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Neurodegenerative disorders include Alzheimer\u2019s, Parkinson\u2019s, and prion diseases among others. These disorders are characterized by the accumulation of aggregating proteins forming amyloid, responsible for the disease\u2010associated pathological lesions. The aggregation of amyloidogenic proteins can result either in gaining of toxic functions, derived from the damage provoked by these deposits in affected tissue, or in a loss of functions, due to the sequestration and the consequent inability of the aggregating protein to ensure its physiological role. While it is widely accepted that aging represents the main risk factor for neurodegeneration, there is still no clear cut\u2010off line between the two conditions. Indeed, many of the pathways that are commonly altered in neurodegeneration\u2014misfolded protein accumulation, chronic inflammation, mitochondrial dysfunction, impaired iron homeostasis, epigenetic modifications\u2014have been often correlated also with healthy aging. This overlap could be explained by the fact that the continuous accumulation of cellular damages, together with a progressive decline in metabolic efficiency during aging, makes the neurons more vulnerable to toxic injuries. 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