ArticleProceedings of the National Academy of Sciences of the United States of America2019
Alzheimer's-like pathology in aging rhesus macaques: Unique opportunity to study the etiology and treatment of Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 75 citations in OpenAlex.
- Plasma and cerebrospinal fluid proteomics reveal distinct patterns of senescence and neuropathology in aging rhesus macaques.GeroScience · 2026Article
- Dorsolateral Prefrontal Cortex Circuitry at the Intersection of Cognition and Disease.Biological psychiatry · 2026Review
- Spatial statistics and point pattern analysis reveal lifespan trajectories of microglial density and clustering in the primate hippocampus.Scientific reports · 2026Article
- γ-Radiation Induces Long-Term Dose-Related Proteomic and Phosphorylated-Tau Species Changes in Non-Human Primate Hippocampus.Research square · 2026Article
- Inflammatory mechanisms underlying early Alzheimer's disease pathology: evidence from the aging rhesus macaque brain.Frontiers in cellular neuroscience · 2026Review
- Ryanodine receptor 2-mediated calcium leak is associated with increased glyoxalase I in the aging brain.JCI insight · 2025Article
- Single-cell, multi-region profiling of the macaque brain across the lifespan.bioRxiv : the preprint server for biology · 2025Article
- Understanding Tau pathology: Insights from animal models.Zoological research · 2025Review
- Mesenchymal stem cell-derived exosomes: Shaping the next era of Alzheimer's disease treatment.World journal of stem cells · 2025Review
- Article
- 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
- Advancement in modeling of Alzheimer's disease: a comprehensive review of preclinical screening platforms.Frontiers in aging neuroscience · 2025Review
- Dysregulated calcium signaling in the aged macaque entorhinal cortex associated with tau hyperphosphorylation.Frontiers in aging neuroscience · 2025Article
- Dysregulated calcium signaling in the aged primate association cortices: vulnerability to Alzheimer's disease neuropathology.Frontiers in aging neuroscience · 2025Review
- Mediterranean diet protects against a neuroinflammatory cortical transcriptome: Associations with brain volumetrics, peripheral inflammation, social isolation, and anxiety in nonhuman primates (Macaca fascicularis).Brain, behavior, and immunity · 2024Article
- Cognitive Deficits and Alzheimer's Disease-Like Pathologies in the Aged Chinese Tree Shrew.Molecular neurobiology · 2024Article
- Genetically modified non-human primate models for research on neurodegenerative diseases.Zoological research · 2024Review
- A nonhuman primate model with Alzheimer's disease-like pathology induced by hippocampal overexpression of human tau.Alzheimer's research & therapy · 2024Article
- Pathological Markers of Alzheimer's Disease and Related Dementia in the Rhesus Macaque Amygdala.Journal of Alzheimer's disease reports · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Although mouse models of Alzheimer's disease (AD) have provided tremendous breakthroughs, the etiology of later onset AD remains unknown. In particular, tau pathology in the association cortex is poorly replicated in mouse models. Aging rhesus monkeys naturally develop cognitive deficits, amyloid plaques, and the same qualitative pattern and sequence of tau pathology as humans, with tangles in the oldest animals. Thus, aging rhesus monkeys can play a key role in AD research. For example, aging monkeys can help reveal how synapses in the prefrontal association cortex are uniquely regulated compared to the primary sensory cortex in ways that render them vulnerable to calcium dysregulation and tau phosphorylation, resulting in the selective localization of tau pathology observed in AD. The ability to assay early tau phosphorylation states and perform high-quality immunoelectron microscopy in monkeys is a great advantage, as one can capture early-stage degeneration as it naturally occurs in situ. Our immunoelectron microscopy studies show that phosphorylated tau can induce an "endosomal traffic jam" that drives amyloid precursor protein cleavage to amyloid-β in endosomes. As amyloid-β increases tau phosphorylation, this creates a vicious cycle where varied precipitating factors all lead to a similar phenotype. These data may help explain why circuits with aggressive tau pathology (e.g., entorhinal cortex) may degenerate prior to producing significant amyloid pathology. Aging monkeys therefore can play an important role in identifying and testing potential therapeutics to protect the association cortex, including preventive therapies that are challenging to test in humans.
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