Clinical trials of neuroprotection for Parkinson’s disease

LeWitt, Peter A.

doi:10.1212/wnl.63.7_suppl_2.s23

Cited by 49 publications

(29 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MAO-B can catalyze dopamine to homovaniuic acid (HVA) and produce hydrogen peroxide in the brain, liver, intestinal mucosa and other organs, and induce oxidative stress and result in neuron death [1,2]. Inhibitors of MAO-B not only lead to enhanced dopaminergic neurotransmission, but also prevent activation of toxin and free radical formation, and then alleviated the process of neuron denaturalization.…”

Section: Introductionmentioning

confidence: 99%

Rapid screening of monoamine oxidase B inhibitors in natural extracts by capillary electrophoresis after enzymatic reaction at capillary inlet

Zhang

et al. 2010

Journal of Chromatography B

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Rapid screening of monoamine oxidase B inhibitors in natural extracts by capillary electrophoresis after enzymatic reaction at capillary inlet

Zhang

et al. 2010

Journal of Chromatography B

View full text Add to dashboard Cite

“…47,76,77 Minocycline, an antibiotic in the tetracycline family, displays neuroprotective prosperity in various models of neurodegenerative disorders including PD through inhibiting the activation of caspase 1 and caspase 3. 78,79 In addition, minocycline inhibits microglia activation. 78,79 Clinical trials of minocycline for its efficacy and toxicity in PD are now underway.…”

Section: Antiapoptotic Approaches In Pdmentioning

confidence: 99%

Neuroprotective Therapy in Parkinson Disease

Chen¹

2006

American Journal of Therapeutics

View full text Add to dashboard Cite

During the past decade, there has been a remarkable progress in our understanding of the biology of Parkinson disease (PD), which has been translated into searching for novel therapy for PD. Much focus is shifted from the development of drugs that only relieve PD symptoms to new generation of remedies that can potentially protect dopaminergic neurons and modify the disease course. Several novel therapeutic approaches have been tested in preclinical experiments and in clinical trials, including molecules targeting on genes involved in the pathogenesis of the disease, neurotrophic factors critical for dopaminergic neuron survival and function, new generation of dopamine receptor agonists that may possess neuroprotective effects, and agents of antioxidation, antiinflammation, and antiapoptosis. The results of these studies will shed new light to our hope that PD can be cured in the future.

show abstract

“…In developing therapeutic strategies for PD, pilot trials with antioxidants did not provide unequivocal results, and as yet, have not provided the expected results [40,69]. However, a phase II trial of high-doses of coenzyme Q10 in early diagnosed PD patients, appeared to slow disease progression [69].…”

Section: Perspectives For Drug Developmentmentioning

confidence: 99%

Mitochondrial Toxins in Basal Ganglia Disorders: From Animal Models to Therapeutic Strategies

Bonsi

Cuomo

Martella

et al. 2006

View full text Add to dashboard Cite

Current knowledge of the pathogenesis of basal ganglia disorders, such as Huntington's disease (HD) and Parkinson's disease (PD) appoints a central role to a dysfunction in mitochondrial metabolism. The development of animal models, based upon the use of mitochondrial toxins has been successfully introduced to reproduce human disease, leading to important acquisitions. Most notably, experimental evidence supports the existence, within basal ganglia, of a peculiar regional vulnerability to distinct mitochondrial toxins. MPTP and rotenone, both selective inhibitors of mitochondrial complex I have been extensively used to mimic PD. Accordingly, in human PD, a specific dysfunction of complex I activity was found in vulnerable dopaminergic neurons of the substantia nigra. Conversely, in HD a selective impairment of mitochondrial succinate dehydrogenase, key enzyme in complex II activity was found in medium spiny neurons of the caudate-putamen. The relevance of such finding is further demonstrated by the evidence that toxins able to primarily target mitochondrial complex II, such as malonic acid and 3-nitropropionic acid (3-NP), strikingly reproduce the main phenotypic and pathological features of HD.Despite the advances obtained from these experimental models, a deeper understanding of the molecular and cellular mechanisms underlying such neuronal vulnerability is lacking.The present review provides a brief survey of currently utilized animal models of mitochondrial intoxication, in attempt to address the cellular mechanisms triggered by energy metabolism failure and to identify potential therapeutic targets.

show abstract

Clinical trials of neuroprotection for Parkinson’s disease

Cited by 49 publications

References 71 publications

Rapid screening of monoamine oxidase B inhibitors in natural extracts by capillary electrophoresis after enzymatic reaction at capillary inlet

Rapid screening of monoamine oxidase B inhibitors in natural extracts by capillary electrophoresis after enzymatic reaction at capillary inlet

Neuroprotective Therapy in Parkinson Disease

Mitochondrial Toxins in Basal Ganglia Disorders: From Animal Models to Therapeutic Strategies

Contact Info

Product

Resources

About