High-fat diet-induced activation of SGK1 promotes Alzheimer's disease-associated tau pathology.


Journal

Human molecular genetics
ISSN: 1460-2083
Titre abrégé: Hum Mol Genet
Pays: England
ID NLM: 9208958

Informations de publication

Date de publication:
28 08 2021
Historique:
received: 27 01 2021
revised: 31 03 2021
accepted: 18 04 2021
pubmed: 24 4 2021
medline: 31 3 2022
entrez: 23 4 2021
Statut: ppublish

Résumé

Type 2 diabetes mellitus (T2DM) has long been considered a risk factor for Alzheimer's disease (AD). However, the molecular links between T2DM and AD remain obscure. Here, we reported that serum-/glucocorticoid-regulated kinase 1 (SGK1) is activated by administering a chronic high-fat diet (HFD), which increases the risk of T2DM, and thus promotes Tau pathology via the phosphorylation of tau at Ser214 and the activation of a key tau kinase, namely, GSK-3ß, forming SGK1-GSK-3ß-tau complex. SGK1 was activated under conditions of elevated glucocorticoid and hyperglycemia associated with HFD, but not of fatty acid-mediated insulin resistance. Elevated expression of SGK1 in the mouse hippocampus led to neurodegeneration and impairments in learning and memory. Upregulation and activation of SGK1, SGK1-GSK-3ß-tau complex were also observed in the hippocampi of AD cases. Our results suggest that SGK1 is a key modifier of tau pathology in AD, linking AD to corticosteroid effects and T2DM.

Identifiants

pubmed: 33890983
pii: 6246109
doi: 10.1093/hmg/ddab115
pmc: PMC8411983
doi:

Substances chimiques

Immediate-Early Proteins 0
Mapt protein, mouse 0
Multiprotein Complexes 0
tau Proteins 0
Glycogen Synthase Kinase 3 beta EC 2.7.11.1
Gsk3b protein, mouse EC 2.7.11.1
Protein Serine-Threonine Kinases EC 2.7.11.1
serum-glucocorticoid regulated kinase EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1693-1710

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Auteurs

Montasir Elahi (M)

Department of Diagnosis, Prevention and Treatment of Dementia, Juntendo University Graduate of Medicine, Tokyo, Japan.
Department of Neurology, Juntendo University Graduate of Medicine, Tokyo, Japan.
Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo, Japan.

Yumiko Motoi (Y)

Department of Diagnosis, Prevention and Treatment of Dementia, Juntendo University Graduate of Medicine, Tokyo, Japan.
Department of Neurology, Juntendo University Graduate of Medicine, Tokyo, Japan.

Shotaro Shimonaka (S)

Department of Diagnosis, Prevention and Treatment of Dementia, Juntendo University Graduate of Medicine, Tokyo, Japan.

Yoko Ishida (Y)

Department of Cell Biology and Neuroscience, Juntendo University Graduate of Medicine, Tokyo, Japan.

Hiroyuki Hioki (H)

Department of Cell Biology and Neuroscience, Juntendo University Graduate of Medicine, Tokyo, Japan.

Masashi Takanashi (M)

Department of Neurology, Juntendo University Graduate of Medicine, Tokyo, Japan.

Koichi Ishiguro (K)

Department of Neurology, Juntendo University Graduate of Medicine, Tokyo, Japan.

Yuzuru Imai (Y)

Department of Neurology, Juntendo University Graduate of Medicine, Tokyo, Japan.
Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo, Japan.

Nobutaka Hattori (N)

Department of Diagnosis, Prevention and Treatment of Dementia, Juntendo University Graduate of Medicine, Tokyo, Japan.
Department of Neurology, Juntendo University Graduate of Medicine, Tokyo, Japan.
Department of Research for Parkinson's Disease, Juntendo University Graduate School of Medicine, Tokyo, Japan.

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Classifications MeSH