Cited by 290Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Detection of a Novel Intraneuronal Pool of Insoluble Amyloid β Protein that Accumulates with Time in Culture

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Skovronsky, Daniel M., Doms, Robert W., Lee, Virginia M.-Y.·1998·The Journal of Cell Biology

DOI 10.1083/jcb.141.4.1031PMC PMC2132781

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Abstract

The amyloid-β peptide (Aβ) is produced at several sites within cultured human NT2N neurons with Aβ1-42 specifically generated in the endoplasmic reticulum/intermediate compartment. Since Aβ is found as insoluble deposits in senile plaques of the AD brain, and the Aβ peptide can polymerize into insoluble fibrils in vitro, we examined the possibility that Aβ1-40, and particularly the more highly amyloidogenic Aβ1-42, accumulate in an insoluble pool within NT2N neurons. Remarkably, we found that formic acid extraction of the NT2N cells solubilized a pool of previously undetectable Aβ that accounted for over half of the total intracellular Aβ. Aβ1-42 was more abundant than Aβ1-40 in this pool, and most of the insoluble Aβ1-42 was generated in the endoplasmic reticulum/intermediate compartment pathway. High levels of insoluble Aβ were also detected in several nonneuronal cell lines engineered to overexpress the amyloid-β precursor protein. This insoluble intracellular pool of Aβ was exceptionally stable, and accumulated in NT2N neurons in a time-dependent manner, increasing 12-fold over a 7-wk period in culture. These novel findings suggest that Aβ amyloidogenesis may be initiated within living neurons rather than in the extracellular space. Thus, the data presented here require a reexamination of the prevailing view about the pathogenesis of Aβ deposition in the AD brain.

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Luo, Y., & Butko, P. (2005) · Oxidative stress and disease · doi:10.1201/9781420026559.ch23
Recombinant AAV Gene Therapy and Delivery
Carty, N. (2009) · Digital Commons - University of South Florida (University of South Florida)
N-truncated Aβ4-x peptides in Alzheimer's disease: generation, degradation, and relationship with neuropathological hallmarks
Zampar, S. (2021) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-9004
High reelin expression can explain why the entorhinal cortex is a cradle for Alzheimer’s diseasePreprint
Kobro‐Flatmoen, A., Hussan, J. R., Hunter, P. J., & Omholt, S. W. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.06.04.655278
High reelin expression may explain why a subgroup of entorhinal cortex neurons functions as an initial nucleation site of Alzheimer’s disease
Kobro‐Flatmoen, A., Hussan, J. R., Hunter, P. J., & Omholt, S. W. (2026) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1014532
To Study the Effect of Nilotinib, a Tyrosine Kinase Inhibitor, on Learning and Memory and Its Comparison with Nitric Oxide Synthase Inhibitor in an Animal Model of Alzheimer’s Disease
Kumar, A., Fatima, N., Kumar, P., Nath, R., Sachan, A. K., Dixit, R., & Pal, R. (2026) · Annals of Neurosciences · doi:10.1177/09727531261470562
Amyloid precursor protein (APP) and copper homeostasis in the human neuroblastoma cell line SH-SY5Y
Klein, J. (2011)

Authors: Skovronsky, D. M., Doms, R. W., & Lee, V. M.-Y.
Affiliations: University of Pennsylvania (US)
ORCID: Lee, Virginia M.-Y.
Venue: The Journal of Cell Biology
Publisher: Rockefeller University Press
Published: 1998-05-18
Volume: 141
Issue: 4
Pages: 1031-1039
ISSN: 0021-9525 (ISSN-L)
1540-8140
DOI: 10.1083/jcb.141.4.1031
PMC: PMC2132781
OpenAlex: W2130792655
Cited by: 290
References: 36
Citations by year: 2026: 2 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 6 · 2021: 3 · 2019: 8 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 6 · 2014: 3 · 2013: 8 · 2012: 8
FWCI: 15.16
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: cc-by-nc-sa
Locations: The Journal of Cell Biology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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-beta 42, Aβ40, endoplasmic reticulum, amyloidogenesis, Alzheimer's disease, amyloid plaques, amyloid precursor protein overexpression, formic acid extraction
MeSH terms: Alzheimer Disease, Animals, Brain, Cell Line, Endoplasmic Reticulum, Genetic Vectors, Cricetinae, Humans, Neurons, Peptide Fragments, Recombinant Proteins, Semliki forest virus, Solubility, Subcellular Fractions, Transfection, Tumor Cells, Cultured, Amyloid beta-Peptides, CHO Cells, Carcinoma, Embryonal

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Detection of a Novel Intraneuronal Pool of Insoluble Amyloid β Protein that Accumulates with Time in Culture

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