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Thus, in vitro Notch overexpression or PDX models are unsuitable for testing our hypothesis that RSL3 targets the astrocyte-like state

Such TBI-induced actions, whether occurring early or later in life, can readily increase the vulnerability of the brain to other neurodegenerative events as detailed in the two hit hypothesis of the Latent Early-life Associated Regulation (LEARn) model of Lahiri et al., [92, 93], whereby genetic and environmental risk factors combine in an epigenetic pathway to trigger the etiology of a later neurobiological disorder (such as TBI leading to AD)

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Can these differences be therapeutically exploited