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Oxidative stress factors in Parkinson's disease

Neural Regeneration Research 2021年第7期16卷 1383-1391页

作者： jolanta dorszewska Marta Kowalska Michał Prendecki Thomas Piekut Joanna Kozłowska Wojciech Kozubski Laboratory of Neurobiology Department of NeurologyPoznan University of Medical SciencesPoznanPoland Chair and Department of Neurology Poznan University of Medical SciencesPoznanPoland

Parkinson's disease(PD) is the second most common cause of *** the last two decades, various hypotheses have been proposed to explain the etiology of *** these is the oxidant-antioxidant theory, which asserts that local and systemic oxidative damage triggered by reactive oxygen species and other free radicals may promote dopaminergic neuron *** reactive oxygen species formation, one of the underlying causes of pathology in the course of PD has been evidenced by various studies showing that oxidized macromolecules including lipids, proteins, and nucleic acids accumulate in brain tissues of PD *** oxidation may produce various lesions in the course of *** incurred as a result of DNA oxidation may further enhance reactive oxygen species production in the brains of PD patients, exacerbating neuronal loss due to defects in the mitochondrial electron transport chain, antioxidant depletion, and exposure to toxic oxidized *** protein products of SNCA, PRKN, PINK1, DJ1, and LRRK2 genes are associated with disrupted oxidoreductive homeostasis in *** is the first gene linked with familial PD and is currently known to be affected by six mutations correlated with the disorder: A53T, A30P, E46K, G51D, H50Q and *** encodes Parkin, an E3 ubiquitin ligase which mediates the proteasome degradation of redundant and disordered proteins such as glycosylated α-*** 100 mutations have been found among the 12 exons of ***1, a mitochondrial kinase highly expressed in the brain, may undergo loss of function mutations which constitute approximately 1–8% of early onset PD *** than 50 PD-promoting mutations have been found in *** in DJ-1, a neuroprotective protein, are a rare cause of early onset PD and constitute only 1% of *** 20 mutations have been found in DJ1 among PD patients thus *** in the LRRK2 gene are the most common known cause of familial autosomal d

关键词： genetic factors molecular parameters oxidative stress Parkinson's disease pharmacotherapy surgical therapies

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Homocysteine and asymmetric dimethylarginine concentrations in the plasma of Alzheimer’s disease patients with varying degrees of dementia

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Advances in Alzheimer's Disease 2013年第1期2卷 1-6页

作者： jolanta dorszewska jolanta Florczak-Wyspianska Anna Oczkowska Mateusz Dezor Michal Prendecki Wojciech Kozubski Laboratory of Neurobiology Department of NeurologyPoznan University of Medical SciencesPoznanPoland Chair and Department of Neurology Poznan University of Medical SciencesPoznanPoland

Alzheimer’s disease (AD) is accompanied by elevated levels of homocysteine (Hcy). Homocysteine may induce elevated concentration of asymmetric dimethylarginine (ADMA). Both Hcy and ADMA are the amino acids thought to represent risk factors of vascular diseases. Studies were conducted on the plasma levels of Hcy and methionine (Met), estimated by HPLC with electrochemical detection, as well as on levels of ADMA and arginine (Arg), estimated by HPLC with fluorescent detection, in the AD patients with benign through to severe dementia estimated by MMSE scale and in a control group. The studies disclosed elevated levels of Hcy and ADMA in AD (Hcy, p < 0.001) as compared to controls, as well as in subjects older than 60 years of age (Hcy, p < 0.01). The AD patients with severe dementia have shown elevated levels of Hcy (p < 0.05) as compared to the patients with moderate dementia. The concentration of Metand Arg showed a downward trend in AD patientswith severe dementia. The highest levels of ADMA have been demonstrated in AD patients in the early stages of the disease. In parallel, in AD with varying degrees of dementia and subjects older than 60 years of age a disturbed turnover was observed of Hcy to Met and of Arg to ADMA. Similarly to Hcy, ADMA seems to be a potential risk factor of AD and important factor for progress of dementia.

