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Caudate nucleus
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===Parkinson's disease=== [[Parkinson's disease]] is likely the most studied basal ganglia disorder. Patients with this progressive neurodegenerative disorder often first experience movement related symptoms (the three most common being tremors at rest, muscular rigidity, and [[akathisia]]) which are later combined with various cognitive deficiencies, including dementia.<ref>{{cite book|last=Kolb|first=Bryan|author2=Ian Q. Whishaw|title=An Introduction to Brain and Behavior|url=https://archive.org/details/introductiontobr00kolb|url-access=registration|year=2001|publisher=Worth Publishers|location=New York|isbn=978-1429242288|page=[https://archive.org/details/introductiontobr00kolb/page/590 590]|edition=4th}}</ref> Parkinson's disease depletes dopaminergic neurons in the nigrostriatal tract, a dopamine pathway that is connected to the head of the caudate. As such, many studies have correlated the loss of dopaminergic neurons that send axons to the caudate nucleus and the degree of dementia in Parkinson's patients.<ref name="Grahn 2009 146">{{cite journal | vauthors = Grahn JA, Parkinson JA, Owen AM | title = The role of the basal ganglia in learning and memory: neuropsychological studies | journal = Behavioural Brain Research | volume = 199 | issue = 1 | pages = 53β60 | date = April 2009 | pmid = 19059285 | doi = 10.1016/j.bbr.2008.11.020 | s2cid = 15685091 }}</ref> And while a relationship has been drawn between the caudate and Parkinson's motor deficiencies, the caudate has also been associated with Parkinson's concomitant cognitive impairments. One review contrasts the performance of patients with Parkinson's and patients that strictly had frontal-lobe damage in the [[Tower of London test]]. The differences in performance between the two types of patients (in a test that, in short, requires subjects to select appropriate intermediate goals with a larger goal in mind) draws a link between the caudate and goal-directed action. However, the studies are not conclusive. While the caudate has been associated with executive function (see "Goal-Directed Action"), it remains "entirely unclear whether executive deficits in [Parkinson's patients] reflect pre-dominantly their cortical or subcortical damage."<ref name="Grahn 2009 146"/>
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