The misfolded pro-inflammatory protein S100A9 disrupts memory via neurochemical remodelling instigating an Alzheimer’s disease-like cognitive deficit

•Protein S100A9 oligomers and/or fibrils were given intranasally for 14 days in mice.•S100A9 oligomers and fibrils but not their mixture evoked passive avoidance amnesia.•The dopaminergic system was the primary disrupted target of S100A9 species amnesia.•Native S100A9 had no amnestic effect but disrupted brain monoamine neurochemistry.•The new findings are relevant to dementia management via a neuroprotective strategy.