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57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

12. - 15.09.2012, Erlangen

Banner: 57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie

Mixed Alzheimer’s disease and Lewy body dementia

Meeting Abstract

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  • presenting/speaker Lauren Walker - Newcastle University, Institute for Ageing and Health, Newcastle, United Kingdom
  • Alan Thomas - Newcastle University, Institute for Ageing and Health, Newcastle, United Kingdom
  • Chris Morris - Newcastle University, Institute for Ageing and Health, Newcastle, United Kingdom
  • Johannes Attems - Newcastle University, Institute for Ageing and Health, Newcastle, United Kingdom

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP4.23

DOI: 10.3205/12dgnn100, URN: urn:nbn:de:0183-12dgnn1000

Veröffentlicht: 11. September 2012

© 2012 Walker et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Introduction: The ageing brain is characterized by the presence of multiple pathologies and cases that neuropathologically fulfill criteria for both Alzheimer's disease (AD, e.g., NIA-AA criteria: High AD Neuropathologic Change) and Dementia with Lewy bodies (DLB; e.g., McKeith neocortical Lewy body disease) may be classified as mixed dementia: AD and DLB (mixed AD/DLB). Here, we compare mixed AD/DLB cases that clinically presented as either AD or DLB.

Methods: We investigated eight cases (75% female; mean age 74.5±3.4 yrs) that neuropathologically fulfilled the criteria for both AD and DLB. Clinically, four cases each were diagnosed as either AD or DLB. Tau, amyloid-β (Aβ) and α-synuclein (α-syn) pathologies were assessed semiquantitatively according to standardized criteria on 4 (Tau, Aβ) and 5 tiered (α-syn) scales in neocortical, limbic and brainstem regions.

Results: Tau pathology was severe in all regions, except for one case that showed only moderate neocortical tau pathology and was clinically diagnosed as AD. The severity of both α-syn and Aβ pathology varied between cases but no significant differences were seen between clincial AD and DLB cases.

Discussion: Using semiquantitative methods we could not find significant differences in the amount of neuropathological hallmark lesions between clinical AD and DLB cases that neuropathologically fulfilled the criteria for both AD and DLB. Our findings suggest that a more quantitative approach is warranted in order to clarify if the actual amount of neuropathological burden has any influcence on the clinical presentation. Hence, quantification of neuropathology is currently performed in this study group.