In a phase IIa clinical study, several encouraging results were obtained for various types of readouts: It was found that the AD-related alteration in the EEG power spectrum was changed towards normal, a clear indication of the reduction of the synaptic marker neurogranin and the inflammatory marker YKL-40—all of which are in support of protecting impaired synapses [47]. This evidence concerns the gene CHI3L1 and Alzheimer disease.