On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease

For 50 years ago was introduced L-3,4-dihydroxyphenylalanine (L-dopa) in Parkinson's disease treatment and during this significant advances has been done but what trigger the degeneration of the nigrostriatal system remain unknown. There is a general agreement in the scientific community that m...

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Main Author: Juan Segura-Aguilar
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2017-01-01
Series:Neural Regeneration Research
Subjects:
Online Access:http://www.nrronline.org/article.asp?issn=1673-5374;year=2017;volume=12;issue=6;spage=897;epage=901;aulast=Segura-Aguilar
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author Juan Segura-Aguilar
author_facet Juan Segura-Aguilar
author_sort Juan Segura-Aguilar
collection DOAJ
description For 50 years ago was introduced L-3,4-dihydroxyphenylalanine (L-dopa) in Parkinson's disease treatment and during this significant advances has been done but what trigger the degeneration of the nigrostriatal system remain unknown. There is a general agreement in the scientific community that mitochondrial dysfunction, protein degradation dysfunction, alpha-synuclein aggregation to neurotoxic oligomers, neuroinflammation, oxidative and endoplasmic reticulum stress are involved in the loss of dopaminergic neurons containing neuromelanin in Parkinson's disease. The question is what triggers these mechanisms. The age of normal onset in idiopathic Parkinson's disease suggests that environmental factors such as metals, pollutants or genetic mutations cannot be involved because these factors are related to early onset of Parkinsonism. Therefore, we have to search for endogenous neurotoxins and neuroprotection in order to understand what trigger the loss of dopaminergic neurons. One important feature of Parkinson's disease is the rate of the degenerative process before the motor symptoms are evident and during the disease progression. The extremely slow rate of Parkinson's disease suggests that the neurotoxins and the neuroprotection have to be related to dopamine metabolism. Possible candidates for endogenous neurotoxins are alpha-synuclein neurotoxic oligomers, 4-dihydroxyphenylacetaldehyde and ortho-quinones formed during dopamine oxidation to neuromelanin. Vesicular monoamine transporter-2, DT-diaphorase and glutathione transferase M2-2 seems to be the most important neuroprotective mechanism to prevent neurotoxic mechanism during dopamine oxidation.
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spelling doaj.art-3a505d006d7848b08b5590b77647d9e92022-12-22T03:55:54ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742017-01-0112689790110.4103/1673-5374.208560On the role of endogenous neurotoxins and neuroprotection in Parkinson's diseaseJuan Segura-AguilarFor 50 years ago was introduced L-3,4-dihydroxyphenylalanine (L-dopa) in Parkinson's disease treatment and during this significant advances has been done but what trigger the degeneration of the nigrostriatal system remain unknown. There is a general agreement in the scientific community that mitochondrial dysfunction, protein degradation dysfunction, alpha-synuclein aggregation to neurotoxic oligomers, neuroinflammation, oxidative and endoplasmic reticulum stress are involved in the loss of dopaminergic neurons containing neuromelanin in Parkinson's disease. The question is what triggers these mechanisms. The age of normal onset in idiopathic Parkinson's disease suggests that environmental factors such as metals, pollutants or genetic mutations cannot be involved because these factors are related to early onset of Parkinsonism. Therefore, we have to search for endogenous neurotoxins and neuroprotection in order to understand what trigger the loss of dopaminergic neurons. One important feature of Parkinson's disease is the rate of the degenerative process before the motor symptoms are evident and during the disease progression. The extremely slow rate of Parkinson's disease suggests that the neurotoxins and the neuroprotection have to be related to dopamine metabolism. Possible candidates for endogenous neurotoxins are alpha-synuclein neurotoxic oligomers, 4-dihydroxyphenylacetaldehyde and ortho-quinones formed during dopamine oxidation to neuromelanin. Vesicular monoamine transporter-2, DT-diaphorase and glutathione transferase M2-2 seems to be the most important neuroprotective mechanism to prevent neurotoxic mechanism during dopamine oxidation.http://www.nrronline.org/article.asp?issn=1673-5374;year=2017;volume=12;issue=6;spage=897;epage=901;aulast=Segura-AguilarVMAT-2; monoamine oxidase; 34-Dihydroxyphenylacetaldehyde; 34-dihydroxyphenylacetic acid; dopamine; L-dopa; aminochrome; neuromelanin
spellingShingle Juan Segura-Aguilar
On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease
Neural Regeneration Research
VMAT-2; monoamine oxidase; 3
4-Dihydroxyphenylacetaldehyde; 3
4-dihydroxyphenylacetic acid; dopamine; L-dopa; aminochrome; neuromelanin
title On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease
title_full On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease
title_fullStr On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease
title_full_unstemmed On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease
title_short On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease
title_sort on the role of endogenous neurotoxins and neuroprotection in parkinson s disease
topic VMAT-2; monoamine oxidase; 3
4-Dihydroxyphenylacetaldehyde; 3
4-dihydroxyphenylacetic acid; dopamine; L-dopa; aminochrome; neuromelanin
url http://www.nrronline.org/article.asp?issn=1673-5374;year=2017;volume=12;issue=6;spage=897;epage=901;aulast=Segura-Aguilar
work_keys_str_mv AT juanseguraaguilar ontheroleofendogenousneurotoxinsandneuroprotectioninparkinsonsdisease