Cited by 184Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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The p75 Neurotrophin Receptor Promotes Amyloid-β(1-42)-Induced Neuritic Dystrophy In Vitro and In Vivo

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Knowles, Juliet K., Rajadas, Jayakumar, Nguyen, Thuy-Vi V., Yang, Tao, LeMieux, Melburne C., Vander Griend, Lilith, Ishikawa, Chihiro, Massa, Stephen M., Wyss-Coray, Tony, Longo, Frank M.·2009·The Journal of Neuroscience

DOI 10.1523/jneurosci.0620-09.2009PMC PMC2771439

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Abstract

Oligomeric forms of amyloid-beta (Abeta) are thought to play a causal role in Alzheimer's disease (AD), and the p75 neurotrophin receptor (p75(NTR)) has been implicated in Abeta-induced neurodegeneration. To further define the functions of p75(NTR) in AD, we examined the interaction of oligomeric Abeta(1-42) with p75(NTR), and the effects of that interaction on neurite integrity in neuron cultures and in a chronic AD mouse model. Atomic force microscopy was used to ascertain the aggregated state of Abeta, and fluorescence resonance energy transfer analysis revealed that Abeta oligomers interact with the extracellular domain of p75(NTR). In vitro studies of Abeta-induced death in neuron cultures isolated from wild-type and p75(NTR-/-) mice, in which the p75(NTR) extracellular domain is deleted, showed reduced sensitivity of mutant cells to Abeta-induced cell death. Interestingly, Abeta-induced neuritic dystrophy and activation of c-Jun, a known mediator of Abeta-induced deleterious signaling, were completely prevented in p75(NTR-/-) neuron cultures. Thy1-hAPP(Lond/Swe) x p75(NTR-/-) mice exhibited significantly diminished hippocampal neuritic dystrophy and complete reversal of basal forebrain cholinergic neurite degeneration relative to those expressing wild-type p75(NTR). Abeta levels were not affected, suggesting that removal of p75(NTR) extracellular domain reduced the ability of excess Abeta to promote neuritic degeneration. These findings indicate that although p75(NTR) likely does not mediate all Abeta effects, it does play a significant role in enabling Abeta-induced neurodegeneration in vitro and in vivo, establishing p75(NTR) as an important therapeutic target for AD.

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Authors: Knowles, J. K., Rajadas, J., Nguyen, T.-V. V., Yang, T., LeMieux, M. C., Vander Griend, L., Ishikawa, C., Massa, S. M., Wyss-Coray, T., & Longo, F. M.
Affiliations: Stanford University (US)
University of North Carolina at Chapel Hill (US)
VA Palo Alto Health Care System (US)
San Francisco VA Medical Center (US)
Corresponding author: Longo, Frank M.
ORCID: Knowles, Juliet K.
Rajadas, Jayakumar
Nguyen, Thuy-Vi V.
Yang, Tao
Massa, Stephen M.
Longo, Frank M.
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2009-08-26
Volume: 29
Issue: 34
Pages: 10627-10637
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.0620-09.2009
PMC: PMC2771439
OpenAlex: W2090434536
Cited by: 184
References: 70
Citations by year: 2026: 10 · 2025: 6 · 2024: 6 · 2023: 4 · 2022: 9 · 2021: 14 · 2020: 11 · 2019: 11 · 2018: 4 · 2017: 10 · 2016: 17 · 2015: 14 · 2014: 17 · 2013: 15 · 2012: 12
FWCI: 7.73
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 184 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Alzheimer's Association
U.S. Public Health Service (F30 NA051971)
National Institute of Neurological Disorders and Stroke (F30NS051971)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: p75 neurotrophin receptor, amyloid-beta 42, Alzheimer's disease, neuritic dystrophy, amyloid-beta oligomers, c-Jun activation, cholinergic neurons, hippocampus, APP transgenic mice, therapeutic target
MeSH terms: Acetylcholinesterase, Alzheimer Disease, Analysis of Variance, Animals, Cell Survival, Cells, Cultured, Disease Models, Animal, Embryo, Mammalian, Enzyme-Linked Immunosorbent Assay, Exons, Hippocampus, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nerve Degeneration, Neurons, Peptide Fragments, Spectrophotometry, Atomic, Amyloid beta-Peptides, Neurites, Prosencephalon, Amyloid beta-Protein Precursor, Receptor, Nerve Growth Factor, Fluorescence Resonance Energy Transfer, Mice

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The p75 Neurotrophin Receptor Promotes Amyloid-β(1-42)-Induced Neuritic Dystrophy In Vitro and In Vivo

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