ArticlePloS one2012
Acetyl-L-carnitine improves behavior and dendritic morphology in a mouse model of Rett syndrome.
Article in PloS one, 2012. 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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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, 30 citations in OpenAlex.
- Regulation of oligodendrocyte metabolism and myelination by acetyl-L-carnitine in a mouse model of post-weaning social isolation.Translational psychiatry · 2026Article
- Acetyl-carnitine improves hyperactivity and learning deficits inLife science alliance · 2026Article
- Increasing histone acetylation improves sociability and restores learning and memory in KAT6B-haploinsufficient mice.The Journal of clinical investigation · 2024Article
- Review
- Drug Studies on Rett Syndrome: From Bench to Bedside.Journal of autism and developmental disorders · 2020Review
- Metabolic Signatures Differentiate Rett Syndrome From Unaffected Siblings.Frontiers in integrative neuroscience · 2020Article
- Early Postnatal Treatment with Valproate InducesInternational journal of molecular sciences · 2019Article
- Treating Rett syndrome: from mouse models to human therapies.Mammalian genome : official journal of the International Mammalian Genome Society · 2019Review
- l-Acetylcarnitine: A Mechanistically Distinctive and Potentially Rapid-Acting Antidepressant Drug.International journal of molecular sciences · 2017Review
- Autism spectrum disorder-associated genes and the development of dentate granule cells.Medical molecular morphology · 2017Review
- Alterations in the carnitine cycle in a mouse model of Rett syndrome.Scientific reports · 2017Article
- Stress-induced structural plasticity of medial amygdala stellate neurons and rapid prevention by a candidate antidepressant.Molecular psychiatry · 2017Article
- Loss of MeCP2 in the rat models regression, impaired sociability and transcriptional deficits of Rett syndrome.Human molecular genetics · 2016Article
- MeCP2 deficiency results in robust Rett-like behavioural and motor deficits in male and female rats.Human molecular genetics · 2016Article
- Evidence of Mitochondrial Dysfunction within the Complex Genetic Etiology of Schizophrenia.Molecular neuropsychiatry · 2015Review
- Alterations in the cholinergic system of brain stem neurons in a mouse model of Rett syndrome.American journal of physiology. Cell physiology · 2014Article
- Rett syndrome and MeCP2.Neuromolecular medicine · 2014Review
- The effect of two-week L-carnitine supplementation on exercise -induced oxidative stress and muscle damage.Asian journal of sports medicine · 2014Article
- Upregulation of mGlu2 receptors via NF-κB p65 acetylation is involved in the Proneurogenic and antidepressant effects of acetyl-L-carnitine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rett syndrome (RTT) is a devastating neurodevelopmental disorder affecting 1 in 10,000 girls. Approximately 90% of cases are caused by spontaneous mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MeCP2). Girls with RTT suffer from severe motor, respiratory, cognitive and social abnormalities attributed to early deficits in synaptic connectivity which manifest in the adult as a myriad of physiological and anatomical abnormalities including, but not limited to, dimished dendritic complexity. Supplementation with acetyl-L-carnitine (ALC), an acetyl group donor, ameliorates motor and cognitive deficits in other disease models through a variety of mechanisms including altering patterns of histone acetylation resulting in changes in gene expression, and stimulating biosynthetic pathways such as acetylcholine. We hypothesized ALC treatment during critical periods in cortical development would promote normal synaptic maturation, and continuing treatment would improve behavioral deficits in the Mecp2(1lox) mouse model of RTT. In this study, wildtype and Mecp2(1lox) mutant mice received daily injections of ALC from birth until death (postnatal day 47). General health, motor, respiratory, and cognitive functions were assessed at several time points during symptom progression. ALC improved weight gain, grip strength, activity levels, prevented metabolic abnormalities and modestly improved cognitive function in Mecp2 null mice early in the course of treatment, but did not significantly improve motor or cognitive functions assessed later in life. ALC treatment from birth was associated with an almost complete rescue of hippocampal dendritic morphology abnormalities with no discernable side effects in the mutant mice. Therefore, ALC appears to be a promising therapeutic approach to treating early RTT symptoms and may be useful in combination with other therapies.
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