Thalamic D2 receptors in dementia with Lewy bodies, Parkinson's disease, and Parkinson's disease dementia.
Dementia with Lewy bodies (DLB) is characterized by progressive dementia with two of three core symptoms; Parkinsonism, visual hallucinations or disturbances of consciousness/fluctuating attention. Dementia in Parkinson's disease (PDD) has similar neuropsychiatric characteristics. Reduced nigrothalamic dopamine and altered thalamic D2 receptors may mediate some of the non-motor symptoms of DLB and PDD. The study aims were to ascertain whether thalamic D2 density was altered in Parkinson's disease (PD), PDD and DLB, and whether D2 density was related to core symptoms. Thalamic D2 receptor binding was measured by post-mortem autoradiography in 18 cases of DLB, 13 PDD, 6 PD and 14 normal elderly controls. Highest D2 density in control cases was in the intralaminar, midline, anterior and mediodorsal nuclei. In PD without dementia D2 binding was elevated above controls in all thalamic regions, significantly in reticular, laterodorsal, centromedian, ventral centromedian, parafascicular, paraventricular, ventroposterior, ventrolateral posterior, and ventrointermedius nuclei. Compared to controls, DLB cases with Parkinsonism (DLB+EPS) had significantly elevated D2 receptor density in laterodorsal and ventrointermedius nuclei; PDD cases had significantly raised density in the ventrointermedius, and DLB cases without Parkinsonism (DLB-EPS) did not show increased D2 density in any areas. In DLB and PDD cases with disturbances of consciousness, cases treated with neuroleptics had higher D2 binding in all thalamic regions, significantly in the mediodorsal and ventrolateral posterior nuclei. D2 receptor binding did not vary with cognitive decline (MMSE) or visual hallucinations, but was significantly higher with increased extrapyramidal symptoms.
Piggott
Margaret A
MA
IAH Research Laboratories, Institute for Ageing and Health, University of Newcastle-upon-Tyne, Newcastle General Hospital, Westgate Road, Newcastle-upon-Tyne, UK. m.a.piggott@ncl.ac.uk
Ballard
Clive G
CG
Dickinson
Heather O
HO
McKeith
Ian G
IG
Perry
Robert H
RH
Perry
Elaine K
EK
D000368:Aged; D000369:Aged, 80 and over; D014150:Antipsychotic Agents / Q000627:therapeutic use; D001344:Autopsy; D001345:Autoradiography; D001480:Basal Ganglia Diseases / Q000378:metabolism / Q000523:psychology; D002540:Cerebral Cortex / Q000473:pathology; D003244:Consciousness Disorders / Q000378:metabolism / Q000523:psychology; D003704:Dementia / Q000209:etiology / Q000378:metabolism* / Q000523:psychology; D005260:Female; D006212:Hallucinations / Q000378:metabolism / Q000523:psychology; D006801:Humans; D016631:Lewy Bodies / Q000473:pathology; D020961:Lewy Body Disease / Q000378:metabolism* / Q000473:pathology / Q000523:psychology; D008297:Male; D009069:Movement Disorders / Q000378:metabolism / Q000523:psychology; D009483:Neuropsychological Tests; D010300:Parkinson Disease / Q000150:complications / Q000378:metabolism* / Q000523:psychology; D017448:Receptors, Dopamine D2 / Q000378:metabolism*; D013787:Thalamic Nuclei / Q000378:metabolism / Q000473:pathology; D013788:Thalamus / Q000378:metabolism* / Q000473:pathology
D014150:Antipsychotic Agents; D017448:Receptors, Dopamine D2