Neurofilament light gene deletion exacerbates amyloid, dystrophic neurite, and synaptic pathology in the APP/PS1 transgenic model of Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with the loss of cognitive function. Neurofilament (NF) triplet proteins, the major structural (intermediate filament) proteins of neurons, are expressed in a subset of pyramidal cells that show a high degree of vulnerability to degeneration in AD. Alterations in the NF triplet proteins in amyloid-beta (Aβ) plaque-associated dystrophic neurites (DNs) represent the first cytoskeletal aberration to occur in the neocortex in the earliest stages of AD. We generated transgenic APP/PS1 (APPswe/PSEN1dE9) mice on the neurofilament light knockout (NFL KO) background to explore the role of NFL deletion in the context of DN formation, synaptic changes, and other neuropathologic features. Our analysis demonstrated that NFL deficiency significantly increased neocortical DN pathology, Aβ deposition, synapse vulnerability, and microgliosis in APP/PS1 mice. Thus, NFs may have a role in protecting neurites from dystrophy and in regulating cellular pathways related to the generation of Aβ plaques.
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NFL gene deletion increased amyloid plaque load and synaptic pathology in APP/PS1 TG mice.
“Surprisingly, NFL gene deletion increased amyloid plaque load and synaptic pathology in APP/PS1 TG mice (Fernandez-Martos et al., 2015).”
From Disrupted structural connectivity in ArcAβ mouse model of Aβ amyloidosis (2020) · cites this paper as Fernandez-Martos et al., 2015
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References 73 · Cited by 38
- Authors
- Fernandez-Martos, C. M., King, A. E., Atkinson, R. A. K., Woodhouse, A., & Vickers, J. C.
- Affiliations
- University of Tasmania (AU)
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 36
- Issue
- 10
- Pages
- 2757-2767
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W1842037003
- Cited by
- 38
- References
- 73
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 5 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 1 · 2019: 6 · 2018: 3 · 2017: 3 · 2016: 7
- FWCI
- 3.19
- Type
- journal article
- Language
- en
- Open access
- green
- figshare.com
- Licence
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- eCite Digital Repository (University of Tasmania) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- J.O. and J.R. Wicking Trust
- National Health and Medical Research Council
- Research Enhancement Grants Scheme of The University of Tasmania
- Topics
- Health Sciences › Medicine › Physiology › 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
- neurofilament light chain, neurofilament triplet proteins, Alzheimer's disease, APP/PS1 mice, amyloid plaques, dystrophic neurites, synaptic pathology, microglial activation, intermediate filaments, neocortex
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Hippocampus, Mice, Transgenic, Synapses, Amyloid beta-Peptides, Neurites, Neurofilament Proteins, Gene Deletion, Microglia, Disease Progression, Neocortex, Plaque, Amyloid
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