There is damage because the Parkinson Disease profactors in the Complex I of the mitochondria, this cause an increase in the p53 mutate form and this can lead to unnecessary apopototic activity in the dopaminergic neuron of the nigralsubstancia.
Previously studies have shown that
Transcript of "Carlos santos review revised ed"
Mitochondrial Dysfunctional Activity and the Relationship with Parkinson’s Disease<br />Carlos Santos Pérez, RISE Student<br />December <br />
Abstract<br />Parkinson Disease is one of the most dangerous neurodegenerative diseases. The symptoms of this disease can be stiffness of the muscle, trembling and also difficulty in swallowing, speaking and chewing. Some studies and researches found a relationship between Parkinson Disease and Mitochondrial Dysfunctional Activity. In fact the researchers discuss that the p53 agent could be a pro apoptotic agent and in that way it could help to the death of the dopaminergic cells. This dopaminergic cells are the cells that controls the movement specifically the motor system. Also it exists some proapoptotic agents and agents that inhibit the apoptotic phases. It have been proven that the mitochondrial activity of the cell regulate this apoptotical function. It can be inferred from that position that it can exists a relation between the DNA that contain the mitochondria and its activity. That’s why it can be mention that polymorphism can be mediators in the deregulation of the complex I activity of the electron transfer chain reaction of the cellular respiration. On the other hand researchers mentioned in this review paper found that polymorphism are not the causes of the Deregulated Activity of the Mitochondria. This decreasing activity o the Complex I of the Electron Transfer Chain is because of the presence of neurotoxin that are also proapoptotic factors. In addition it have to be mention that this decreasing of the mitochondrial activity it is not only because of the neurotoxin it is also because of the presence of Calcium in the cells. <br />
Outline<br />Parkinson Disease <br />Mitochondrial Apoptosis Activity and p53<br />Decreasing of the Complex I Activity and Cellular Respiration<br />Nitric Oxide Association withMitochondrial Polymorphism <br />Endoplasmic Reticulum and Mitochondrial Dysfunctional Activity<br />Deletion of mitochondrial DNA agents that can induce PD<br />The imbalance of Redox in Patient with Parkinson Disease and Oxidative Stress<br />
Parkinson Disease <br />The cause of Parkinson Disease (PD) in a patient is the absence of dopamine. <br />Symptoms:<br />Trembling of the extremities<br />Stiffness<br />Slowness <br />Poor balance or coordination<br />Mitochondrial Dysfunction may represent a presage of PD. <br />
Mitochondrial Apoptosis Activity and p53<br />Apoptosis - programmed cell death<br />In vitro and in vivo models of Parkinson Disease, <br />1-methyl-4phenyl-1,2,3,6-tetrachydropyridine (MPTP),<br /> Rotenone and 6-hydroxydopamine <br />mediators to abrogate for dysfunctional activity in the Complex I of the mitochondria <br />cause and induce Parkinson Disease in animasl and for in vitro cases (Blum et al 2001). <br />P53- tumor suppressant that is important for the mitochondrial function <br />
Decrease of the Complex I Activity and Cellular Respiration<br />Complex I of the Mitochondria – Electron Transport Chain (ETC)<br />Significant reduction in activity of the complex I in the mitochondria. <br />Levodopa is provoking the deregulation behavior of the mitochondria in PD Patients.<br />Relation with neurotoxin MPTP <br />metabolized by mitochondrial monoamine oxidase (Chiba et al. 1984; Barnajee et al. 2008) <br />accumulated in the mitochondrial and quickly affected the ETC<br />
Nitric Oxide Association withMitochondrial Polymorphism <br />Nitric Oxide (NO) in a pathological function can provoke - DNA damage, lipid peroxidation, proteins nitrosylation and mitochondrial dysfunction (Huerta et al. 2006). <br />NO overproduction in the neuronal cells may cause formation of free radicals<br />can contribute to the death of neuronal cell and every type of cells <br />Huerta et al. prepared a methodology to genotype 450 PD patients and a control group for three mitochondrial polymorphisms that have been previously link to PD <br />
Deletion of Mitochondrial DNA Agents that can Induce PD<br /> Mitochondrial 4977b deletion had proven to be related with Parkinson Disease and the movement disorders cause by the neurological system.<br /> There is a uncertainty as to what caused the deletion of this mtDNA: the aging or the PD itself. <br />The study sample consists of 47 PD patients. Zhang et al. found that PD was not related to Mitochondrial 4977b deletion. <br />Finally they concluded that 4977b deletion may not be directly related toPD. <br />
Imbalance of Redox in Patient with Parkinson Disease and Oxidative Stress<br />The autooxidation of the dopamin produces semiquinones that are very reactive compounds of cellular respiration.<br />They specifically occur in the ETC and can also generate free radicals. <br />Levodopa and this can cause an overproduction of hydrogen peroxide that is also negative for the dopaminergic cells <br /> it accelerates the process of apoptosis <br />In normal conditions the hydrogen peroxide should be inhibited by glutathion in a catalyzed reaction by glutathionproxidase<br />
Conclusion<br />It can be infer that neurotoxins are not the only the factors that may affect the dopaminergic cells. <br />
References<br />Moniz D, Esteves R, Cardoso S, Oliviera C. 2009. Endoplasmic Reticulum and Mitochondria interplay mediates apoptotic cell death: Relevance To Parkinson’s Disease. Neurochemistry International 55: 341-348.<br />Zhang J, Montine TJ, Smith MA, Siedlak SL, Gu G, Robertson D and Perry G. 2002. The mitochondrial common deletion in Parkinson’s disease and related movement disorders. Parkinsonism and Related Disorders 8:165-170.<br />Huerta et al.2007.No association between Parkinson’s disease and three polymorphism in the eNOS, nNOS, and iNOS genes. Vol 463. 202-205.<br />Shults C. Mitochondrial dysfunction and possible treatments in Parkinson’s Disease.2004. Mithocondrion 4. 641-648.<br />Blum D., Torch S., Lambeng N., Nissou M., Benabid A. L., Sadoul R. and Verna J. M. 2001. Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease. Prog. Neurobiol. 65,135–172. <br />Chinta S Andersen J.2008. Redox Imbalance in Parkinson’s Disease. Biochimica et BiophysiaActa 1788.1362-1368.<br />Duncan J, Heales S. 2005. Nitric Oxide and Neurologican Disorders. Molecular aspects of Medicien26. 67-90. <br />
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