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.
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
Ferri A;
2002
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
