Aberrant protein aggregation and late manifestation are common features of human neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases.Why these maladies onset late in life and whether the aging process plays active roles in allowing their manifestation are key questions that we address in my lab. To test whether the alteration of aging can postpone the onset of neurodegeneration-linked toxic protein aggregation we employed model worms and discovered that reducing the activity of theInsulin/IGF signaling pathway (IIS), a well-established aging regulating pathway, protects the animals from toxicity of the human Alzheimer’s disease-associated peptide, Aβ. Recently we found that NT219, a chemical IGF1 inhibitor, mitigates the symptoms that emanate from the aggregation of human Aβ in models worms. We also study how aging affects the cell biology of protein aggregates, specifically of the prion protein and how protein homeostasis is regulated by neurons at the organismal level. Our research is aimed to harness the mechanisms that prevent the onset of neurodegenerative diseases early in life, to protect the elderly from these devastating maladies.