Parvalbumin-Positive Neuron Loss and Amyloid-β Deposits in the Frontal Cortex of Alzheimer’s Disease-Related Mice
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Alzheimer's disease (AD) has several hallmark features including amyloid-β (Aβ) plaque deposits and neuronal loss. Here, we characterized Aβ plaque aggregation and parvalbumin-positive (PV) GABAergic neurons in 6-9-month-old 5xFAD mice harboring mutations associated with familial AD. We used immunofluorescence staining to compare three regions in the frontal cortex-prelimbic (PrL), cingulate (Cg, including Cg1 and Cg2), and secondary motor (M2) cortices-along with primary somatosensory (S1) cortex. We quantified the density of Aβ plaques, which showed significant laminar and regional vulnerability. There were more plaques of larger sizes in deep layers compared to superficial layers. Total plaque burden was higher in frontal regions compared to S1. We also found layer- and region-specific differences across genotype in the density of PV interneurons. PV neuron density was lower in 5xFAD mice than wild-type, particularly in deep layers of frontal regions, with Cg (-50%) and M2 (-39%) exhibiting the largest reduction. Using in vivo two-photon imaging, we longitudinally visualized the loss of frontal cortical PV neurons across four weeks in the AD mouse model. Overall, these results provide information about Aβ deposits and PV neuron density in a widely used mouse model for AD, implicating deep layers of frontal cortical regions as being especially vulnerable.
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In 5xFAD mice, significantly reduced PV-positive neuron numbers were shown in cingulate and motor cortices, cortical layer IV, and hippocampal CA1-3 and dentate gyrus subfields.
“In 5xFAD mice, significantly reduced PV-positive neuron numbers were shown in cingulate and motor cortices [127], as well as cells in the cortical layer IV [128] or the hippocampal CA1–3 and dentate gyrus subfields [126].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [127]
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Mølgaard, S., Ulrichsen, M., Boggild, S., Holm, M., Vægter, C. B., Nyengaard, J. R., & Glerup, S. (2014) · F1000Research · doi:10.12688/f1000research.5349.2 · Cited by 16 · see citing works
Crowe, S. E., & Ellis‐Davies, G. C. R. (2013) · Journal of Comparative Neurology · doi:10.1002/cne.23306 · Cited by 15 · see citing works
Crowe, S. E., & Ellis‐Davies, G. C. R. (2013) · The Journal of Comparative Neurology · doi:10.1002/cne.23336 · Cited by 14 · see citing works
Immunofluorescent visualization of mouse interneuron subtypes
Mølgaard, S., Ulrichsen, M., Boggild, S., Holm, M., Vægter, C. B., Nyengaard, J. R., & Glerup, S. (2015) · F1000Research · doi:10.12688/f1000research.5349.3 · Cited by 11 · see citing works
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Microglia facilitate loss of perineuronal nets in the Alzheimer's disease brain
Crapser, J. D., Spangenberg, E. E., Barahona, R. A., Arreola, M. A., Hohsfield, L. A., & Green, K. N. (2020) · EBioMedicine · doi:10.1016/j.ebiom.2020.102919 · Cited by 280 · see citing works
Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models
Wirths, O., & Zampar, S. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21218144 · Cited by 75 · see citing works
Giesers, N. K., & Wirths, O. (2020) · ASN Neuro · doi:10.1177/1759091420925356 · Cited by 47 · see citing works
- Authors
- Ali, F., Baringer, S. L., Neal, A., Choi, E. Y., & Kwan, A. C.
- Affiliations
- Yale University (US)
- University of New Haven (US)
- Corresponding author
- Ali, Farhan
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2019-12-12
- Volume
- 72
- Issue
- 4
- Pages
- 1323-1339
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC7123545
- OpenAlex
- W2986996850
- Cited by
- 43
- References
- 93
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 5 · 2023: 11 · 2022: 5 · 2021: 6 · 2020: 5
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P50AG047270)
- National Institute of Mental Health (R01MH112750)
- 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
- Alzheimer's disease, amyloid plaques
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Frontal Lobe, Male, Mice, Transgenic, Neurons, Parvalbumins, Amyloid beta-Peptides, Mice, Plaque, Amyloid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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