Cited by 1,774Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43)

Iwatsubo, Takeshi, Odaka, Asano, Suzuki, Nobuhiro, Mizusawa, Hidehiro, Nukina, Nobuyuki, Ihara, Yasuo·1994·Neuron

Abstract

To learn about the carboxy-terminal extent of amyloid beta-protein (A beta) composition of senile plaques (SPs) in the brain affected with Alzheimer's disease (AD), we employed two end-specific monoclonal antibodies as immunocytochemical probes: one is specific for A beta 40, the carboxyl terminus of A beta 1-40, while the other is specific for A beta 42(43). In the AD cortex, all SPs that were labeled with an authentic antibody were A beta 42(43) positive, while only one-third of which, on the average, were A beta 40 positive. There was a strong correlation between A beta 40 positivity and mature plaques. Two familial AD cortices with the mutation of beta-amyloid protein precursor 717 (beta APP717) (Val to Ile) showed a remarkable predominance of A beta 42(43)-positive, A beta 40-negative plaques. Diffuse plaques, representing the earliest stage of A beta deposition, were exclusively positive for A beta 42(43), but completely negative for A beta 40.

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Crossref · 10.1016/0896-6273(94)90458-8

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41 of 41 references verified0 citation errors · 0 not checkable

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  • Aβs ending at Aβ42(43) are critically important in AD where they deposit selectively in plaques of all kinds.

    “These observations indicate that Aps ending at Ap42(43), which are a minor component of the Ap in human cerebrospinal fluid and plasma, are critically important in AD where they deposit selectively in plaques of all kinds.”

    From Amyloid β Protein (Aβ) in Alzheimeri's Disease Brain (1995) · cites this paper as [21]

  • The immunocytochemical results demonstrate that BC-05 intensely stains all types of senile plaques, that vessels are stained by both BC-05 and BA-27, and that BA-27 stains plaques poorly.

    “The immunocytochemical results shown here and in a recent report by Iwatsubo et al. (21) demonstrate that BC-05 intensely stains all types of senile plaques, that vessels are stained by both BC-OS and BA-27, and that BA-27 stains plaques poorly, in many cases only faintly staining occasional cored plaques (Fig. 3).”

    From Amyloid β Protein (Aβ) in Alzheimeri's Disease Brain (1995) · cites this paper as [21]

  • From studies of trisomy 21 brains, it is generally believed that, in human AD, Aβ deposition begins with the formation of diffuse plaques.

    “From studies of trisomy 21 brains (Iwatsubo et al., 1994), it is generally believed that, in human AD, A␤ deposition begins with the formation of diffuse plaques.”
  • Aβ1-42 is deposited early and selectively in senile plaques.

    “there is good evidence that A␤1-42 is deposited early and selectively in senile plaques (Iwatsubo et al., 1994).”
  • Aβ42 is the main component of amyloid plaques and is neurotoxic.

    “Indeed, Aβ42 is the main component of amyloid plaques and is shown to be neurotoxic [30].”

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Authors
Iwatsubo, T., Odaka, A., Suzuki, N., Mizusawa, H., Nukina, N., & Ihara, Y.
Affiliations
  • Takeda (Japan) (JP)
  • The University of Tokyo (JP)
  • University of Tsukuba (JP)
Venue
Neuron
Publisher
Elsevier BV
Published
1994-07
Volume
13
Issue
1
Pages
45-53
ISSN
0896-6273 (ISSN-L)
OpenAlex
W1991435932
Cited by
1,774
References
41
Citations by year
2026: 30 · 2025: 41 · 2024: 53 · 2023: 49 · 2022: 49 · 2021: 55 · 2020: 68 · 2019: 49 · 2018: 41 · 2017: 49 · 2016: 52 · 2015: 45 · 2014: 68 · 2013: 69 · 2012: 66
FWCI
35.75
Type
journal article
Language
en
Open access
closed
Locations
  • Neuron (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
amyloid-beta, Aβ40, amyloid plaques, Alzheimer's disease, familial Alzheimer's disease, plaque maturation, diffuse plaques, immunocytochemistry
MeSH terms
Adult, Aged, Aged, 80 and over, Alzheimer Disease, Antibodies, Monoclonal, Brain, Cerebral Cortex, Female, Humans, Immunoenzyme Techniques, Male, Middle Aged, Mutation, Peptide Fragments, Amyloid beta-Peptides

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