Ageing and protein aggregation-mediated disorders: from invertebrates to mammals
Late onset is a common hallmark character of numerous disorders including human neurodegenerative maladies such as Huntington's, Parkinson's and Alzheimer's diseases. Why these diseases manifest in aged individuals and why distinct disorders share strikingly similar emergence patterns...
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Published in | Philosophical transactions of the Royal Society of London. Series B. Biological sciences Vol. 366; no. 1561; pp. 94 - 98 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
The Royal Society
12.01.2011
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Subjects | |
Online Access | Get full text |
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Summary: | Late onset is a common hallmark character of numerous disorders including human neurodegenerative maladies such as Huntington's, Parkinson's and Alzheimer's diseases. Why these diseases manifest in aged individuals and why distinct disorders share strikingly similar emergence patterns were until recently unsolved enigmas. During the past decade, invertebrate-based studies indicated that the insulin/IGF signalling pathway (IIS) mechanistically links neurodegenerative-associated toxic protein aggregation and ageing; yet, until recently it was unclear whether this link is conserved from invertebrates to mammals. Recent studies performed in Alzheimer's mouse models indicated that ageing alteration by IIS reduction slows the progression of Alzheimer's-like disease, protects the brain and mitigates the behavioural, pathological and biochemical impairments associated with the disease. Here, we review these novel studies and discuss the potential of ageing alteration as a therapeutic approach for the treatment of late onset neurodegeneration. |
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Bibliography: | Discussion Meeting issue 'The new science of ageing' organized and edited by Linda Partridge, Gillian Bates and Janet Thornton |
ISSN: | 0962-8436 1471-2970 |
DOI: | 10.1098/rstb.2010.0271 |