关键词： Homocysteine ADMA Dementia Alzheimer’s Disease

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Activated Caspase-3 and Neurodegeneration and Synaptic Plasticity in Alzheimer’s Disease

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Advances in Alzheimer's Disease 2015年第3期4卷 63-77页

作者： Anna Plociennik MichalPrendecki Ewelina Zuba Marcin Siudzinski jolanta dorszewska Laboratory of Neurobiology Department of NeurologyPoznan University of Medical SciencesPoznanPoland

In Alzheimer’s disease (AD) there is a loss of neurons in different areas of the brain, including hippocampus, temporal and frontal cortex. Molecular mechanism of neuronal death in AD is not clear. It seems that apoptosis is a major form of neuronal cell death in this neurodegenerative disease. Neurons in both experimental animals and AD brains showed apoptotic changes, including DNA fragmentation, microRNA expression and caspase-3 activation. Activated caspase-3 may lead to amyloid precursor protein (APP) cleavage, extracellular senile plaques (SPs) and intracellular neurofibrillary tangles (NFTs) formation and neuronal loss, and it contributes to synaptic plasticity and cognitive dysfunction, especially in early stage of AD. Moreover, changes of caspase-3 activity were observed after therapy with memantine (NMDA receptor antagonist), donepezil and ladostigil (acetylcholinesterase inhibitors) in AD patients. It has been shown that both mementine and acetylcholinesterase inhibitors protect neurons from the caspase-3 activation. It seems that caspase-3 may be a potential diagnostic factor and target for pharmacotherapy of AD patients.

关键词： Caspase-3 MicroRNA Apoptosis Synaptic Plasticity Experimental Models AD

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Mutations of TP53 Gene and Oxidative Stress in Alzheimer’s Disease Patients

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Advances in Alzheimer's Disease 2014年第1期3卷 24-32页

作者： jolanta dorszewska Agata Rozycka Anna Oczkowska jolanta Florczak-Wyspianska Michal Prendecki Mateusz Dezor Izabela Postrach Pawel P.Jagodzinski Wojciech Kozubski Laboratory of Neurobiology Department of NeurologyPoznan University of Medical SciencesPoznanPoland Department of Biochemistry and Molecular Biology Poznan University of Medical SciencesPoznanPoland Chair and Department of Neurology Poznan University of Medical Sciences10Fredry Str.61-701 PoznanPoland

Alzheimer’s disease (AD) leads to the generation of β-amyloid (Aβ), which may damage DNA and thus lead to apoptosis induction by the p53 pathway. Dysfunction of the p53 protein may then be connected with the development of AD. Studies were conducted on 28 AD patients and 30 non-AD controls. Analysis of TP53 mutations in exon 7 was performed on DNA isolated from whole blood and biochemical parameters in the peripheral lymphocytes of these individuals. Our study showed a silent mutation TP53 C708T (21%) [p TP53 C748A (4%) only in the AD patients. Moreover, in AD patients with the TP53 C748A mutation, the level of 8-oxo-2’- deoxyguanosine (8-oxo2dG) was more than 5 times higher than the average level in this study group. In AD patients with the wild-type TP53 gene, the level of 8-oxo2dG was correlated with the level of protein p53 (R = +0.7388, p TP53 (p TP53 (C748A, C708T) may be associated with pathogenesis of AD.

关键词： TP53 8-oxo2dG p53 OGG1 AD

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Homocysteine and asymmetric dimethylarginine concentrations in the plasma of Alzheimer’s disease patients with varying degrees of dementia

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Advances in Alzheimer's Disease（阿尔茨海默氏病研究进展） 2013年第1期

作者： jolanta dorszewska jolanta Florczak-Wyspiańska Anna Oczkowska Mateusz Dezor Michał Prendecki Wojciech Kozubski Laboratory of Neurobiology Department of Neurology Poznan University of Medical Sciences Chair and Department of Neurology Poznan University of Medical Sciences

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Mutations of TP53 Gene and Oxidative Stress in Alzheimer’s Disease Patients

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Advances in Alzheimer's Disease（阿尔茨海默氏病研究进展） 2014年第1期

作者： jolanta dorszewska Agata Ró？ycka Anna Oczkowska jolanta Florczak-Wyspiańska Micha？ Prendecki Mateusz Dezor Izabela Postrach Pawe？ P. Jagodzinski Wojciech Kozubski

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