ArticleMolecular neurobiology2022
DHCR24 Knockdown Induces Tau Hyperphosphorylation at Thr181, Ser199, Ser262, and Ser396 Sites via Activation of the Lipid Raft-Dependent Ras/MEK/ERK Signaling Pathway in C8D1A Astrocytes.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 27 citations in OpenAlex.
- Cholesterol metabolism in neurodegenerative diseases: mechanisms and therapeutic advances.Molecular neurodegeneration · 2026Review
- DHCR24 in cholesterol metabolism and diseases of the nervous system.Lipids in health and disease · 2026Review
- Article
- Analysis of the potential regulatory mechanism of PIEZO1 in Alzheimer's disease based on RNA sequencing.IBRO neuroscience reports · 2025Article
- Mesenchymal stem cell application in Alzheimer's disease.Regenerative therapy · 2025Review
- Lipidome disruption in Alzheimer's disease brain: detection, pathological mechanisms, and therapeutic implications.Molecular neurodegeneration · 2025Review
- High mRNA Expression of 24 Dehydrocholesterol Reductase (DHCR24) in the Treatment of Doxorubicin-Induced Heart Failure in Rats.International journal of molecular sciences · 2025Article
- The role of protein phosphorylation modifications mediated by iron metabolism regulatory networks in the pathogenesis of Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- Identifying biomarkers of hepatic fatty acid metabolism disorder in sevoflurane-induced brain developmental injury by bioinformatics analysis.Frontiers in molecular neuroscience · 2025Article
- The role of small GTPases in Alzheimer's disease tau pathologies.Frontiers in cellular neuroscience · 2025Review
- A study on the functional role of the DHCR24 gene in gonadal differentiation and development of Macrobrachium nipponense.Scientific reports · 2024Article
- Interaction Between DHCR24 and hsa_circ_0015335 Facilitates Cognitive Impairment in Cerebral Small Vessel Disease Patients.CNS neuroscience & therapeutics · 2024Article
- Navigating the metabolic maze: anomalies in fatty acid and cholesterol processes in Alzheimer's astrocytes.Alzheimer's research & therapy · 2024Review
- Review
- The interaction between ageing and Alzheimer's disease: insights from the hallmarks of ageing.Translational neurodegeneration · 2024Review
- American Ginseng for the Treatment of Alzheimer's Disease: A Review.Molecules (Basel, Switzerland) · 2023Review
- DHCR24 reverses Alzheimer's disease-related pathology and cognitive impairment via increasing hippocampal cholesterol levels in 5xFAD mice.Acta neuropathologica communications · 2023Article
- White matter injury, cholesterol dysmetabolism, and APP/Abeta dysmetabolism interact to produce Alzheimer's disease (AD) neuropathology: A hypothesis and review.Frontiers in aging neuroscience · 2023Article
- Exploring the role of statin interventions on cognitive function by Mendelian randomization study.Journal of Alzheimer's disease reportsArticle
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9 authors at 1 institution in 1 country.
Funding
Abstract
The synthetase 3β-hydroxysterol-Δ24 reductase (DHCR24) is a key regulator involved in cholesterol synthesis and homeostasis. A growing body of evidence indicates that DHCR24 is downregulated in the brain of various models of Alzheimer's disease (AD), such as astrocytes isolated from AD mice. For the past decades, astrocytic tau pathology has been found in AD patients, while the origin of phosphorylated tau in astrocytes remains unknown. A previous study suggests that downregulation of DHCR24 is associated with neuronal tau hyperphosphorylation. Herein, the present study is to explore whether DHCR24 deficiency can also affect tau phosphorylation in astrocytes. Here, we showed that DHCR24 knockdown could induce tau hyperphosphorylation at Thr181, Ser199, Thr231, Ser262, and Ser396 sites in C8D1A astrocytes. Meanwhile, we found that DHCR24-silencing cells had reduced the level of free cholesterol in the plasma membrane and intracellular organelles, as well as cholesterol esters. Furthermore, reduced cellular cholesterol level caused a decreased level of the caveolae-associated protein, cavin1, which disrupted lipid rafts/caveolae and activated rafts/caveolae-dependent Ras/MEK/ERK signaling pathway. In contrast, overexpression of DHCR24 prevented the overactivation of Ras/MEK/ERK signaling by increasing cellular cholesterol content, therefore decreasing tau hyperphosphorylation in C8D1A astrocytes. Herein, we firstly found that DHCR24 knockdown can lead to tau hyperphosphorylation in the astrocyte itself by activating lipid raft-dependent Ras/MEK/ERK signaling, which might contribute to the pathogenesis of AD and other degenerative tauopathies.
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