Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease
Dietary restriction (DR) extends lifespan in diverse organisms and, in animal and cellular models, can delay a range of aging-related diseases including Alzheimer's disease (AD). A better understanding of the mechanisms mediating these interactions, however, may reveal novel pathways involved i...
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ftucl:oai:eprints.ucl.ac.uk.OAI2:134784 2023-05-15T15:09:54+02:00 Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease Kerr, F Augustin, H Piper, MDW Gandy, C Allen, MJ Lovestone, S Partridge, L 2011-11 http://discovery.ucl.ac.uk/134784/ eng eng ELSEVIER SCIENCE INC open Neurobiology of Aging , 32 (11) 1977 - 1989. (2011) Alzheimer's disease Aging Dietary restriction Neuronal function Drosophila caloric restriction life-span caenorhabditis-elegans a-beta amyloid neuropathology axonal-transport mouse model melanogaster expression phenotypes Article 2011 ftucl 2016-10-20T22:17:57Z Dietary restriction (DR) extends lifespan in diverse organisms and, in animal and cellular models, can delay a range of aging-related diseases including Alzheimer's disease (AD). A better understanding of the mechanisms mediating these interactions, however, may reveal novel pathways involved in AD pathogenesis, and potential targets for disease-modifying treatments and biomarkers for disease progression. Drosophila models of AD have recently been developed and, due to their short lifespan and susceptibility to genetic manipulation, we have used the fly to investigate the molecular connections among diet, aging and AD pathology. DR extended lifespan in both Arctic mutant A beta 42 and WT 4R tau over-expressing flies, but the underlying molecular pathology was not altered and neuronal dysfunction was not prevented by dietary manipulation. Our data suggest that DR may alter aging through generalised mechanisms independent of the specific pathways underlying AD pathogenesis in the fly, and hence that lifespan-extending manipulations may have varying effects on aging and functional declines in aging-related diseases. Alternatively, our analysis of the specific effects of DR on neuronal toxicity downstream of A beta and tau pathologies with negative results may simply confirm that the neuro-protective effects of DR are upstream of the initiating events involved in the pathogenesis of AD. (C) 2009 Elsevier Inc. All rights reserved. Article in Journal/Newspaper Arctic University College London: UCL Discovery Arctic |
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University College London: UCL Discovery |
op_collection_id |
ftucl |
language |
English |
topic |
Alzheimer's disease Aging Dietary restriction Neuronal function Drosophila caloric restriction life-span caenorhabditis-elegans a-beta amyloid neuropathology axonal-transport mouse model melanogaster expression phenotypes |
spellingShingle |
Alzheimer's disease Aging Dietary restriction Neuronal function Drosophila caloric restriction life-span caenorhabditis-elegans a-beta amyloid neuropathology axonal-transport mouse model melanogaster expression phenotypes Kerr, F Augustin, H Piper, MDW Gandy, C Allen, MJ Lovestone, S Partridge, L Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease |
topic_facet |
Alzheimer's disease Aging Dietary restriction Neuronal function Drosophila caloric restriction life-span caenorhabditis-elegans a-beta amyloid neuropathology axonal-transport mouse model melanogaster expression phenotypes |
description |
Dietary restriction (DR) extends lifespan in diverse organisms and, in animal and cellular models, can delay a range of aging-related diseases including Alzheimer's disease (AD). A better understanding of the mechanisms mediating these interactions, however, may reveal novel pathways involved in AD pathogenesis, and potential targets for disease-modifying treatments and biomarkers for disease progression. Drosophila models of AD have recently been developed and, due to their short lifespan and susceptibility to genetic manipulation, we have used the fly to investigate the molecular connections among diet, aging and AD pathology. DR extended lifespan in both Arctic mutant A beta 42 and WT 4R tau over-expressing flies, but the underlying molecular pathology was not altered and neuronal dysfunction was not prevented by dietary manipulation. Our data suggest that DR may alter aging through generalised mechanisms independent of the specific pathways underlying AD pathogenesis in the fly, and hence that lifespan-extending manipulations may have varying effects on aging and functional declines in aging-related diseases. Alternatively, our analysis of the specific effects of DR on neuronal toxicity downstream of A beta and tau pathologies with negative results may simply confirm that the neuro-protective effects of DR are upstream of the initiating events involved in the pathogenesis of AD. (C) 2009 Elsevier Inc. All rights reserved. |
format |
Article in Journal/Newspaper |
author |
Kerr, F Augustin, H Piper, MDW Gandy, C Allen, MJ Lovestone, S Partridge, L |
author_facet |
Kerr, F Augustin, H Piper, MDW Gandy, C Allen, MJ Lovestone, S Partridge, L |
author_sort |
Kerr, F |
title |
Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease |
title_short |
Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease |
title_full |
Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease |
title_fullStr |
Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease |
title_full_unstemmed |
Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease |
title_sort |
dietary restriction delays aging, but not neuronal dysfunction, in drosophila models of alzheimer's disease |
publisher |
ELSEVIER SCIENCE INC |
publishDate |
2011 |
url |
http://discovery.ucl.ac.uk/134784/ |
geographic |
Arctic |
geographic_facet |
Arctic |
genre |
Arctic |
genre_facet |
Arctic |
op_source |
Neurobiology of Aging , 32 (11) 1977 - 1989. (2011) |
op_rights |
open |
_version_ |
1766340990687248384 |