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Mitochondrial neuronal uncoupling proteins:a target for potential disease-modification in parkinson’s disease Philip

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Translational Neurodegeneration 2012年第1期1卷 11-19页

作者： WL Ho Jessica WM Ho Hui-Fang Liu Danny HF so Zero HM Tse Koon-Ho Chan David B Ramsden shu-Leong Ho Division of Neurology Department of MedicineUniversity of Hong KongPokfulamHong Kong SARChina school of Medicine and school of Biosciences University of BirminghamBirminghamUK Research Centre of Heart BrainHormone and Healthy Aging(HBHA)University of Hong KongPokfulamHong Kong SARChina

This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in parkinson’s disease(PD).Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation,but as an integral part of this process,superoxides and other reactive oxygen species are also *** free radical production contributes to oxidative *** have evolved to handle such stress via various endogenous anti-oxidant *** such family of proteins is the mitochondrial uncoupling proteins(UCPs),which are anion carriers located in the mitochondrial inner *** are five known homologues(UCP1 to 5),of which UCP4 and 5 are predominantly expressed in neural *** a series of previous publications,we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium(MPP+;toxic metabolite of MPTP)and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential,and reducing oxidative *** also showed how their expression can be influenced by nuclear factor kappa-B(NF-B)signaling pathway specifically in ***,we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin(hormone produced by adipocytes)acting via UCP2 against MPP+-induced *** is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with *** expression,which can be induced,may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease.

关键词： uncoupling proteins mitochondria parkinson??s disease ATP oxidative stress neuroprotection

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Norepinephrine:the next therapeutics frontier for parkinson’s disease

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Translational Neurodegeneration 2012年第1期1卷 20-23页

作者： Peter A LeWitt Department of Neurology Henry Ford Hospital and Wayne State University School of MedicineDetroitMichigan USA

Tissue concentrations of norepinephrine(NE)are markedly decreased in various regions of the parkinson’s disease(PD)*** in the substantia nigra pars compacta,neuronal dropout and Lewy bodies are prominent changes affecting the locus coeruleus,which is the source of ascending NErgic *** the major roles of NE throughout the brain,there has been only minimal exploration of pharmacological intervention with NErgic *** operations,“freezing”of gait,tremor,dyskinesia,REM sleep regulation,and other aspects of brain function are tied into signaling by NE,and there is also evidence that it may have a role in the neurodegenerative process *** article reviews the reported pharmacological experience in PD therapeutics.

关键词： Norepinephrine parkinson??s disease neuropharmacology

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