The role of tau in Aβ toxicity via Fyn-kinase modulation is further supported by studies reporting that absence of tau in dendritic spines prevented the toxic effects of AβOs mediated by GluN2B-NMDA receptors [133], and whereas a reduction in tau levels prevented the cognitive impairment in AD transgenic mice overexpressing Aβ, overexpression of Fyn can enhance their cognitive impairment [134]. Here, GRIN2B is linked to Alzheimer disease.