ArticleMolecular psychiatry2026
Elevated SGK1 increases Tau phosphorylation and microtubule instability in Alzheimer's patient-derived cortical neurons.
Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Oligodendrocyte-Targeted SGK1.1 Inhibition Alleviates White Matter Injury and Cognitive Impairment in Alzheimer's Disease via Modulation of HDAC2 Phosphorylation.CNS neuroscience & therapeutics · 2026Article
- Cognitive and synaptic impairment induced by deficiency of autism risk gene Smarcc2 and its rescue by histone deacetylase inhibition.Molecular psychiatry · 2026Article
- Tuberostemonine ameliorates Alzheimer's disease pathology by suppression of the p38 MAPK signaling pathway.iScience · 2026Article
- Retinal proteome changes mirror brain pathology and reveal synaptic and cytoskeletal dysfunction in Alzheimer's disease.Acta neuropathologica · 2026Article
- SGK1-mediated deficits in microglial phagocytosis drive pathological progression in amyotrophic lateral sclerosis.Journal of neuroinflammation · 2026Article
- Correlation Between SGK1 Expression Level and Multiple Myeloma Progression After Autologous Hematopoietic Stem Cell Transplantation.Biochemical genetics · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- GATA4-Driven Transcription of HtrA1 Promotes Cellular Senescence in Ménière's Disease and Age-Related Audio-Vestibular Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SGK1 inhibition supports neuroprotection in spinal cord injury by suppressing oxidative stress and AIM2 activation via FoxO1 mediated mitophagy.Journal of neuroinflammation · 2026Article
- SGK1 inhibition restores excitability of cortical neurons derived from Alzheimer's disease patients.Neurobiology of disease · 2026Article
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6 authors.
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Abstract
Hyperphosphorylation of Tau and the ensuing microtubule destabilization are linked to synaptic dysfunction in Alzheimer's disease (AD). We find a marked increase of phosphorylated Tau (pTau) in cortical neurons differentiated from induced pluripotent stem cells (iPSCs) of AD patients. It is accompanied by significantly elevated expression of Serum and Glucocorticoid-regulated Kinase-1 (SGK1), which is induced by cellular stress, and Histone Deacetylase 6 (HDAC6), which deacetylates tubulin to destabilize microtubules. Indeed, acetylated tubulin and microtubule stability are significantly lower in AD-derived cortical neurons. SGK1 inhibitors or shRNA decrease Tau phosphorylation and HDAC6 levels while increasing acetylated tubulin in AD neurons. Overexpression of SGK1 in normal neurons does the opposite. These results suggest that elevation of the cellular stress-induced SGK1 increases Tau phosphorylation and HDAC6 expression, which destabilize microtubules to compromise many cellular functions subserving cognition. The coordinated increases in SGK1, pTau, and HDAC6, as well as the corresponding decrease in acetylated tubulin and microtubule stability in AD neurons, offer attractive targets for therapeutic development.
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