NAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy.
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| Title: | NAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy. |
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| Authors: | Quraishe, S, Cowan, C M, Mudher, A |
| Source: | Molecular Psychiatry. Jul2013, Vol. 18 Issue 7, p834-842. 9p. 5 Graphs. |
| Subjects: | Alzheimer's disease, Axonal transport, Biological transport, Microtubules, Neurodegeneration |
| Abstract: | Alzheimer's disease (AD) is a devastating neurodegenerative disease causing irreversible cognitive decline in the elderly. There is no disease-modifying therapy for this condition and the mechanisms underpinning neuronal dysfunction and neurodegeneration are unclear. Compromised cytoskeletal integrity within neurons is reported in AD. This is believed to result from loss-of-function of the microtubule-associated protein tau, which becomes hyper-phosphorylated and deposits into neurofibrillary tangles in AD. We have developed a Drosophila model of tauopathy in which abnormal human tau mediates neuronal dysfunction characterised by microtubule destabilisation, axonal transport disruption, synaptic defects and behavioural impairments. Here we show that a microtubule-stabilising drug, NAPVSIPQ (NAP), prevents as well as reverses these phenotypes even after they have become established. Moreover, it does not alter abnormal tau levels indicating that it by-passes toxic tau altogether. Thus, microtubule stabilisation is a disease-modifying therapeutic strategy protecting against tau-mediated neuronal dysfunction, which holds great promise for tauopathies like AD. [ABSTRACT FROM AUTHOR] |
| Copyright of Molecular Psychiatry is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
| FullText | Links: – Type: pdflink Text: Availability: 0 |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 88306733 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: NAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Quraishe%2C+S%22">Quraishe, S</searchLink><br /><searchLink fieldCode="AR" term="%22Cowan%2C+C+M%22">Cowan, C M</searchLink><br /><searchLink fieldCode="AR" term="%22Mudher%2C+A%22">Mudher, A</searchLink> – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Molecular+Psychiatry%22">Molecular Psychiatry</searchLink>. Jul2013, Vol. 18 Issue 7, p834-842. 9p. 5 Graphs. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Alzheimer's+disease%22">Alzheimer's disease</searchLink><br /><searchLink fieldCode="DE" term="%22Axonal+transport%22">Axonal transport</searchLink><br /><searchLink fieldCode="DE" term="%22Biological+transport%22">Biological transport</searchLink><br /><searchLink fieldCode="DE" term="%22Microtubules%22">Microtubules</searchLink><br /><searchLink fieldCode="DE" term="%22Neurodegeneration%22">Neurodegeneration</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Alzheimer's disease (AD) is a devastating neurodegenerative disease causing irreversible cognitive decline in the elderly. There is no disease-modifying therapy for this condition and the mechanisms underpinning neuronal dysfunction and neurodegeneration are unclear. Compromised cytoskeletal integrity within neurons is reported in AD. This is believed to result from loss-of-function of the microtubule-associated protein tau, which becomes hyper-phosphorylated and deposits into neurofibrillary tangles in AD. We have developed a Drosophila model of tauopathy in which abnormal human tau mediates neuronal dysfunction characterised by microtubule destabilisation, axonal transport disruption, synaptic defects and behavioural impairments. Here we show that a microtubule-stabilising drug, NAPVSIPQ (NAP), prevents as well as reverses these phenotypes even after they have become established. Moreover, it does not alter abnormal tau levels indicating that it by-passes toxic tau altogether. Thus, microtubule stabilisation is a disease-modifying therapeutic strategy protecting against tau-mediated neuronal dysfunction, which holds great promise for tauopathies like AD. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Molecular Psychiatry is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1038/mp.2013.32 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 9 StartPage: 834 Subjects: – SubjectFull: Alzheimer's disease Type: general – SubjectFull: Axonal transport Type: general – SubjectFull: Biological transport Type: general – SubjectFull: Microtubules Type: general – SubjectFull: Neurodegeneration Type: general Titles: – TitleFull: NAP (davunetide) rescues neuronal dysfunction in a Drosophila model of tauopathy. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Quraishe, S – PersonEntity: Name: NameFull: Cowan, C M – PersonEntity: Name: NameFull: Mudher, A IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 07 Text: Jul2013 Type: published Y: 2013 Identifiers: – Type: issn-print Value: 13594184 Numbering: – Type: volume Value: 18 – Type: issue Value: 7 Titles: – TitleFull: Molecular Psychiatry Type: main |
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