title: Decreased striatal dopamine-receptor binding in sporadic ALS: glutamate hyperactivity?
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.
authors.affiliation: Department of Neurology, University Hospital Nijmegen, The Netherlands.
authors.forename: O J
authors.initials: OJ
authors.lastname: Vogels
authors.forename: W J
authors.initials: WJ
authors.lastname: Oyen
authors.forename: B G
authors.initials: BG
authors.lastname: van Engelen
authors.forename: G W
authors.initials: GW
authors.lastname: Padberg
authors.forename: M W
authors.initials: MW
authors.lastname: Horstink
mesh_terms: D000368:Aged; D000690:Amyotrophic Lateral Sclerosis / Q000378:metabolism*; D003342:Corpus Striatum / Q000378:metabolism*; D006801:Humans; D008875:Middle Aged; D010865:Pilot Projects; D017448:Receptors, Dopamine D2 / Q000187:drug effects / Q000378:metabolism*; D019782:Riluzole / Q000494:pharmacology*
chemical_list: D017448:Receptors, Dopamine D2; D019782:Riluzole