Pathological Substrates of Cognitive Decline in Alzheimer’s DiseaseGiannakopoulos P.a,c · Gold G.b · von Gunten A.c · Hof P.R.d,e · Bouras C.a,d
Departments of aPsychiatry and bGeriatrics, University of Geneva School of Medicine, Chêne-Bourg, Geneva, cDivision of Old Age Psychiatry, University of Lausanne School of Medicine, Lausanne, Switzerland; Departmentsof dNeuroscience and eGeriatrics and Adult Development, Mount Sinai School of Medicine, New York, N.Y., USA
Do you have an account?
- Rent for 48h to view
- Buy Cloud Access for unlimited viewing via different devices
- Synchronizing in the ReadCube Cloud
- Printing and saving restrictions apply
Rental: USD 8.50
Cloud: USD 20.00
The progressive development of Alzheimer’s disease (AD)-related lesions such as neurofibrillary tangles,amyloid deposits and synaptic loss within the cerebral cortex is a main event of brain aging.Recent neuropathologic studies strongly suggested that the clinical diagnosis of dementia dependsmore on the severity and topography of pathologic changes than on the presence of a qualitativemarker. However, several methodological problems such as selection biases, case-control design,density-based measures, and masking effects of concomitant pathologies should be taken intoaccount when interpreting these data. In last years, the use of stereologic counting permitted todefine reliably the cognitive impact of AD lesions in the human brain. Unlike fibrillar amyloid depositsthat are poorly or not related to the dementia severity, the use of this method documented thattotal neurofibrillary tangles and neuron numbers in the CA1 field are the best correlates of cognitivedeterioration in brain aging. Loss of dendritic spines in neocortical but not hippocampal areas has amodest but independent contribution to dementia. In contrast, the importance of early dendriticand axonal tau-related pathologic changes such as neuropil threads remains doubtful. Despite theseprogresses, neuronal pathology and synaptic loss in cases with pure AD pathology cannot explainmore than 50% of clinical severity. The present review discusses the complex structure/function relationshipsin brain aging and AD within the theoretical framework of the functional neuropathologyof brain aging.
© 2009 S. Karger AG, Basel
Article / Publication Details
Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.