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• W2928486542 abstract "Los estudios en el laboratorio han permitido identificar cambios del metabolismo de halógenos en suero y líquido cefalorraquídeo (LCR) de pacientes con enfermedad de Parkinson, que indican la presencia de «autohalogenación acelerada» del LCR de los pacientes o aumento de haloperoxidasas, en concreto, tiroperoxidasa en sangre y lactoperoxidasa en LCR. Además, se ha detectado un exceso en suero y LCR de algunos derivados halogenados, como proteínas con halogenación avanzada tipo advanced oxidation protein products (AOPP). Estos hechos, «autohalogenación acelerada» e incremento de haloperoxidasas y proteínas AOPP, indican la presencia de estrés halogenativo en la enfermedad de Parkinson. Además, un derivado halogenado, la 3-yodo-L-tirosina, muestra toxicidad parkinsoniana en modelos experimentales, pues se ha observado que induce agregados de α-sinucleína y daño de las neuronas de dopamina en cerebro e intestino en ratones. La hipótesis que se maneja es que en la enfermedad de Parkinson existe un exceso halogenativo, relacionado con una alteración haloenzimática de síntesis o degradación de oxiácidos de halógenos y sus derivados halogenados. Este estrés halogenativo se relacionaría con el daño del sistema nervioso. Laboratory studies identified changes in the metabolism of halogens in the serum and cerebrospinal fluid (CSF) of patients with Parkinson's disease, which indicates the presence of «accelerated self-halogenation» of CSF and/or an increase in haloperoxidases, specifically serum thyroperoxidase and CSF lactoperoxidase. Furthermore, an excess of some halogenated derivatives, such as advanced oxygenation protein products (AOPP), has been detected in the CSF and serum. «Accelerated self-halogenation» and increased levels of haloperoxidases and AOPP proteins indicate that halogenative stress is present in Parkinson's disease. In addition, 3-iodo-L-tyrosine, a halogenated derivative, shows «parkinsonian» toxicity in experimental models, since it has been observed to induce α-synuclein aggregation and damage to dopaminergic neurons in the mouse brain and intestine. The hypothesis is that patients with Parkinson's disease display halogenative stress related to a haloenzymatic alteration of the synthesis or degradation of oxyacid of halogens and their halogenated derivatives. This halogenative stress would be related to nervous system damage." @default.
• W2928486542 created "2019-04-11" @default.
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• W2928486542 date "2022-10-01" @default.
• W2928486542 modified "2023-10-01" @default.
• W2928486542 title "¿Presenta la enfermedad de Parkinson una haloenzimopatía?" @default.
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• W2928486542 doi "https://doi.org/10.1016/j.nrl.2018.12.008" @default.
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