Memory and executive function in sporadic and familial Parkinson's disease

Citation
K. Dujardin et al., Memory and executive function in sporadic and familial Parkinson's disease, BRAIN, 124, 2001, pp. 389-398
Citations number
60
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
BRAIN
ISSN journal
00068950 → ACNP
Volume
124
Year of publication
2001
Part
2
Pages
389 - 398
Database
ISI
SICI code
0006-8950(200102)124:<389:MAEFIS>2.0.ZU;2-G
Abstract
Some studies have demonstrated that the motor symptomatology in sporadic an d familial Parkinson's disease was identical, From a physiopathological poi nt of view and perhaps in the future from a therapeutic point of view it se ems important to determine whether sporadic and familial Parkinson's diseas e are also similar with regard to cognitive impairment, The aim of the pres ent study was to assess cognitive functions in patients suffering from spor adic and familial Parkinson's disease. Executive functions and memory were investigated in particular, Two groups of 12 patients with Parkinson's dise ase (sporadic and familial) and 12 healthy controls performed a set of task s known to evaluate different aspects of executive function and memory, One -way analysis of variance tested for significant group effects, and when ju stified, post hoc analysis was performed, Cognitive impairment was differen t in sporadic and familial forms of Parkinson's disease, Indeed, although e xecutive function was impaired in both groups of patients, deficits in test s of explicit memory recall were only observed in patients with sporadic Pa rkinson's disease, Although the impairment observed in both groups of patie nts suggests a disruption of the striatoprefrontal circuits, this disruptio n seems to be quantitatively more important and more widespread in the spor adic patients than in the familial ones. In both patient groups, the defici ts probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested, In this group, a xenobiotic could b e responsible for an acquired metabolic defect involving more widespread st ructures of the striatoprefrontal circuits, leading to disruption of nondop aminergic loops, Cholinergic deprivation is considered in particular.