Peer-reviewed veterinary case report
NAP (davunetide) enhances cognitive behavior in the STOP heterozygous mouse--a microtubule-deficient model of schizophrenia.
- Journal:
- Peptides
- Year:
- 2010
- Authors:
- Merenlender-Wagner, Avia et al.
- Affiliation:
- Department of Human Molecular Genetics and Biochemistry
- Species:
- rodent
Abstract
NAP (generic name, davunetide) is an active fragment of activity-dependent neuroprotective protein (ADNP). ADNP-/- embryos exhibit CNS dysgenesis and die in utero. ADNP+/- mice survive but demonstrate cognitive dysfunction coupled with microtubule pathology. NAP treatment ameliorates, in part, ADNP-associated dysfunctions. The microtubule, stable tubule-only polypeptide (STOP) knockout mice were shown to provide a reliable model for schizophrenia. Here, STOP-/- as well as STOP+/- showed schizophrenia-like symptoms (hyperactivity) that were ameliorated by chronic treatment with the antipsychotic drug, clozapine. Daily intranasal NAP treatment significantly decreased hyperactivity in the STOP+/- mice and protected visual memory.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/20417241/