Animal studies aiming on Alzheimers’ disease either focusing on the enzyme 12/15–lipoxygenase catalyzing the deoxygenation of polyunsaturated fatty acids, or focusing on the carboxy terminal fragments of the human amyloid precursor protein (betaCTF99) revealed CREB alterations and corresponding anxiety changes (Lee et al., 2006; Joshi et al., 2014). This evidence concerns the gene CREB1 and early-onset autosomal dominant Alzheimer disease.