Sarcopenia-associated phenotypes involving pathological changes in muscle strength and function along with cognitive decline are observed in human AD patients.73,74 It is noteworthy that HDACs play key regulatory roles in skeletal muscle metabolism and have been linked to the development of muscle atrophy and dysfunction.75 In view of this, the data suggest that the gut microbial dysbiosis initiated temporal changes in HDACs in skeletal muscle, leading to sarcopenia-related phenotypes that are therapeutically targeted by the HDAC-inhibitory function of TB/butyrate. Here, HDAC9 is linked to Alzheimer disease.