Genetic and pharmacological evidence that endogenous nociceptin/orphanin FQ contributes to dopamine cell loss in Parkinson's disease

Abstract Parkinson’s disease is characterized by dopamine cell loss of the substantia nigra. Parkinson’s disease and the neurotoxin 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine may destroy dopamine neurons through oxidative stress. Coenzyme Q is a cofactor of mitochondrial uncoupling proteins that enhances state-4 respiration and eliminate superoxides. Here we report that short-term oral administration of coenzyme Q induces nigral mitochondrial uncoupling and prevents dopamine cell loss after 1-methyl-4-phenyl-1,2,5,6 tetrahydropyridine administration in monkeys.

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Faculty Opinions recommendation of Synapsin III deficiency hampers α-synuclein aggregation, striatal synaptic damage and nigral cell loss in an AAV-based mouse model of Parkinson's disease.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.733700001.793551488 ◽

2018 ◽

Author(s):

Vladimir Uversky

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Mouse Model ◽

Cell Loss ◽

Synapsin Iii

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Dopamine cell transplantation in Parkinson's disease: challenge and perspective

British Medical Bulletin ◽

10.1093/bmb/ldr040 ◽

2011 ◽

Vol 100 (1) ◽

pp. 173-189 ◽

Cited By ~ 14

Author(s):

Yilong Ma ◽

Shichun Peng ◽

Vijay Dhawan ◽

David Eidelberg

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cell Transplantation ◽

Dopamine Cell

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Parkinsonism, Parkinson’s disease, and related conditions

Oxford Textbook of Geriatric Medicine ◽

10.1093/med/9780198701590.003.0116 ◽

2017 ◽

pp. 897-906

Author(s):

John V. Hindle ◽

Sion Jones ◽

Glesni Davies

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Older People ◽

Lewy Bodies ◽

Cell Loss ◽

Brain Regions ◽

Motor Symptoms ◽

Advanced Care Planning ◽

Non Motor Symptoms

Parkinson’s disease (PD) is a progressive neurodegenerative condition characterized clinically by fatiguable bradykinesia, rigidity and tremor and pathologically by deposition of Lewy bodies and cell loss in the substantia nigra and other brain regions. Parkinsonism is the term used to describe the clinical features of conditions resembling PD. Their management requires specialist assessment and a multidisciplinary approach. Levodopa remains the mainstay of treatment for PD. Although other treatments are used, older people are more sensitive to their side effects. Non-motor symptoms, particularly neuropsychiatric problems, significantly impact quality of life and need special consideration in older people. Towards the later stage of the disease, management can be complex, and should involve advanced care planning.

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PAX6 expression may be protective against dopaminergic cell loss in Parkinson's disease

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527314666150821101757 ◽

2016 ◽

Vol 15 (1) ◽

pp. 73-79 ◽

Cited By ~ 6

Author(s):

Meghan G. Thomas ◽

Caitlyn Welch ◽

Leah Stone ◽

Peter Allan ◽

Roger A. Barker ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cell Loss ◽

Pax6 Expression ◽

Dopaminergic Cell

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Neuroprotection in Parkinson’s disease: facts and hopes

Journal of Neural Transmission ◽

10.1007/s00702-019-02115-8 ◽

2019 ◽

Vol 127 (5) ◽

pp. 821-829 ◽

Cited By ~ 5

Author(s):

András Salamon ◽

Dénes Zádori ◽

László Szpisjak ◽

Péter Klivényi ◽

László Vécsei

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Cell Loss ◽

Substantia Nigra Pars Compacta ◽

Neuroprotective Agents ◽

Dopaminergic Cell ◽

Pathological Mechanism ◽

Positive Results

AbstractParkinson’s disease (PD) is the second most common neurodegenerative disease worldwide. Behind the symptoms there is a complex pathological mechanism which leads to a dopaminergic cell loss in the substantia nigra pars compacta. Despite the strong efforts, curative treatment has not been found yet. To prevent a further cell death, numerous molecules were tested in terms of neuroprotection in preclinical (in vitro, in vivo) and in clinical studies as well. The aim of this review article is to summarize our knowledge about the extensively tested neuroprotective agents (Search period: 1991–2019). We detail the underlying pathological mechanism and summarize the most important results of the completed animal and clinical trials. Although many positive results have been reported in the literature, there is still no evidence that any of them should be used in clinical practice (Cochrane analysis was performed). Therefore, further studies are needed to better understand the pathomechanism of PD and to find the optimal neuroprotective agent(s).

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