Several studies have reported reduced SCFAs-producing species and SCFA levels in individuals with mild cognitive impairment (MCI) and AD patients.292–295 Notably, reduced fecal levels of SCFAs were negatively associated with Aβ deposition in patients with MCI.293 In addition, increased levels of HDAC2 and HDAC6 were detected in AD mouse models and AD patients.296,297 Thus, HDAC inhibition represents a promising approach for the treatment of AD. Here, HDAC9 is linked to Alzheimer disease.