ArticleAging cell2019
Brains of rhesus monkeys display Aβ deposits and glial pathology while lacking Aβ dimers and other Alzheimer's pathologies.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 28 citations in OpenAlex.
- Repeated Intra-cisterna Magna Injections with Amyloid-beta Oligomers to Induce Alzheimer's Disease in Cynomolgus Monkey (Experimental neurobiology · 2026Article
- Spatial statistics and point pattern analysis reveal lifespan trajectories of microglial density and clustering in the primate hippocampus.Scientific reports · 2026Article
- Integrating neuroinflammation biomarkers into the ATN(X) framework: Advances in Alzheimer's pathogenesis, diagnosis, and insights from non-human primate models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Expression patterns of blood-based biomarkers of neurodegeneration and inflammation across adulthood in rhesus macaques.Experimental gerontology · 2025Article
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- In Vivo Seeding of Amyloid-β Protein and Implications in Modeling Alzheimer's Disease Pathology.Biomolecules · 2025Review
- An update on mammalian and non-mammalian animal models for biomarker development in neurodegenerative disorders.Cellular and molecular life sciences : CMLS · 2025Review
- A study on the variation of cytokine and electrolyte levels in rhesus macaques, cynomolgus monkeys, and Assamese macaques.Animal models and experimental medicine · 2025Article
- Tau and tauopathies across primate species: implications for modeling neurodegenerative disorders.Frontiers in aging neuroscience · 2025Review
- Animal models of Alzheimer's disease: Current strategies and new directions.Zoological research · 2024Review
- Review
- Review
- Cognitive Deficits and Alzheimer's Disease-Like Pathologies in the Aged Chinese Tree Shrew.Molecular neurobiology · 2024Article
- A nonhuman primate model with Alzheimer's disease-like pathology induced by hippocampal overexpression of human tau.Alzheimer's research & therapy · 2024Article
- Amyloid-β Pathology Is the Common Nominator Proteinopathy of the Primate Brain Aging.Journal of Alzheimer's disease : JAD · 2024Review
- Attenuation of amyloid-β-induced mitochondrial dysfunction by active components of anthocyanins in HT22 neuronal cells.MedComm · 2023Article
- Expression of tau and phosphorylated tau in the brain of normal and hemiparkinsonian rhesus macaques.The Journal of comparative neurology · 2023Article
- XperCT-guided Intra-cisterna Magna Injection of Streptozotocin for Establishing an Alzheimer's Disease Model Using the Cynomolgus Monkey (Experimental neurobiology · 2022Article
- Comparative neuropathology in aging primates: A perspective.American journal of primatology · 2021Review
- Deconstructing Alzheimer's Disease: How to Bridge the Gap between Experimental Models and the Human Pathology?International journal of molecular sciences · 2021Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Cerebral amyloid beta (Aβ) deposits are the main early pathology of Alzheimer's disease (AD). However, abundant Aβ deposits also occur spontaneously in the brains of many healthy people who are free of AD with advancing aging. A crucial unanswered question in AD prevention is why AD does not develop in some elderly people, despite the presence of Aβ deposits. The answer may lie in the composition of Aβ oligomer isoforms in the Aβ deposits of healthy brains, which are different from AD brains. However, which Aβ oligomer triggers the transformation from aging to AD pathogenesis is still under debate. Some researchers insist that the Aβ 12-mer causes AD pathology, while others suggest that the Aβ dimer is the crucial molecule in AD pathology. Aged rhesus monkeys spontaneously develop Aβ deposits in the brain with striking similarities to those of aged humans. Thus, rhesus monkeys are an ideal natural model to study the composition of Aβ oligomer isoforms and their downstream effects on AD pathology. In this study, we found that Aβ deposits in aged monkey brains included 3-mer, 5-mer, 9-mer, 10-mer, and 12-mer oligomers, but not 2-mer oligomers. The Aβ deposits, which were devoid of Aβ dimers, induced glial pathology (microgliosis, abnormal microglia morphology, and astrocytosis), but not the subsequent downstream pathologies of AD, including Tau pathology, neurodegeneration, and synapse loss. Our results indicate that the Aβ dimer plays an important role in AD pathogenesis. Thus, targeting the Aβ dimer is a promising strategy for preventing AD.
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