IL1B and Alzheimer disease: In contrast, the lack of evidence of autophagic failure in age-matched patients without AD suggests that it is logical to assume that whatever level of neuronal stress that is tolerable is consonant with tolerable levels of IL-1β in which parkin is sufficiently activated for ubiquitination to meet the challenge of the propensity of excess IL-1β to induce synthesis and activation of kinases that favor untoward phosphorylation of important proteins involved in clearance and in synthesis of proteins important in neuronal repair.