Genetic and pharmacological evidence of intraneuronal Aβ accumulation in APP transgenic mice
Abstract
Intraneuronal punctate immunostaining in Alzheimer's disease brain and amyloid‐β precursor protein (APP) transgenic mice has been suggested to represent Aβ, but this is somewhat controversial. Here we show that both biochemical Aβ levels and intraneuronal immunostaining are reduced in APP transgenic mice when γ‐secretase is inhibited. Moreover, BACE‐1 deficient APP transgenic mice show neither Aβ production nor intraneuronal immunostaining. Our findings suggest that the punctate immunostaining with APP antibodies is due to Aβ that has accumulated inside neurons. Similar type of intraneuronal Aβ accumulation, which precedes senile plaque formation, may link Aβ to tauopathy and neurodegeneration in Alzheimer's disease pathogenesis.
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Intraneuronal Aβ disappears in AD transgenic mice when Aβ levels are reduced either by treatment with γ-secretase inhibitor or by crossing the mice with BACE knockout mice.
“Confirmation for the presence of intraneuronal Aβ was provided by a study that showed the disappearance of intraneuronal Aβ in AD transgenic mice when Aβ levels were reduced either by treatment with γ-secretase inhibitor or by crossing the mice with BACE knockout mice [145].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [145]
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References 19 · Cited by 21
- Authors
- Philipson, O., Lannfelt, L., & Nilsson, L. N. G.
- Affiliations
- Uppsala University (SE)
- Corresponding author
- Nilsson, Lars N.G.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2009-08-14
- Volume
- 583
- Issue
- 18
- Pages
- 3021-3026
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W1980275843
- Cited by
- 21
- References
- 19
- Citations by year
- 2025: 1 · 2019: 2 · 2017: 1 · 2016: 2 · 2014: 1 · 2013: 3 · 2012: 4
- FWCI
- 2.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- FEBS Letters (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 precursor protein, APP transgenic mice, gamma-secretase inhibition, amyloid-beta production, amyloid plaques, tauopathy, neurodegeneration, Alzheimer's disease pathogenesis
- MeSH terms
- Alzheimer Disease, Animals, Immunohistochemistry, Mice, Transgenic, Neurons, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, Mice, Amyloid Precursor Protein Secretases
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