Abstract

Parkinson's disease (PD) has historically been considered a motor disorder induced by a loss of dopaminergic neurons in the substantia nigra pars compacta. More recently, it has been recognized to have significant non-motor symptoms, most prominently cognitive symptoms associated with a dysexecutive syndrome. It is common in the literature to see motor and cognitive symptoms treated separately and, indeed, there has been a general call for specialized treatment of the latter, particularly in the more severe cases of PD with mild cognitive impairment and dementia. Animal studies have similarly been developed to model the motor or non-motor symptoms. Nevertheless, considerable research has established that segregating consideration of cognition from the precursors to motor movement, particularly movement associated with goal-directed action, is difficult if not impossible. Indeed, on some contemporary views cognition is embodied in action control, something that is particularly prevalent in theory and evidence relating to the integration of goal-directed and habitual control processes. The current paper addresses these issues within the literature detailing animal models of cognitive dysfunction in PD and their neural and neurochemical bases. Generally, studies using animal models of PD provide some of the clearest evidence for the integration of these action control processes at multiple levels of analysis and imply that consideration of this integrative process may have significant benefits for developing new approaches to the treatment of PD.

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