Fig. 1.

Experimental evidence that regulation of parkin expression and phosphorylation is related to glial activation and excess IL-1β in Alzheimer brain and in AD Model Systems. a Parkin in neurons in brains of age-matched control patients (AMC) is diffusely distributed within the cytoplasm whereas parkin in neurons in brains of Alzheimer patients (AD) is present in rosette-like aggregates (b). c Parkin in Alzheimer brain is colocalized with tau aggregates. d Activated glia overexpressing IL-1α (brown) are immediately adjacent to parkin-immunoreactive neurons (blue), scale bar 20 μM. e Comparative levels of IL-1α, IL-1β, and parkin mRNAs in wild-type littermates or PD-APP mice. f Representative western immunoblot showing proteins from NT2 cells either treated, or not, overnight with IL-1β. g Phospho-parkin levels (P-parkin Ser₆₅) in two representative western immunoblots of proteins from NT2 cell and rat primary neuron cultures treated, or not, with IL-1β. h Quantification of parkin in untreated and treated cell cultures (n = 6), data is mean ± SEM (**p < 0.01). i, j Quantification of P-parkin levels in IL-1β treated or untreated cultures in NT2 cells (i) and primary rat neurons (j)