ArticleProceedings of the National Academy of Sciences of the United States of America2012
Postsynaptic dysfunction is associated with spatial and object recognition memory loss in a natural model of Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
72 citing papers in PubMed, 140 citations in OpenAlex.
- Article
- Age-Associated Behavioral Alterations in Laboratory-Housed Octodon degus.bioRxiv : the preprint server for biology · 2026Article
- Circadian Changes in CA1 LTP Are Driven by Shifts in Excitation-Inhibition Balance and Reverse Direction after Puberty in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
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- Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- The Role of Astrocytes in Synaptic Dysfunction and Memory Deficits in Alzheimer's Disease.Biomolecules · 2025Review
- Article
- Exploring efficient and effective mammalian models for Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Alterations in zinc, copper, and iron levels in the retina and brain of Alzheimer's disease patients and the APP/PS1 mouse model.Metallomics : integrated biometal science · 2024Article
- Investigating the Potential Therapeutic Mechanisms of Puerarin in Neurological Diseases.Molecular neurobiology · 2024Review
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- Clinical application of sparse canonical correlation analysis to detect genetic associations with cortical thickness in Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Identification of Alzheimer's Disease by Imaging: A Comprehensive Review.International journal of environmental research and public health · 2023Review
- Age-Dependent Behavioral and Synaptic Dysfunction Impairment Are Improved with Long-Term Andrographolide Administration in Long-Lived Female Degus (International journal of molecular sciences · 2023Article
- mGluR-dependent plasticity in rodent models of Alzheimer's disease.Frontiers in synaptic neuroscience · 2023Article
- Impact of prolonged chronic social isolation stress on behavior and multifractal complexity of metabolic rate inFrontiers in behavioral neuroscience · 2023Article
- Clinical effects of novel susceptibility genes for beta-amyloid: a gene-based association study in the Korean population.Frontiers in aging neuroscience · 2023Article
- Cognitively impaired aged Octodon degus recapitulate major neuropathological features of sporadic Alzheimer's disease.Acta neuropathologica communications · 2022Article
- The Long-Term Pannexin 1 Ablation Produces Structural and Functional Modifications in Hippocampal Neurons.Cells · 2022Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
Abstract
Alzheimer's disease (AD) is an age-related neurodegenerative disorder associated with progressive memory loss, severe dementia, and hallmark neuropathological markers, such as deposition of amyloid-β (Aβ) peptides in senile plaques and accumulation of hyperphosphorylated tau proteins in neurofibrillary tangles. Recent evidence obtained from transgenic mouse models suggests that soluble, nonfibrillar Aβ oligomers may induce synaptic failure early in AD. Despite their undoubted value, these transgenic models rely on genetic manipulations that represent the inherited and familial, but not the most abundant, sporadic form of AD. A nontransgenic animal model that still develops hallmarks of AD would be an important step toward understanding how sporadic AD is initiated. Here we show that starting between 12 and 36 mo of age, the rodent Octodon degus naturally develops neuropathological signs of AD, such as accumulation of Aβ oligomers and phosphorylated tau proteins. Moreover, age-related changes in Aβ oligomers and tau phosphorylation levels are correlated with decreases in spatial and object recognition memory, postsynaptic function, and synaptic plasticity. These findings validate O. degus as a suitable natural model for studying how sporadic AD may be initiated.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.