Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease

Namba, Yoshio; Tomonaga, Masanori; Kawasaki, Hiroshi; Otomo, Eiichi; Ikeda, Kazuhiko

doi:10.1016/0006-8993(91)91092-f

Cited by 1,157Alzheimer's disease research and treatmentsPrion Diseases and Protein MisfoldingNeuroinflammation and Neurodegeneration Mechanisms

Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease

Namba, Yoshio, Tomonaga, Masanori, Kawasaki, Hiroshi, Otomo, Eiichi, Ikeda, Kazuhiko·1991·Brain Research

DOI 10.1016/0006-8993(91)91092-f

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Abstract

During the course of our immunohistochemical studies on the change of lipids in Alzheimer's disease brains by using antibody to apolipoprotein E, a protein having a special relevance to nervous tissue, we unexpectedly found that apo E immunoreactivity was associated with amyloid in both senile plaques and cerebral vessels and neurofibrillary tangles. The immunoreactivity was also found in amyloid of kuru plaques in Creutzfeldt-Jakob disease. Pretreatment of the sections with formic acid greatly enhanced immunoreactivity of senile and kuru plaques to antibody to apo E.

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Along with other amyloid-associated proteins, apoE is found in amyloid plaques.
“Along with other amyloid-associated proteins, apoE is found in amyloid plaques (Namba et al., 1991; Wisniewski and Frangione, 1992).”
From Anti-apoE immunotherapy inhibits amyloid accumulation in a transgenic mouse model of Aβ amyloidosis (2012) · cites this paper as Namba et al., 1991
The reduced amyloid deposition in Ldlr-overexpressing mice may stem from the interaction between APOE and Aβ and their subsequent uptake via these receptors.
“Because APOE co‐localizes with Aβ, 17 the reduced amyloid deposition in Ldlr‐overexpressing mice may stem from the interaction between APOE and Aβ and their subsequent uptake via these receptors.”
From Deletion of neuronal Idol ameliorates Alzheimer's disease–related pathologies via APOE receptors (2025) · cites this paper as [17]
ApoE colocalizes with Aβ plaques.
“and it also colocalizes with A␤ plaques (Namba et al., 1991).”
From Anti-ApoE Antibody Given after Plaque Onset Decreases Aβ Accumulation and Improves Brain Function in a Mouse Model of Aβ Amyloidosis (2014) · cites this paper as Namba et al., 1991
ApoE colocalizes with amyloid plaques.
“Interestingly, apoE colocalizes with amyloid plaques (Namba et al., 1991).”
From Apolipoprotein E in Synaptic Plasticity and Alzheimer’s Disease: Potential Cellular and Molecular Mechanisms (2014) · cites this paper as Namba et al., 1991
The degree of co-localization between apoE and Aβ deposition appeared to decrease in brains carrying the APOE3-Jac variant compared to those from APOE3.
“As apoE co-deposits with Aβ in the amyloid plaques (13–15), we examined and found that the degree of co-localization between apoE and Aβ deposition appeared to decrease in the brains carrying APOE3-Jac variant compared to those from APOE3 (Fig. S1C–F).”
From APOE3 -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [15]

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Authors: Namba, Y., Tomonaga, M., Kawasaki, H., Otomo, E., & Ikeda, K.
Affiliations: Tokyo Institute of Psychiatry (JP)
The University of Tokyo (JP)
Yokufukai Hospital (JP)
Corresponding author: Namba, Yoshio
ORCID: Kawasaki, Hiroshi
Ikeda, Kazuhiko
Venue: Brain Research
Publisher: Elsevier BV
Published: 1991-02
Volume: 541
Issue: 1
Pages: 163-166
ISSN: 0006-8993 (ISSN-L)
DOI: 10.1016/0006-8993(91)91092-f
OpenAlex: W2072682191
Cited by: 1,157
References: 24
Citations by year: 2026: 11 · 2025: 19 · 2024: 13 · 2023: 19 · 2022: 30 · 2021: 34 · 2020: 28 · 2019: 33 · 2018: 19 · 2017: 26 · 2016: 19 · 2015: 17 · 2014: 23 · 2013: 20 · 2012: 21
FWCI: 23.38
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Brain Research (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: apolipoprotein E, Alzheimer's disease, Creutzfeldt-Jakob disease, kuru plaques, amyloid plaques, neurofibrillary tangles, formic acid pretreatment, immunoreactivity
MeSH terms: Alzheimer Disease, Amyloid, Apolipoproteins E, Brain, Humans, Immunohistochemistry, Creutzfeldt-Jakob Syndrome, Kuru, Neurofibrils

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Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease

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