Fig. 1

αCaMKII is dysregulated in the Alzheimer’s disease hippocampus. αCaMKII-expressing neurons are selectively lost in the hippocampal CA1 subfield in AD [50, 51], a region that shows devastating atrophy when compared to age-matched controls [54]. Remaining pyramidal neurons of this region show increased expression of αCaMKII. This increased expression may critically contribute to tau hyperphosphorylation and other neurodegenerative processes, such as caspase-3 overactivation, in CA1 pyramidal neurons [for references, see main text]. On the other hand, CA3 pyramidal neurons and granule cells of the DG do not develop these changes in total αCaMKII. They do however show a change in subcellular distribution of T286-autophosphorylated αCaMKII (inset) [59]. This change is suggested to shift CaMKII activity from the synapse to soma leading to synaptic deficits, neurodegenerative processes, and impaired memory formation. AD, Alzheimer’s disease; CA1/3, Cornu Amonis areas 1/3; αCaMKII, α subunit of calcium/calmodulin-dependent protein kinase II; DG, dentate gyrus