Idiopathic nondementing Parkinson’s disease (PD) is marked by progressive loss of dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area. Recent brain imaging work implicates these stru...Idiopathic nondementing Parkinson’s disease (PD) is marked by progressive loss of dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area. Recent brain imaging work implicates these structures in dopamine modulated networks subserving episodic memory. These findings are of relevance to PD because they suggest that dopamine depletion contributes to the disease-dependent decline in episodic memory, and therefore, this decline should, at least partially, be remediated by dopaminergic medication. Recognition memory (RM), recollection and familiarity during recognition was examined in 17 PD patients, 12 of whom were medicated with a D2 dopamine agonist (pramipexole or ropinirole) and l-dopa, with a further 5 PD control patients on l-dopa but no D2 agonist. Memory was tested “ON” and, following a period of medication withdrawal, “OFF” and compared to a group of 14 matched healthy volunteers (HV). The HVs were also tested twice in the absence of medication. The patients on the agonists PD showed significant impairments in recollection ON- and OFF-medication, whereas the l-dopa control patients exhibited a decline in OFF-recollection only. RM and familiarity were spared in both groups ON- and OFF-medication. These findings suggest that D2 dopamine agonists (combined with l-dopa) contribute to disease-dependent episodic memory impairment.展开更多
文摘Idiopathic nondementing Parkinson’s disease (PD) is marked by progressive loss of dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area. Recent brain imaging work implicates these structures in dopamine modulated networks subserving episodic memory. These findings are of relevance to PD because they suggest that dopamine depletion contributes to the disease-dependent decline in episodic memory, and therefore, this decline should, at least partially, be remediated by dopaminergic medication. Recognition memory (RM), recollection and familiarity during recognition was examined in 17 PD patients, 12 of whom were medicated with a D2 dopamine agonist (pramipexole or ropinirole) and l-dopa, with a further 5 PD control patients on l-dopa but no D2 agonist. Memory was tested “ON” and, following a period of medication withdrawal, “OFF” and compared to a group of 14 matched healthy volunteers (HV). The HVs were also tested twice in the absence of medication. The patients on the agonists PD showed significant impairments in recollection ON- and OFF-medication, whereas the l-dopa control patients exhibited a decline in OFF-recollection only. RM and familiarity were spared in both groups ON- and OFF-medication. These findings suggest that D2 dopamine agonists (combined with l-dopa) contribute to disease-dependent episodic memory impairment.
