Identification of Correlative Shifts in Indices of Brain Cholesterol Metabolism in the C57BL6/Mecp2tm1.1Bird Mouse, a Model for Rett Syndrome
Abstract
Rett syndrome (RS) is a pervasive neurodevelopmental disorder resulting from loss‐of‐function mutations in the X‐linked gene methyl‐Cpg‐binding protein 2 (MECP2). Using a well‐defined model for RS, the C57BL6/Mecp2tm1.1Bird mouse, we have previously found a moderate but persistently lower rate of cholesterol synthesis, measured in vivo, in the brains of Mecp2−/y mice, starting from about the third week after birth. There was no genotypic difference in the total cholesterol concentration throughout the brain at any age. This raised the question of whether the lower rate of cholesterol synthesis in the mutants was balanced by a fall in the rate at which cholesterol was converted via cholesterol 24‐hydroxylase (Cyp46A1) to 24 S‐hydroxycholesterol (24 S‐OHC), the principal route through which cholesterol is ordinarily removed from the brain. Here, we show that while there were no genotypic differences in the concentrations in plasma and liver of three cholesterol precursors (lanosterol, lathosterol, and desmosterol), two plant sterols (sitosterol and campesterol), and two oxysterols (27‐hydroxycholesterol [27‐OHC] and 24 S‐OHC), the brains of the Mecp2 −/y mice had significantly lower concentrations of all three cholesterol precursors, campesterol, and both oxysterols, with the level of 24 S‐OHC being ~20% less than in their Mecp2 +/y controls. Together, these data suggest that coordinated regulation of cholesterol synthesis and catabolism in the central nervous system is maintained in this model for RS. Furthermore, we speculate that the adaptive changes in these two pathways conceivably resulted from a shift in the permeability of the blood–brain barrier as implied by the significantly lower campesterol and 27‐OHC concentrations in the brains of the Mecp2−/y mice.
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An independent group showed significant dysregulated expression of genes involved in cholesterol biosynthesis, such as Hmgcr and Squalene Epoxidase (Sqle), in both brains and livers of Mecp2-null mice and a concurrent reduction of cholesterol precursors and a decrease of cholesterol biosynthesis in the brain.
“Few months after, an independent group showed significant dysregulated expression of genes involved in cholesterol biosynthesis, such as Hmgcr and Squalene Epoxidase (Sqle), in both brains and livers of Mecp2-null mice and a concurrent reduction of cholesterol precursors and a decrease of cholesterol biosynthesis in the brain [77,78,79].”
From Loss of Mevalonate/Cholesterol Homeostasis in the Brain: A Focus on Autism Spectrum Disorder and Rett Syndrome (2019) · cites this paper as [79]
Mecp2 KO mice exhibit a reduced rate of brain cholesterol biosynthesis, downregulation of key metabolic enzymes, and decreased levels of cholesterol precursors, despite accumulation of cholesterol in the brain.
“In particular, Mecp2 KO mice exhibit a reduced rate of brain cholesterol biosynthesis, together with the downregulation of key metabolic enzymes and decreased levels of cholesterol precursors, despite the accumulation of cholesterol in the brain (Ben-Shachar et al., 2009;Buchovecky et al., 2013b;Lütjohann et al., 2018;Urdinguio et al., 2008Urdinguio et al., , 2008;;Villani et al., 2016).”
From Impaired astrocyte-to-neuron cholesterol trafficking drives synaptic dysfunction in Rett syndrome (2026) · cites this paper as Lütjohann et al., 2018
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Impaired astrocyte-to-neuron cholesterol trafficking drives synaptic dysfunction in Rett syndrome
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“…2005; J.-P. Liu et al., 2010; Pfrieger, 2003), as well as by accumulating evidence of altered brain cholesterol metabolism in RTT (Ben-Shachar et al., 2009; Buchovecky et al., 2013b; Lopez et al., 2017; Lütjohann et al., 2018; Urdinguio et al., 2008; Villani et al., 2016; Zandl-Lang et al., 2022).”
- Authors
- Lütjohann, D., Lopez, A. M., Chuang, J., Kerksiek, A., & Turley, S. D.
- Affiliations
- University of Bonn (DE)
- The University of Texas Southwestern Medical Center (US)
- Children's Medical Center (US)
- Corresponding author
- Turley, Stephen D.
- Venue
- Lipids
- Publisher
- Wiley
- Published
- 2018-04
- Volume
- 53
- Issue
- 4
- Pages
- 363-373
- ISSN
- 0024-4201 (ISSN-L)
- 1558-9307
- OpenAlex
- W2804993959
- Cited by
- 11
- References
- 62
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 3 · 2019: 1
- FWCI
- 0.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Lipids (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Rett Syndrome Research Trust (RSRT7349)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Physiology › Lysosomal Storage Disorders Research
- Keywords
- Rett syndrome, MeCP2, brain cholesterol metabolism, cholesterol biosynthesis, cholesterol 24-hydroxylase, CYP46A1, 24S-hydroxycholesterol, 27-hydroxycholesterol, oxysterols, phytosterols, cholesterol precursors, blood-brain barrier permeability, neurodevelopmental disorders
- MeSH terms
- Animals, Behavior, Animal, Brain, Disease Models, Animal, Hydroxycholesterols, Lovastatin, Mice, Inbred C57BL, Rett Syndrome, Mice, Methyl-CpG-Binding Protein 2
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