The rationale for our design is simply that, since σ-1, HDAC-6, and OS (e.g., mitochondria and lipid peroxidation), are independently potentially druggable targets in neurodegenerative pathologies [1,3,19,20], it is plausible that single compounds designed with the trio-target capabilities (i.e., σ-1 activation and HDAC-6 and OS inhibitions) could yield novel mechanistic molecules with advantageous neuroprotective properties for testing in AD models. The gene discussed is HDAC6; the disease is Alzheimer disease.