Publication:
The Distribution Pattern of Pathology and Cholinergic Deficits in Amygdaloid Complex in Alzheimer's Disease and Dementia with Lewy Bodies

dc.authorscopusid35581243200
dc.authorscopusid7004878675
dc.authorscopusid12141144100
dc.authorscopusid7202233944
dc.authorscopusid7004050836
dc.authorscopusid7402423425
dc.contributor.authorŞahin, H.A.
dc.contributor.authorEmre, M.
dc.contributor.authorZiabreva, I.
dc.contributor.authorPerry, E.
dc.contributor.authorCelasun, B.
dc.contributor.authorPerry, R.
dc.date.accessioned2020-06-21T15:29:13Z
dc.date.available2020-06-21T15:29:13Z
dc.date.issued2006
dc.departmentOndokuz Mayıs Üniversitesien_US
dc.department-temp[Şahin] Hüseyin Alparslan, Department of Neurology, Ondokuz Mayis Üniversitesi, Samsun, Turkey; [Emre] Murat, Department of Neurology, İstanbul Tıp Fakültesi, Istanbul, Turkey; [Ziabreva] Iryna, Newcastle General Hospital, Newcastle, Tyne and Wear, United Kingdom; [Perry] Elaine K., Newcastle General Hospital, Newcastle, Tyne and Wear, United Kingdom; [Celasun] Bülent, Department of Pathology, Gülhane Eğitim ve Araştırma Hastanesi, Ankara, Turkey; [Perry] Robert Henry, Department of Neuropathology, Newcastle General Hospital, Newcastle, Tyne and Wear, United Kingdomen_US
dc.description.abstractWe 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 α-synuclein burden was significantly higher in all nuclei in both AD and DLB. Compared to AD α-synuclein burden was higher in all nuclei in DLB. There were no correlations between the distribution pattern of hyperphosphorylated tau-pathology, amyloid plaques and α-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. © Springer-Verlag 2006.en_US
dc.identifier.doi10.1007/s00401-005-0003-2
dc.identifier.endpage125en_US
dc.identifier.issn0001-6322
dc.identifier.issn1432-0533
dc.identifier.issue2en_US
dc.identifier.pmid16468020
dc.identifier.scopus2-s2.0-33646184840
dc.identifier.scopusqualityQ1
dc.identifier.startpage115en_US
dc.identifier.urihttps://doi.org/10.1007/s00401-005-0003-2
dc.identifier.volume111en_US
dc.identifier.wosWOS:000236214000004
dc.identifier.wosqualityQ1
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofActa Neuropathologicaen_US
dc.relation.journalActa Neuropathologicaen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAlzheimer Diseaseen_US
dc.subjectAmygdalaen_US
dc.subjectCholinergic Systemen_US
dc.subjectDementia with Lewy Bodiesen_US
dc.titleThe Distribution Pattern of Pathology and Cholinergic Deficits in Amygdaloid Complex in Alzheimer's Disease and Dementia with Lewy Bodiesen_US
dc.typeArticleen_US
dspace.entity.typePublication

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