Ageing and protein aggregation-mediated disorders: From invertebrates to mammals

Andrew Dillin*, Ehud Cohen

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

50 Scopus citations


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.

Original languageAmerican English
Pages (from-to)94-98
Number of pages5
JournalPhilosophical Transactions of the Royal Society B: Biological Sciences
Issue number1561
StatePublished - 12 Jan 2011


  • Ageing
  • Insulin/IGF-1 signalling
  • Neurodegeneration
  • Proteotoxicity


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