ParkinsonCanadaV1, PubMed, Corpus, bibRecord, 001419

Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease.

Identifieur interne : 001419 ( PubMed/Corpus ); précédent : 001418; suivant : 001420

Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease.

Auteurs : Paul S. Fitzmaurice ; Lee Ang ; Mark Guttman ; Ali H. Rajput ; Yoshiaki Furukawa ; Stephen J. Kish

Source :

Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2003.

RBID : pubmed:14502663

English descriptors

KwdEn :
- Aged, Antioxidants (metabolism), Glutathione (deficiency), Humans, Multiple System Atrophy (metabolism), Oxidative Stress, Parkinson Disease (metabolism), Substantia Nigra (metabolism), Supranuclear Palsy, Progressive (metabolism), Uric Acid (metabolism).
MESH :
- chemical , deficiency : Glutathione.
- chemical , metabolism : Antioxidants, Uric Acid.
- metabolism : Multiple System Atrophy, Parkinson Disease, Substantia Nigra, Supranuclear Palsy, Progressive.
- Aged, Humans, Oxidative Stress.

Abstract

The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [-30%], PSP [-21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [-20%]). GSH levels were normal in all examined normal and degenerating extra-nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (-19 to -30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD.

DOI: 10.1002/mds.10486
PubMed: 14502663

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pubmed:14502663

Le document en format XML

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<author><name sortKey="Fitzmaurice, Paul S" sort="Fitzmaurice, Paul S" uniqKey="Fitzmaurice P" first="Paul S" last="Fitzmaurice">Paul S. Fitzmaurice</name>
<affiliation><nlm:affiliation>Human Neurochemical Pathology Laboratory, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. Paul_fitzmaurice@camh.net</nlm:affiliation>
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<author><name sortKey="Ang, Lee" sort="Ang, Lee" uniqKey="Ang L" first="Lee" last="Ang">Lee Ang</name>
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<author><name sortKey="Guttman, Mark" sort="Guttman, Mark" uniqKey="Guttman M" first="Mark" last="Guttman">Mark Guttman</name>
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<author><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H" last="Rajput">Ali H. Rajput</name>
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<author><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name>
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<term>Supranuclear Palsy, Progressive (metabolism)</term>
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<front><div type="abstract" xml:lang="en">The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [-30%], PSP [-21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [-20%]). GSH levels were normal in all examined normal and degenerating extra-nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (-19 to -30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD.</div>
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<Abstract><AbstractText>The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [-30%], PSP [-21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [-20%]). GSH levels were normal in all examined normal and degenerating extra-nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (-19 to -30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD.</AbstractText>
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Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease.

Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease.

Source :

English descriptors

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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