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Alzheimer’s disease (AD) is the most common form of neurodegenerative dementia. While major histopathological hallmarks of AD are amyloid‐β (Aβ) plaques and neurofibrillary tau tangles, soluble oligomeric forms of Aβ and tau (TauO) have been identified as the most neurotoxic species involved in synaptic degeneration. Previous studies associate alterations of the phosphatase calcineurin (CaN) to AβO‐driven toxicity. We previously have shown that CaN mediates both the neurotoxic and cognitive effects of AβO and elevated CaN levels have been also shown in AD patients, suggesting a central role of CaN in AD onset and/or clinical progression. Our previous studies in mouse models demonstrated that an acute treatment with the CaN inhibitor FK506/Tacrolimus in Tg2576 acutely injected intracerebroventricularly with AβO restores memory function in these cognitively impaired animals …