Neuritic (Senile) Plaques and Filamentous Changes in Aged Rhesus Monkeys
Abstract
Three rhesus monkeys, whose approximate ages were 16 to 18 years old, and one 22 to 23 years old, were studied for age changes in the nervous system. The brains of all four were slightly shrunken and the meninges were fibrotic. The vessels were stiff and fibrosed, but were not atheromatous. The lateral ventricles were mildly dilated. Bodian preparations of the oldest monkey and of one of the 16− to 18-year-old monkeys revealed the presence of neuritic (senile) plaques. Serial one-micron toluidine blue-stained sections showed that some plaques were closely associated with capillaries. Electron microscopic studies revealed that the plaques were identical to those of human Alzheimer's disease except that the typical twisted tubules were absent. Outside the plaques there were scattered neurites showing degeneration of the type found in the neuritic plaques. Furthermore, two forms of rare pathological fibrillar material were found in 3 animals. One was made up of pairs of helically wound 100 Å filaments with a twist every 500 Å. The other fibrillar structures were made up of bundles of parallel filamentous elements, each about 130 Å thick, with a distinctly granular structure on longitudinal section. A list of other abnormalities includes vascular amyloidosis, lipofuscin accumulation, dark neurons undergoing phagocytosis, myelin remodeling, aggregates of large electron-dense droplets, enlarged mitochondria and mitochondria with paracrystalline inclusions, corpora amylacea, Rosenthal fibers and two types of virus-like particles.
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The neuropathologic hallmarks of AD are neurofibrillary tangles (including pretangles) and AβPs (including diffuse and neuritic plaques).
“The neuropathologic hallmarks of AD are neurofibrillary tangles (NFTs; including pretangles) and AβPs (including diffuse and neuritic plaques, which may also be referred to as “senile plaques” [2, 18, 19]; Fig. 1 and Table 1).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [18]
NPs represent a nidus in which extracellular plaque substance(s) seem to induce intracellular degenerative changes with tau pathology.
“The particular toxic substance(s) within NPs still have not been completely characterized (90, 103, 278), but NPs represent a nidus in which extracellular plaque substance(s) seem to induce intracellular degenerative changes with tau pathology (18, 50, 279-281).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [18]
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“Wisniewski et al. (1973) found similar plaques in ageing rhesus monkeys, including PHF, though neurons showing tangles were not identified.”
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“…of aged nonhuman primates, rhesus monkeys (Abraham et al., 1989; Iwatsubo et al., 1994; Poduri et al., 1994; Struble et al., 1985; Uno et al., 1996; Wisniewski et al., 1973), chimpanzees (Fukumoto et al., 1996; Gearing et al., 1994), Japanese monkeys (Iwata, 1986), squirrel monkeys (Walker et al.,…”
BackgroundIn situ hybridization histochemistry and the study of gene expression in the human brain
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“The appearance and composition of the plaques we examined were consistent with those of the primitive type described in earlier ultrastructural studies of aged monkeys (Martin et al. 1994; Peters 1991; Struble et al. 1985; Wisniewski et al. 1973).”
BackgroundResultBrain aging in normotensive and hypertensive strains of rats
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Synthetic amyloid β-protein fails to produce specific neurotoxicity in monkey cerebral cortex
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Age‐related ubiquitin deposits in dystrophic neurites: an immunoelectron microscopic study
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MRI description of cerebral atrophy in mouse lemur primates
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Viral-based gene transfer to the mammalian CNS for functional genomic studies
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Neurofibrillary pathology: Current status and research perspectives
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Self-citationPathology of animal amyloidoses
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Reduction of inclusion body pathology in ApoE-deficient mice fed a combination of antioxidants
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- Authors
- Wiśniewski, H. M., Ghetti, B., & Terry, R. D.
- Affiliations
- Albert Einstein College of Medicine (US)
- ORCID
- Ghetti, Bernardino
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 1973-10
- Volume
- 32
- Issue
- 4
- Pages
- 566-584
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W2090601883
- Cited by
- 272
- References
- 0
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 6 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 1 · 2016: 2 · 2013: 2 · 2012: 4
- FWCI
- 8.85
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- neuritic plaques, amyloid plaques, Alzheimer's disease, rhesus monkeys, brain aging, fibrillar material, helical filaments, vascular amyloidosis, lipofuscin, myelin remodeling, corpora amylacea, Rosenthal fibers, virus-like particles, mitochondrial inclusions, meningeal fibrosis
- MeSH terms
- Aging, Amyloid, Animals, Haplorhini, Basal Ganglia, Brain, Brain Chemistry, Cerebral Cortex, Dementia, Disease Models, Animal, Female, Humans, Macaca, Male, Medulla Oblongata, Microscopy, Electron, Nerve Degeneration, Neurofibrils, Pons, Spinal Cord
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