Caloric Restriction Improves Spatial Learning Deficits in Tau Mice.

Background: Caloric restriction (CR) has been recognized for its benefits in delaying age-related diseases and extending lifespan. While its effects on amyloid pathology in Alzheimer's disease (AD) mouse models are well-documented, its effects on tauopathy, another hallmark of AD, are less explored.

Objective: To assess the impact of a short-term 30% CR regimen on age-dependent spatial learning deficits and pathological features in a tauopathy mouse model.

Oxytocin prevents dysregulation of the acute stress response and glucocorticoid-induced oxidative stress in chronically isolated prairie voles.

Chronic social isolation can lead to dysregulation of many physiological and psychological processes, including the ability to respond to acute stressors. Previous work in our lab reported that six weeks of social isolation in prairie voles (Microtus ochrogaster) caused increased glucocorticoid levels, oxidative damage, telomere degradation and anhedonia, and that oxytocin treatment prevented all of these changes. Following these results, we investigated how chronic social isolation with and without oxytocin treatment affected glucocorticoid (CORT) and oxidative stress responses to an acute stressor, a 5-min resident-intruder (R-I) test at the end of the social isolation period.

Untangling senescent and damage-associated microglia in the aging and diseased brain.

Microglial homeostasis has emerged as a critical mediator of health and disease in the central nervous system. In their neuroprotective role as the predominant immune cells of the brain, microglia surveil the microenvironment for debris and pathogens, while also promoting neurogenesis and performing maintenance on synapses. Chronological ageing, disease onset, or traumatic injury promotes irreparable damage or deregulated signaling to reinforce neurotoxic phenotypes in microglia.