Deletion of Specific Sphingolipids in Distinct Neurons Improves Spatial Memory in a Mouse Model of Alzheimer’s Disease
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Alzheimer’s disease (AD) is characterized by progressive neurodegeneration and a concomitant loss of synapses and cognitive abilities. Recently, we have proposed that an alteration of neuronal membrane lipid microdomains increases neuronal resistance towards amyloid-β stress in cultured neurons and protects from neurodegeneration in a mouse model of AD. Lipid microdomains are highly enriched in a specific subclass of glycosphingolipids, termed gangliosides. The enzyme glucosylceramide synthase (GCS) catalyzes the rate-limiting step in the biosynthesis of these gangliosides. The present work now demonstrates that genetic GCS deletion in subsets of adult forebrain neurons significantly improves the spatial memory and counteracts the loss of dendritic spines in the hippocampal dentate gyrus of 5x familial AD mice (5xFAD//Ugcgf/f//Thy1-CreERT2//EYFP mice), when compared to 5xFAD//Ugcgf/f littermates (5xFAD mice). Aberrantly activated glial cells and their expression of pro-inflammatory cytokines have emerged as the major culprits for synaptic loss in AD. Typically, astrocytic activation is accompanied by a thickening of astrocytic processes, which impairs astrocytic support for neuronal synapses. In contrast to 5xFAD mice, 5xFAD//Ugcgf/f//Thy1-CreERT2//EYFP display a less pronounced thickening of astrocytic processes and a lower expression of TNF-α and IL1-α in the hippocampus. Thus, this work further emphasizes that GCS inhibition may constitute a potential therapeutic target against AD.
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The CA1 hippocampal pyramidal cell layer has been reported to lack intraneuronal Aβ immunoreactivity while presenting elevated levels of intracellular human APP.
“In particular, the CA1 hippocampal pyramidal cell layer was investigated as it has been reported to lack intraneuronal Aβ immunoreactivity while presenting elevated levels of intracellular human APP [52, 57].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [52]
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Mlinac, K., Heffer, M., & Schnaar, R. L. (2026) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2026.111184 · Cited by 11 · see citing works
Rodent models with neuraminidase deficiencies
Can, M., Basırlı, H., & Seyrantepe, V. (2026) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2026.110778 · Cited by 1 · see citing works
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Dodge, J. C., Tamsett, T. J., Treleaven, C. M., Taksir, T. V., Piepenhagen, P. A., Sardi, S. P., Cheng, S. H., & Shihabuddin, L. S. (2022) · Figshare · doi:10.6084/m9.figshare.19106114
- Authors
- Herzer, S., Hagan, C., von Gerichten, J., Dieterle, V., Munteanu, B., Sandhoff, R., Hopf, C., & Nordström, V.
- Affiliations
- German Cancer Research Center (DE)
- Heidelberg University (DE)
- Corresponding author
- Nordström, Viola
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-06-20
- Volume
- 11
- Pages
- 206-206
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC6019486
- OpenAlex
- W2806775328
- Cited by
- 27
- References
- 68
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 5 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 5 · 2019: 2 · 2018: 1
- FWCI
- 1.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Alzheimer Forschung Initiative (Pilot Grant)
- Deutsche Forschungsgemeinschaft (NO 1107/1-1, HE 7978/1-1)
- Bundesministerium für Bildung und Forschung (grant No. 13FH8I03IA)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
- Keywords
- Alzheimer's disease, glucosylceramide synthase, gangliosides, sphingolipids, lipid microdomains, spatial memory, dendritic spines, dentate gyrus, 5xFAD mice, astrocyte activation, glial activation, inflammatory cytokines, TNF-α, IL-1α, amyloid-beta, neurodegeneration, synaptic loss, therapeutic target
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.
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