ArticleNature communications2016
Early detection of cryptic memory and glucose uptake deficits in pre-pathological APP mice.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Navigating Alzheimer's Disease Mouse Models: Age-Related Pathology and Cognitive Deficits.Biomolecules · 2024Review
- Accelerated long-term forgetting: A sensitive paradigm for detecting subtle cognitive impairment and evaluating BACE1 inhibitor efficacy in preclinical Alzheimer's disease.Frontiers in dementia · 2023Review
- Impact of somatostatin interneurons on interactions between barrels in plasticity induced by whisker deprivation.Scientific reports · 2022Article
- Dopamine, sleep, and neuronal excitability modulate amyloid-β-mediated forgetting in Drosophila.PLoS biology · 2021Article
- Accelerated long-term forgetting is a BACE1 inhibitor-reversible incipient cognitive phenotype in Alzheimer's disease model mice.Neuropsychopharmacology reports · 2021Article
- Neuron-specific deletion of presenilin enhancer2 causes progressive astrogliosis and age-related neurodegeneration in the cortex independent of the Notch signaling.CNS neuroscience & therapeutics · 2021Article
- Accelerated long-term forgetting over three months in asymptomatic APOE ɛ4 carriers.Annals of clinical and translational neurology · 2021Article
- Early β adrenoceptor dependent time window for fear memory persistence in APPswe/PS1dE9 mice.Scientific reports · 2021Article
- Oleocanthal-rich extra-virgin olive oil enhances donepezil effect by reducing amyloid-β load and related toxicity in a mouse model of Alzheimer's disease.The Journal of nutritional biochemistry · 2018Article
- Accelerated long-term forgetting in presymptomatic autosomal dominant Alzheimer's disease: a cross-sectional study.The Lancet. Neurology · 2018Article
- Oleocanthal ameliorates amyloid-β oligomers' toxicity on astrocytes and neuronal cells: In vitro studies.Neuroscience · 2017Article
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Authors and funding
11 authors.
Funding
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.
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