Aging renders the brain vulnerable to amyloid β-protein neurotoxicity

Guela, Changiz; Wu, Chuang-Kuo; Saroff, Daniel; Lorenzo, Alfredo; Yuan, Menglan; Yankner, Bruce A.

doi:10.1038/nm0798-827

Cited by 520Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Aging renders the brain vulnerable to amyloid β-protein neurotoxicity

Guela, Changiz, Wu, Chuang-Kuo, Saroff, Daniel, Lorenzo, Alfredo, Yuan, Menglan, Yankner, Bruce A.·1998·Nature Medicine

DOI 10.1038/nm0798-827

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Abstract

The formation of fibrillar deposits of amyloid beta protein (Abeta) in the brain is a pathological hallmark of Alzheimer's disease (AD). A central question is whether Abeta plays a direct role in the neurodegenerative process in AD. The involvement of Abeta in the neurodegenerative process is suggested by the neurotoxicity of the fibrillar form of Abeta in vitro. However, mice transgenic for the Abeta precursor protein that develop amyloid deposits in the brain do not show the degree of neuronal loss or tau phosphorylation found in AD. Here we show that microinjection of plaque-equivalent concentrations of fibrillar, but not soluble, Abeta in the aged rhesus monkey cerebral cortex results in profound neuronal loss, tau phosphorylation and microglial proliferation. Fibrillar Abeta at plaque-equivalent concentrations is not toxic in the young adult rhesus brain. Abeta toxicity in vivo is also highly species-specific; toxicity is greater in aged rhesus monkeys than in aged marmoset monkeys, and is not significant in aged rats. These results suggest that Abeta neurotoxicity in vivo is a pathological response of the aging brain, which is most pronounced in higher order primates. Thus, longevity may contribute to the unique susceptibility of humans to Alzheimer's disease by rendering the brain vulnerable to Abeta neurotoxicity.

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Aβ-42 is linked to genetic mutations in amyloid precursor protein (APP), leading to excessive amyloid production.
“Aβ-42, a key part of SPs, is linked to genetic mutations in amyloid precursor protein (APP), leading to excessive amyloid production.”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [5]
The neurotoxicity of aggregated Aβ-42 and its role in tau phosphorylation prompts investigation into disease-modifying therapies.
“The neurotoxicity of aggregated Aβ-42 and its role in tau phosphorylation prompts investigation into disease-modifying therapies.5”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [5]

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Authors: Guela, C., Wu, C.-K., Saroff, D., Lorenzo, A., Yuan, M., & Yankner, B. A.
Affiliations: Beth Israel Deaconess Medical Center (US)
Boston Children's Hospital (US)
ORCID: Lorenzo, Alfredo
Yankner, Bruce A.
Venue: Nature Medicine
Publisher: Springer Science and Business Media LLC
Published: 1998-07
Volume: 4
Issue: 7
Pages: 827-831
ISSN: 1078-8956 (ISSN-L)
1546-170X
DOI: 10.1038/nm0798-827
OpenAlex: W2606648674
Cited by: 520
References: 0
Citations by year: 2026: 6 · 2025: 7 · 2024: 9 · 2023: 9 · 2022: 12 · 2021: 12 · 2020: 5 · 2019: 11 · 2018: 11 · 2017: 10 · 2016: 14 · 2015: 9 · 2014: 12 · 2013: 10 · 2012: 15
FWCI: 22.94
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Medicine (publishedVersion)
Funders: National Institute on Aging (AG 10282)
National Institute of Neurological Disorders and Stroke (NS30352)
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: amyloid-beta, amyloid fibrils, neurotoxicity, Alzheimer's disease, brain aging, rhesus monkeys, marmoset monkey, species differences, tau phosphorylation, neuronal loss, microglial proliferation, cerebral cortex, longevity, neurodegeneration

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Aging renders the brain vulnerable to amyloid β-protein neurotoxicity

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