Non-Pharmacological Therapeutic Options for the Treatment of Alzheimer's Disease.

Alzheimer's disease is a growing global crisis in need of urgent diagnostic and therapeutic strategies. The current treatment strategy mostly involves immunotherapeutic medications that have had little success in halting disease progress. Hypotheses for pathogenesis and development of AD have been expanded to implicate both organ systems as well as cellular reactions. Non-pharmacologic interventions ranging from minimally to deeply invasive have attempted to address these diverse contributors to AD. In this review, we aim to delineate mechanisms underlying such interventions while attempting to provide explanatory links between the observed differences in disease states and postulated metabolic or structural mechanisms of change. The techniques discussed are not an exhaustive list of non-pharmacological interventions against AD but provide a foundation to facilitate a deeper understanding of the area of study.

Prehabilitation programs - a systematic review of the economic evidence.

Introduction: Prehabilitation, which involves improving a patient's physical and psychological condition before surgery, has shown potential benefits but has yet to be extensively studied from an economic perspective. To address this gap, a systematic review was conducted to summarize existing economic evaluations of prehabilitation interventions. Methods: The PRISMA Protocols 2015 checklist was followed. Over 16,000 manuscripts were reviewed, and 99 reports on preoperative interventions and screening tests were identified, of which 12 studies were included in this analysis. The costs are expressed in Pounds (GBP, £) and adjusted for inflation to December 2022. Results: The studies were conducted in Western countries, focusing on specific surgical subspecialties. While the interventions and study designs varied, most studies demonstrated cost savings in the intervention group compared to the control group. Additionally, all cost-effectiveness analysis studies favored the intervention group. However, the review also identified several limitations. Many studies had a moderate or high risk of bias, and critical information such as time horizons and discount rates were often missing. Important components like heterogeneity, distributional effects, and uncertainty were frequently lacking as well. The misclassification of economic evaluation types highlighted a lack of knowledge among physicians in prehabilitation research. Conclusion: This review reveals a lack of robust evidence regarding the economics of prehabilitation programs for surgical patients. This suggests a need for further research with rigorous methods and accurate definitions.

Fecal Microbiota Transplantation Reduces Pathology and Improves Cognition in a Mouse Model of Alzheimer's Disease.

Characterized by the presence of amyloid plaques, neurofibrillary tangles and neuroinflammation, Alzheimer's disease (AD) is a progressive neurodegenerative disorder with no known treatment or cure. Global disease projections warrant an urgent and rapid therapeutic for the treatment of this devastating disease. Fecal microbiota transplantation (FMT) is a widely accepted and safely used treatment for recurrent Clostridium difficile infection and other metabolic diseases such as diabetes mellitus. FMT has also been demonstrated to be a possible AD therapeutic. We examined the potential of FMT for the treatment of AD in a robust, mouse model of the disease and report that a brief, 7-day treatment regimen demonstrated 'plaque-busting' and behavior-modifying effects in treated 5xFAD mice. Importantly, we show that donor age plays an important role in the efficacy of the treatment and these findings warrant further investigation in human trials.

Cyclical amyloid beta-astrocyte activity induces oxidative stress in Alzheimer's disease.

Glial cell involvement in Alzheimer's disease (AD) is multi-faceted. The role of astrocytes in AD pathology, both as a causative agent of amyloid-beta (Aß) production as well as a casualty of dysfunction resulting from the presence of Aß has been well-delineated. In this review, we explore the influence of oxidative stress in astrocytes and the subsequent effect on Aß levels in the brain from a perspective of intracellular calcium homeostasis and NADPH oxidase activity. The response of astrocytes to the presence of Aß, as well astrocytic and microglial interaction and inflammatory cytokine release is also discussed, highlighting a cyclical behaviour of these cells in contributing to AD pathogenesis.