, were both ICER Igamma and IIgamma isoforms.
4
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Neuroprotective effects of ginsenosides

80%
Rausch W.-D., Liu S., Gille G., Radad K.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
369-375
EN
Ginseng, the root of the Panax species, is a well-known herbal medicine. Traditionally it has been used in Korea, China and Japan for thousands of years. Nowadays it has become a popular and worldwide known health drug. Current scientific studies demonstrate in vivo and in vitro its beneficial effects in a wide range of pathological conditions such as cardiovascular disease, cancer, immune deficiency and hepatotoxicity. Ginsenosides or ginseng saponins as the active ingredients have antioxidant, anti-inflammatory, anti-apoptotic and immunostimulant properties, which raised speculations that these compounds could positively affect neurodegenerative disorders and delay neuronal aging. Conclusive clinical data in humans are still missing. However, results from animal studies and neuronal cell culture experiments indicate that ginsenosides can counteract and attenuate factors promoting neuronal death as environmental toxins, excitotoxic action of glutamate and rises in intracellular calcium, excessive release of free radicals and apoptotic events. Thus, neuroprotective actions of ginsenosides could come about as a valuable option to slow down neurodegenerative diseases.
5
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Modulation of the composition of AP-1 complex and its impact on transcriptional activity

70%
Kaminska B., Pyrzynska B., Ciechomska I., Wisniewska M.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 3
395-402
EN
AP-1 transcription factor known to play a role in cell proliferation and neuronal activation, it is also involved in apoptosis of cells in response to stress, DNA damaging agents or lack of survival signals. AP-1 DNA binding complex is not a single transcritpion factor but a dimer consisting of members of Fos and Jun families. In this review, we discuss evidence that composition of the AP-1 complex is different under various physiological and pathophysiological conditions. Furthermore, we describe biochemical properties of Fos and Jun proteins that may explain the ability of this transcription factor to activate different sets of genes in response to different stimuli. We propose a hypothesis that AP-1 might contribute to distinct biological processes because an activation of specific signaling pathways results in changes of AP-1 composition and/or phosphorylation status and modulates its transactivating potential towards different promoters.
6
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Mitochondrial DNA in pathogenesis of Alzheimer's and Parkinson's diseases

61%
Maruszak A., Gaweda-Walerych K., Soltyszewski I., Zekanowski C.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 2
153-176
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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