Recent data indicate that overexpression of the enzyme Cu,Zn superoxide dismutase (SOD1) in mice confers neuroprotection against various dopamine neurotoxins like 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), methamphetamine, 6-hydroxydopamine and methylenedioxymethamphetamine. In the present study we investigated whether a mutant form of SOD1 (G93A), occurring in humans affected by amyotrophic lateral sclerosis, leads to a differential vulnerability of nigrostriatal dopaminergic neurons to the chronic dopamine depletion induced by the selective neurotoxin MPTP. Our results indicate that overexpression of both wild-type and human mutant SOD1 induces comparable neuroprotective effects against striatal dopaminergic depletion. q 2002 Elsevier Science Ireland Ltd. All rights reserved.
Resistance to striatal dopamine depletion induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice expressing human mutant Cu,Zn superoxide dismutase.
FORNAI, FRANCESCO;
2002-01-01
Abstract
Recent data indicate that overexpression of the enzyme Cu,Zn superoxide dismutase (SOD1) in mice confers neuroprotection against various dopamine neurotoxins like 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), methamphetamine, 6-hydroxydopamine and methylenedioxymethamphetamine. In the present study we investigated whether a mutant form of SOD1 (G93A), occurring in humans affected by amyotrophic lateral sclerosis, leads to a differential vulnerability of nigrostriatal dopaminergic neurons to the chronic dopamine depletion induced by the selective neurotoxin MPTP. Our results indicate that overexpression of both wild-type and human mutant SOD1 induces comparable neuroprotective effects against striatal dopaminergic depletion. q 2002 Elsevier Science Ireland Ltd. All rights reserved.File | Dimensione | Formato | |
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