ArticleNeurochemical research2007
Inhibition of melatonin biosynthesis induces neurofilament hyperphosphorylation with activation of cyclin-dependent kinase 5.
Article in Neurochemical research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Modulation of neural circuits by melatonin in neurodegenerative and neuropsychiatric disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Melatonin as a Harmonizing Factor of Circadian Rhythms, Neuronal Cell Cycle and Neurogenesis: Additional Arguments for Its Therapeutic Use in Alzheimer's Disease.Current neuropharmacology · 2023Review
- Cellular Mechanisms of Melatonin: Insight from Neurodegenerative Diseases.Biomolecules · 2020Review
- Mechanisms of Melatonin in Alleviating Alzheimer's Disease.Current neuropharmacology · 2017Review
- Minocycline ameliorates D-galactose-induced memory deficits and loss of Arc/Arg3.1 expression.Molecular biology reports · 2016Article
- Cnga2 Knockout Mice Display Alzheimer's-Like Behavior Abnormities and Pathological Changes.Molecular neurobiology · 2016Article
- Activation of Glycogen Synthase Kinase-3 Mediates the Olfactory Deficit-Induced Hippocampal Impairments.Molecular neurobiology · 2015Article
- Progress in the development of new drugs in Alzheimer's disease.The journal of nutrition, health & aging · 2011Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decreased level of melatonin and hyperphosphorylation of neurofilament proteins have been reported in Alzheimer's disease (AD). However, the direct evidence linking melatonin and neurofilament phosphorylation is still lacking. Here, we investigated the effect of inhibiting melatonin biosynthesis on phosphorylation of neurofilament proteins and the involvement of cyclin-dependent kinase 5 (cdk-5) in rats. We observed that injection of haloperidol, a specific inhibitor of 5-hydroxyindole-O-methyltransferase, resulted in significantly decreased level of serum melatonin with a concomitantly increased phosphorylation of neurofilament proteins and activation of cdk-5 in rats. Exogenous supplementation of melatonin partially arrested the hyperphosphorylation of neurofilament and the activation of cdk-5. These results suggest that inhibition of melatonin biosynthesis may activate cdk-5 and thus induces Alzheimer-like hyperphosphorylation of neurofilament proteins.
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