DSP and Alzheimer disease: However, the simplistic model wherein locus coeruleus damage causes reduced NE transmission is challenged by early AD findings, which indicate that cerebrospinal fluid (CSF) shows elevated NE levels and turnover [199, 208]; this is consistent with prodromal symptoms such as anxiety and sleep disturbances, paralleling PD's “reduced fibers with hyperactive phenotype.” These results suggest complex compensatory mechanisms, as observed in DSP‐4‐induced AD models, where reduced noradrenergic gene expression coexists with increased NE turnover and signaling at terminals [209].