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Cerebral Cortex Advance Access first published online on July 16, 2008
This version published online on July 28, 2008
Cerebral Cortex, doi:10.1093/cercor/bhn111
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Widespread Changes in Dendritic Spines in a Model of Alzheimer's Disease

S. Knafo1, L. Alonso-Nanclares1, J. Gonzalez-Soriano2, P. Merino-Serrais1, I. Fernaud-Espinosa1, I. Ferrer3 and J. DeFelipe1

1 Instituto Cajal (CSIC), 28002 Madrid, Spain, 2 Department of Anatomy, Faculty of Veterinary Medicine, Complutense University, 28040 Madrid, Spain, 3 Institut Neuropatología, IDIBELL-Hospital Universitari de Bellvitge, Universitat de Barcelona, Hospitalet de LLobregat, 08907 Barcelona, Spain

Address correspondence to S. Knafo, MD, PhD, Cajal Institute, CSIC, Av. Dr. Arce 37, 28002, Madrid, Spain. Email: shira.knafo{at}gmail.com.

The mechanism by which dementia occurs in patients with Alzheimer's disease (AD) is not known. We assessed changes in hippocampal dendritic spines of APP/PS1 transgenic mice that accumulate amyloid beta throughout the brain. Three-dimensional analysis of 21 507 dendritic spines in the dentate gyrus, a region crucial for learning and memory, revealed a substantial decrease in the frequency of large spines in plaque-free regions of APP/PS1 mice. Plaque-related dendrites also show striking alterations in spine density and morphology. However, plaques occupy only 3.9% of the molecular layer volume. Because large spines are considered to be the physical traces of long-term memory, widespread decrease in the frequency of large spines likely contributes to the cognitive impairments observed in this AD model.

Key Words: Alzheimer's disease • confocal microscopy • dementia • dentate gyrus • transgenic mice

Updated to correct abstract and funding section


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