ReviewJournal of endocrinological investigation2016
Neuroprotective effects of estrogens: the role of cholesterol.
Review in Journal of endocrinological investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
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- DHCR24 in cholesterol metabolism and diseases of the nervous system.Lipids in health and disease · 2026Review
- Transcriptomic and Proteomic Analyses of the Liver and Ileum Identify Key Genes and Pathways Associated with Low and High Groups of Social Genetic Effect of Residual Feed Intake.Animals : an open access journal from MDPI · 2025Article
- Hidden risk patterns among acute ischemic stroke patients identified by latent class analysis.Frontiers in neurology · 2025Article
- The Intersection of cerebral cholesterol metabolism and Alzheimer's disease: Mechanisms and therapeutic prospects.Heliyon · 2024Review
- Huangqi Guizhi Wuwu Decoction Improves Inflammatory Factor Levels in Chemotherapy-induced Peripheral Neuropathy by Regulating the Arachidonic Acid Metabolic Pathway.Current pharmaceutical design · 2024Article
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- Integrated multi-omics and machine learning approach reveals lipid metabolic biomarkers and signaling in age-related meibomian gland dysfunction.Computational and structural biotechnology journal · 2023Article
- The role of DHCR24 in the pathogenesis of AD: re-cognition of the relationship between cholesterol and AD pathogenesis.Acta neuropathologica communications · 2022Review
- Association between lipid metabolism and cognitive function in patients with schizophrenia.Frontiers in psychiatry · 2022Article
- Erzhi pills ameliorate cognitive dysfunction and alter proteomic hippocampus profiles induced by d-galactose and AβPharmaceutical biology · 2021Article
- DHCR24 Knockdown Lead to Hyperphosphorylation of Tau at Thr181, Thr231, Ser262, Ser396, and Ser422 Sites by Membrane Lipid-Raft Dependent PP2A Signaling in SH-SY5Y Cells.Neurochemical research · 2021Article
- SeXX Matters in Multiple Sclerosis.Frontiers in neurology · 2020Review
- A Novel Contrast Agent Based on Magnetic Nanoparticles for Cholesterol Detection as Alzheimer's Disease Biomarker.Nanoscale research letters · 2019Article
- The etiological effect of a new low-frequencyAging · 2018Article
- Estrogen Interactions With Lipid Rafts Related to Neuroprotection. Impact of Brain Ageing and Menopause.Frontiers in neuroscience · 2018Review
- Review
- Hydrogen exerts neuroprotective effects by inhibiting oxidative stress in experimental diabetic peripheral neuropathy rats.Medical gas researchArticle
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionExperimental and clinical evidence suggests that estrogens have protective effects in the brain. Nevertheless, their potential role against neurodegenerative diseases, in particular Alzheimer's disease (AD), is still a matter of debate. The identification of the seladin-1 gene (for SELective Alzheimer's Disease INdicator-1), which appeared to be significantly less expressed in brain region affected in AD, opened a new scenario in the field of neuroprotective mechanisms. Seladin-1 was found to have neuroprotective properties through its anti-apoptotic activity. In addition, it was subsequently demonstrated that seladin-1 also has enzymatic activity, because it catalyzes the conversion of desmosterol into cholesterol. Several studies have shown that an appropriate amount of membrane cholesterol plays a pivotal role to protect nerve cells against β-amyloid toxicity in AD and to counteract the synthesis of β-amyloid. METHODS AND
resultsWe demonstrated that the expression of seladin-1, as well as the synthesis of cell cholesterol, is stimulated by estrogens in human neuronal precursor cells. Cholesterol enriched cells became more resistant against oxidative stress and β-amyloid toxicity. We thus hypothesized that seladin-1 might be a mediator of the neuroprotective effects of estrogens. Indeed, in cells in which seladin-1 gene expression had been silenced by siRNA the protective effects of estrogens were lost. This finding indicates that seladin-1 is a crucial mediator of the neuroprotective effects of these hormones, at least in our cell model.
conclusionsIn summary, these results establish a new link between estrogens and cholesterol, which is represented by the neuroprotective factor seladin-1.
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