The distribution pattern of pathology and cholinergic deficits in amygdaloid complex in Alzheimer's disease and dementia with Lewy bodies.
We studied the distribution pattern of pathology and cholinergic deficits in the subnuclei of the amygdaloid complex (AC) in five patients with Alzheimer's disease (AD), eight with dementia with Lewy bodies (DLB) and five normal controls. In controls, the basal nucleus contained the highest choline acetyltransferase activity; the activity in the lateral and central nuclei and those in the cortical, medial and accessory basal nuclei were comparable. In AD, there was a significant decrease in choline acetyltransferase activity in the accessory basal and lateral nuclei, in DLB a significant decrease was observed in the accessory basal, lateral and cortical nuclei. Compared to controls the hyperphosphorylated tau-pathology burden was significantly higher in the basal, central and medial nuclei in AD and in the central, cortical, lateral and medial nuclei in DLB. The amyloid plaque burden was significantly higher in the accessory basal, basal, lateral and cortical nuclei in AD and in all nuclei in DLB. The alpha-synuclein burden was significantly higher in all nuclei in both AD and DLB. Compared to AD alpha-synuclein burden was higher in all nuclei in DLB. There were no correlations between the distribution pattern of hyperphosphorylated tau-pathology, amyloid plaques and alpha-synuclein-positive structures, and choline acetyltransferase activity, except the lateral nucleus in DLB. In conclusion we found no relationship between the pattern of cholinergic deficits and the distribution pattern of lesions in the AC of patients with AD or DLB. Cholinergic deficits were more prominent in the nuclei of basolateral (BL) group in AD, whereas the nuclei of both BL and corticomedial groups were involved in DLB, which may be due to the involvement of both basal forebrain and brainstem cholinergic nuclei in the latter.
Sahin
Huseyin A
HA
Department of Neurology, Ondokuz Mayis University, Faculty of Medicine, Kurupelit, 55139, Samsun, Turkey. hasahin@omu.edu.tr
Emre
Murat
M
Ziabreva
Iryna
I
Perry
Elaine
E
Celasun
Bulent
B
Perry
Robert
R
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology*; D000679:Amygdala / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology*; D002795:Choline O-Acetyltransferase / Q000172:deficiency*; D005260:Female; D006651:Histocytochemistry; D006801:Humans; D007150:Immunohistochemistry; D016631:Lewy Bodies / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D010766:Phosphorylation; D058225:Plaque, Amyloid / Q000201:enzymology / Q000473:pathology; D051844:alpha-Synuclein / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism
D051844:alpha-Synuclein; D016875:tau Proteins; D002795:Choline O-Acetyltransferase