ASAH1 and Alzheimer disease: Further along these lines, in agreement with our results, a quantitative proteomics study performed on prefrontal cortical samples of human AD brains showed that the proteins CTSD, DB1, ASAH1, and TPPP had enhanced expression in AD compared to controls, while SORBS1 was downregulated.[79] Additionally, a neuropeptidomics study on AD human brain cortical synaptosomes, representing mainly excitatory neuronal endings, compared to age‐matched controls by Podvin et al.[80] found a significant loss of VGF, which also aligns with our results in single AD hiPSC‐neurons.