Voluntary wheel running exercise rescues behaviorally-evoked acetylcholine efflux in the medial prefrontal cortex and epigenetic changes in ChAT genes following adolescent intermittent ethanol exposure.

Adolescent intermittent ethanol (AIE) exposure, which models heavy binge ethanol intake in adolescence, leads to a variety of deficits that persist into adulthood-including suppression of the cholinergic neuron phenotype within the basal forebrain. This is accompanied by a reduction in acetylcholine (ACh) tone in the medial prefrontal cortex (mPFC). Voluntary wheel running exercise (VEx) has been shown to rescue AIE-induced suppression of the cholinergic phenotype.

The Development of a Digital Patient Navigation Tool to Increase Colorectal Cancer Screening Among Federally Qualified Health Center Patients: Acceptability and Usability Testing.

Background: Federally Qualified Health Centers (FQHCs) are an essential place for historically underserved patients to access health care, including screening for colorectal cancer (CRC), one of the leading causes of cancer death in the United States. Novel interventions aimed at increasing CRC screening completion rates at FQHCs are crucial.

Objective: This study conducts user testing of a digital patient navigation tool, called eNav, designed to support FQHC patients in preparing for, requesting, and completing CRC screening tests.

Exercise leads to sex-specific recovery of behavior and pathological AD markers following adolescent ethanol exposure in the TgF344-AD model.

Introduction: Human epidemiological studies suggest that heavy alcohol consumption may lead to earlier onset of Alzheimer's Disease (AD), especially in individuals with a genetic predisposition for AD. Alcohol-related brain damage (ARBD) during a critical developmental timepoint, such as adolescence, interacts with AD-related pathologies to accelerate disease progression later in life. The current study investigates if voluntary exercise in mid-adulthood can recover memory deficits caused by the interactions between adolescence ethanol exposure and AD-transgenes.

Adolescent alcohol exposure alters age-related progression of behavioral and neurotrophic dysfunction in the TgF344-AD model in a sex-specific manner.

Alzheimer's Disease (AD) and heavy alcohol use are widely prevalent and lead to brain pathology. Both alcohol-related brain damage (ABRD) and AD result in cholinergic dysfunction, reductions in hippocampal neurogenesis, and the emergence of hippocampal-dependent cognitive impairments. It is still unknown how ARBD caused during a critical developmental timepoint, such as adolescence, interacts with AD-related pathologies to accelerate disease progression later in life.