Modulation of the aging process through cell signaling represents a recent and exciting area of study with the potential for development of therapeutics to extend human health.

Inducible degradation of the insulin/insulin-like growth factor-1 receptor shows that a doubling in lifespan is possible even at extremely old ages in an organism.

High variability in neuropathology burden and interactions between dementia diagnosis and RNA quality present underappreciated complications when studying dementia in an aged population.

Modulation of histone levels in gut enterocytes by rapamycin treatment alters chromatin organisation and induces intestinal autophagy through transcriptional regulation to prevent age-related decline in the intestine and extend lifespan.

The tyrosine degradation pathway reprogramming connects mitochondrial dysfunction, aging, and production of tyrosine-derived neuromediators that can be targeted with an FDA-approved drug, Tigecycline.

Mice with a mutation that disrupts the release of growth hormone show greatly increased lifespan, which can be further increased by caloric restriction.

Light controls can fine tune microbiome–host interaction to qualitatively regulate host longevity with temporal and spatial precision.

Adiponectin is an essential regulator for healthspan and is indispensable for sustaining a normal lifespan.

Translational evidence indicates APOE2 benefits longevity independent of its protective effects on Alzheimer’s disease, which preserved activity and the metabolism of apoE protein and associated-lipids would be key to understanding.

Lithocholic acid associates with skeletal muscle mass and plays an important role in skeletal muscle hypertrophy through activation of the bile acid receptor.