In vivo characterization of a bigenic fluorescent mouse model of Alzheimer’s disease with neurodegeneration
Open accessAbstract
The loss of cognitive function in Alzheimer's disease (AD) patients is strongly correlated with the loss of neurons in various regions of the brain. We have created a new fluorescent bigenic mouse model of AD by crossing "H-line" yellow fluorescent protein (YFP) mice with the 5xFAD mouse model, which we call the 5XY mouse model. The 5xFAD mouse has been shown to have significant loss of L5 pyramidal neurons by 12 months of age. These neurons are transgenically labeled with YFP in the 5XY mouse, which enable longitudinal imaging of structural changes. In the 5XY mice, we observed an appearance of axonal dystrophies, with two distinct morphologies in the early stages of the disease progression. Simple swelling dystrophies are transient in nature and are not directly associated with amyloid plaques. Rosette dystrophies are more complex structures that remained stable throughout all imaging sessions, and always surrounded an amyloid plaque. Plaque growth was followed over 4 weeks, and significant growth was seen between weekly imaging sessions. In addition to axonal dystrophy appearance and plaque growth, we were able to follow spine stability in 4-month old 5XY mice, which revealed no significant loss of spines. 5XY mice also showed a striking shrinkage of the neocortex at older ages (12-14 months). The 5XY mouse model may be a valuable tool for studying specific events in the degeneration of the neocortex, and may suggest new avenues for therapeutic intervention.
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In 5XFAD pathology, spine loss (4-9 months) occurs subsequent to cognitive dysfunction (3-6 months) and Aβ plaque formation (two months).
“An interesting observation in the progression of 5XFAD pathology is that spine loss (4–9 months) [62] occurs subsequent to cognitive dysfunction (3–6 months) [35,63,64,65,66] and Aβ plaque formation (two months) [67].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [62]
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Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice
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“While previous studies have shown minimal hippocampal synaptic damage in 5XFAD mice [62], the positive impact of CAW on synaptic formation in the hippocampus (or other brain regions) may not require this pathological deficit to be present, to improve neuronal function and provide cognitive benefits.”
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- Authors
- Crowe, S. E., & Ellis‐Davies, G. C. R.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Ellis‐Davies, Graham C.R.
- Venue
- Journal of Comparative Neurology
- Publisher
- Wiley
- Published
- 2013-04-19
- Volume
- 521
- Issue
- 10
- Pages
- 2181-2194
- ISSN
- 0021-9967 (ISSN-L)
- 1096-9861
- PMC
- PMC4134262
- OpenAlex
- W4232747719
- Cited by
- 15
- References
- 66
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 3 · 2017: 1 · 2014: 2 · 2013: 3
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Comparative Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM053395)
- National Institute of Neurological Disorders and Stroke (R01NS069720)
- 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 › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, YFP, axonal dystrophy, amyloid plaques, longitudinal in vivo imaging, neurodegeneration
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Axons, Bacterial Proteins, Disease Models, Animal, Humans, Luminescent Proteins, Mice, Transgenic, Nerve Degeneration, Amyloid beta-Protein Precursor, Pyramidal Cells, Dendritic Spines, Mice, Presenilin-1, Plaque, Amyloid
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