[A new look at the corticostriatal-thalamocortical circuit in sporadic Parkinson's disease].
The traditional model of corticostriatal-thalamocortical projections, with indirect and direct pathways, provides a simplified and useful explanation for the motor deficits (hypokinesia, bradykinesia) that develop in the course of sporadic Parkinson's disease. In the classic model, major emphasis is placed on the dopamine deficiency in the dorsal striatum that occurs as a result of neuronal loss in the substantia nigra of the midbrain. Nevertheless, because the pathological process that underlies Parkinson's disease also involves many key nondopaminergic connectivities, a revised model is needed that incorporates these projections. The focus on damage to nondopaminergic and extranigral sites is becoming increasingly important for clinical practice.
Braak
H
H
Institut für Klinische Neuroanatomie, Goethe-Universität Frankfurt, Theodor Stern Kai 7, 60590, Frankfurt am Main. Braak@em.uni-frankfurt.de
Del Tredici
K
K
D016922:Cellular Senescence / Q000502:physiology; D002540:Cerebral Cortex / Q000503:physiopathology*; D003342:Corpus Striatum / Q000503:physiopathology*; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D018476:Hypokinesia / Q000503:physiopathology; D009415:Nerve Net / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology*; D013788:Thalamus / Q000503:physiopathology*; D051844:alpha-Synuclein / Q000378:metabolism
D051844:alpha-Synuclein; D004298:Dopamine