1999•NeurologyRequires access
Decreased striatal dopamine-receptor binding in sporadic ALS: Glutamate hyperactivity?
Oscar J.M. Vogels, Wim J.G. Oyen, Baziel G.M. van Engelen, George W. Padberg, Martin W.I.M. Horstink
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Abstract
The pathogenesis of ALS may be related to increased glutamatergic excitotoxicity. The striatum receives massive glutamatergic input. Animal studies suggest that glutamate decreases striatal D2-receptor synthesis. In drug-naive, sporadic ALS patients we demonstrated decreased striatal D2-receptor binding in vivo that could be partially reversed by the glutamatergic transmission blocker riluzole. Our findings support the glutamatergic excitotoxicity hypothesis in sporadic ALS.