Early detection of cryptic memory and glucose uptake deficits in pre-pathological APP mice

V. Beglopoulos, J. Tulloch, A. D. Roe, S. Daumas, L. Ferrington, R. Watson, Z. Fan, B. T. Hyman, P. A. T. Kelly, F. Bard and R. G. M. Morris ()
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V. Beglopoulos: Centre for Cognitive and Neural Systems, Edinburgh Neuroscience, The University of Edinburgh
J. Tulloch: Centre for Cognitive and Neural Systems, Edinburgh Neuroscience, The University of Edinburgh
A. D. Roe: Mass General Institute for Neurodegeneration, Massachusetts General Hospital, Harvard Medical School
S. Daumas: Neuroscience Paris Seine, Institut de Biologie Paris Seine, Sorbonne Universités, Pierre and Marie Curie University, UM CR18, INSERM U1130
L. Ferrington: Centre for Cognitive and Neural Systems, Edinburgh Neuroscience, The University of Edinburgh
R. Watson: Centre for Cognitive and Neural Systems, Edinburgh Neuroscience, The University of Edinburgh
Z. Fan: Mass General Institute for Neurodegeneration, Massachusetts General Hospital, Harvard Medical School
B. T. Hyman: Mass General Institute for Neurodegeneration, Massachusetts General Hospital, Harvard Medical School
P. A. T. Kelly: Centre for Cognitive and Neural Systems, Edinburgh Neuroscience, The University of Edinburgh
F. Bard: Janssen Prevention Center, Janssen Pharmaceutical Companies of Johnson & Johnson
R. G. M. Morris: Centre for Cognitive and Neural Systems, Edinburgh Neuroscience, The University of Edinburgh

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: Abstract Earlier diagnosis and treatment of Alzheimer’s disease would greatly benefit from the identification of biomarkers at the prodromal stage. Using a prominent animal model of aspects of the disease, we here show using clinically relevant methodologies that very young, pre-pathological PDAPP mice, which overexpress mutant human amyloid precursor protein in the brain, exhibit two cryptic deficits that are normally undetected using standard methods of assessment. Despite learning a spatial memory task normally and displaying normal brain glucose uptake, they display faster forgetting after a long delay following performance to a criterion, together with a strong impairment of brain glucose uptake at the time of attempted memory retrieval. Preliminary observations suggest that these deficits, likely caused by an impairment in systems consolidation, could be rescued by immunotherapy with an anti-β-amyloid antibody. Our data suggest a biomarker strategy for the early detection of β-amyloid-related abnormalities.

Date: 2016
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DOI: 10.1038/ncomms11761

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