ReviewToxicologic pathology2025
Neuropathology and Biomarker Correlates of Late Onset Alzheimer's Disease in Aged Old World Monkeys.
Review in Toxicologic pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- A Comparative Study of Plasma Biomarkers of Neurodegeneration in Rhesus Monkeys (bioRxiv : the preprint server for biology · 2026Article
- The MacBrain Resource Center (MBRC) rhesus macaque postnatal brain histology datasets: Enabling new discoveries through NHP tissue and digital data Repositories.Journal of anatomy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Non-invasive predictive biomarkers for preclinical Alzheimer's disease (AD) may inform future dementia risk and support early intervention for AD. In this review, we describe clinical, biomarker and neuropathologic characteristics in spontaneously aged Old World monkeys (OWMs) in the context of preclinical AD. Reliable age-related amyloid-β (Aβ) plaque deposition occurs in OWMs. Plaque composition is complex, signifying significant disruption of synaptic connectivity. Pretangle pTau pathology in brainstem nuclei and limbic system prevails, consistent with Braak Stage 1b in macaques. Soluble pTau distribution approximates Braak Stage III-IV stage in perfused frozen macaque tissue, and colocalizes with Aβ and acetylcholinesterase labeling in AD-vulnerable circuits. Tau and Aβ pathology in OWMs is accompanied by fluid biomarker changes consistent with Core 1 AD diagnosis in humans but cannot be visualized using amyloid or tau tracers. Despite age-related cognitive decline, aging OWMs do not experience significant hippocampal atrophy or neuropathologic co-morbidities. Minimal expression of senescence markers implicates differences in rates of biological brain aging between OWMs and humans. OWMs support mechanistic studies and biomarker discovery in the areas of Aβ plaque and pTau evolution and resolution following anti-amyloid or Tau-directed therapeutics, as well as effects of senotherapeutics, lifestyle intervention or co-morbidities on biological brain aging.
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Registered trials
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