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Human tau mutations in cerebral organoids induce a progressive dyshomeostasis of cholesterol

Glasauer, Stella M.K., Goderie, Susan K., Rauch, Jennifer N., Guzman, Elmer, Audouard, Morgane, Bertucci, Taylor, Joy, Shona, Rommelfanger, Emma, Luna, Gabriel, Keane-Rivera, Erica, Lotz, Steven, Borden, Susan, Armando, Aaron M., Quehenberger, Oswald, Temple, Sally, Kosik, Kenneth S.·2022·Stem Cell Reports
DOI 10.1016/j.stemcr.2022.07.011PMC PMC9481908
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  • Increased cholesterol levels are present in tandem with neuronal dysfunction and tau aggregation in several experimental models.

    “Using several experimental models, it has been shown that increased cholesterol levels are present in tandem with neuronal dysfunction and tau aggregation4,5,18–25.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [4]

  • Time points for scRNA-seq were selected based on previous literature suggesting these are time points at which changes in organoid maturation can be observed.

    “Time points were selected based on previous literature that utilizes neural organoids for immunostaining and transcriptomic analysis4,5,47, suggesting these are time points at which changes in organoid maturation can be observed.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [4]

  • HNOs generated from hiPSCs of patients with MAPT mutations provide a complex in vitro model that exhibits transcriptional changes relevant to neurodegeneration.

    “Human neural organoids (HNOs) generated from human induced pluripotent stem cells (hiPSCs) of patients with MAPT mutations provide a complex in vitro model which also exhibits transcriptional changes that are relevant to neurodegeneration4,5.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [4]

  • Our findings of altered lipid profiles and increased tau phosphorylation in HNOs with MAPT mutations coincide with findings from previously published literature using HNO models to study MAPT gene mutations.

    “Importantly, our findings of altered lipid profiles and increased tau phosphorylation in HNOs with MAPT mutations coincide with findings from previously published literature using HNO models to study MAPT gene mutations4,5.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [4]

  • No further investigation into the functional activity of HNOs, autophagy function, lipid droplet accumulation, or mechanism of tau phosphorylation was performed in that study.

    “However, no further investigation into the functional activity of HNOs, autophagy function, lipid droplet accumulation, or mechanism of tau phosphorylation was performed.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [4]

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Research works printed but not linked: 51

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Metadata

Authors
Glasauer, S. M. K., Goderie, S. K., Rauch, J. N., Guzman, E., Audouard, M., Bertucci, T., Joy, S., Rommelfanger, E., Luna, G., Keane-Rivera, E., Lotz, S., Borden, S., Armando, A. M., Quehenberger, O., Temple, S., & Kosik, K. S.
Venue
Stem Cell Reports
Publisher
Elsevier BV
Published
2022-09
Volume
17
Issue
9
Pages
2127-2140
ISSN
2213-6711
DOI
10.1016/j.stemcr.2022.07.011
PMC
PMC9481908
Cited by
46
References
20
Language
en
Licence
Funders
  • National Institutes of Health (1S10OD010786-01)
  • Swiss National Science Foundation (P2ZHP3_174753, P400PB_186800)
  • Larry L. Hillblom Foundation (R35 NS097277)
  • National Institute of Neurological Disorders and Stroke (R35 NS097277)
  • CurePSP (P30 AG066444, P01 AG03991, P01 AG026276)
  • Office of the President, University of California
  • University of California, Santa Barbara
  • Rainwater Charitable Foundation (U54 NS100717-01, AG064116)
  • National Institute on Aging (AG056293)

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