Kathleen Shannak

TL;DR: It is proposed that the motor deficits that are a constant and characteristic feature of idiopathic Parkinson's disease are for the most part a consequence of dopamine loss in the putamen, and that the dopamine-related caudate deficits are less marked or restricted to discrete functions only.

TL;DR: The found reduced levels of three dopamine nerve terminal markers in post–mortem striatum of chronic methamphetamine users suggest that chronic exposure to methamphetamine does not cause permanent degeneration of striatal dopamine nerve terminals at the doses used by the young subjects in this study.

TL;DR: Striatal subdivisions with physiologically higher dopamine metabolism are not at a greater risk of suffering dopamine neuronal damage with advancing age, as would seem to be implied by the oxidative stress hypothesis; thus, formation of dopamine‐derived oxy radicals in the human striatum appears unlikely to be a primary factor responsible for the age‐related striatal dopamine loss.

TL;DR: Postmortem data from 12 patients with PD and 10 matched controls compared with five different DA neuronal markers may help in interpretation of in vivo neuroimaging studies in PD in which only one radioligand is routinely employed.

TL;DR: It is concluded that disturbed dopamine synthetic capacity or a reduced arborization of striatal dopamine terminals may be the major disturbance in dopa‐responsive dystonia.