SynthesisAlzheimer's research & therapy2025
The biological scaling of Alzheimer's disease neuropathological changes across primate species.
Synthesis in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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 neuromodulatory fragility hypothesis of Alzheimer's disease pathogenesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
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Authors and funding
4 authors.
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Abstract
backgroundStudying the spontaneous emergence of biological anomalies within the animal kingdom can provide insights into the causes of diseases. It is often assumed that Alzheimer's Disease (AD), like other neurodegenerative diseases, is specific to humans. However, the age-related occurrence of AD neuropathological changes (ADNC) in non-human primates (NHPs) and their comparison with humans has not been formally studied. Moreover, a conceptual framework for interpreting the spontaneous occurrence of ADNC in NHPs has yet to be established.
methodsWe conducted a systematic review of the available data describing spontaneous ADNC in various NHP species. To study the biological scaling of ADNC, we used logistic regression models to compare NHP and human findings, based on both chronological age and age standardized to each species' maximum longevity.
resultsAmyloid plaques appear in all primate species according to the same temporal dynamics once the theoretical maximum age is considered, and are significantly more frequent in NHPs than in humans. In contrast, tau neurofibrillary tangles are rare in NHPs and only appear at the limit of their life expectancy.
conclusionThe biological scaling of amyloid plaque development follows an isometric model (proportional to lifespan), whereas tau tangles emerge at a similar temporal horizon across primate species, regardless of lifespan (a chronometric model). This temporal decoupling challenges the amyloid cascade hypothesis as a universal, cross-species biological mechanism in late-onset sporadic AD. The occurrence of full-blown ADNC may depend on the phylogenetic temporal coupling of these two biological processes.
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