Aducanumab for the treatment of Alzheimer's disease: a systematic review.

Aducanumab is a novel disease-modifying anti-amyloid-beta (Aß) human monoclonal antibody specifically targeted to the pathophysiology of Alzheimer's disease (AD). It was granted for treating AD in June 2021 by the United States Food and Drug Administration. We systematically analyzed available trials to evaluate the efficacy and safety of aducanumab treating AD. We followed the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analysis) guidelines. We conducted an extensive literature search using the electronic databases MEDLINE through PubMed, EMBASE, Cochrane, Web of Science, and Scopus for suitable studies on aducanumab. We considered human clinical trials of aducanumab, assessing its efficacy and adverse effects in treating AD, excluding any experimental animal studies. We included three randomised controlled trials. Studies reported that aducanumab reduced brain amyloid-beta plaques in a time- and dose-dependent manner (dose-response, P < 0.05) and a slowed decline in cognition (22% reduction) in the high-dose treated group, difference of -0.39 versus placebo in Clinical Dementia Rating Scale Sum Boxes (95% CI, -0.69 to -0.09; P = 0.012) along with a reduced amyloid positron emission tomography standard uptake value ratio score (P < 0.001) and plasma p181-tau (phosphorylated tau) level. Amyloid-related imaging abnormality was reported as a serious adverse event and was profound in high-dose treated group (425/1029 in 10 mg/kg). Aducanumab has been reported to affect two main pathophysiologic hallmarks (Aß and tau) of AD. We suggest future studies addressing aducanumab's efficacy and safety to confirm that the benefit of this drug outweighs the risk.

Empagliflozin Ameliorates Progression From Prediabetes to Diabetes and Improves Hepatic Lipid Metabolism: A Systematic Review.

Diabetes mellitus (DM) and hepatic steatosis are two of the most common metabolic syndromes that affect the health of people globally. Empagliflozin (EMPA) is a promising drug of choice for the diabetic population. Recent studies have shown its beneficial effects not only on diabetic patients but also on patients suffering from cardiac, hepatic, neurological, or pancreatic anomalies. In this paper, we systematically searched electronic databases to compile literature that focuses on EMPA's effect on the prediabetic population, diabetic population, and hepatic lipid metabolism. We focus on the mechanism of EMPA, specifically by which it increases insulin sensitivity and fat browning and reduces fat accumulation. Overall, we hypothesized that by its effect on weight loss and reducing inflammatory markers and insulin resistance (IR), EMPA decreases the rate of prediabetes to diabetes conversion. We concluded that by improving hepatic and serum triglyceride, decreasing visceral fat, and its positive impact on hepatic steatosis, the drug improves hepatic lipid metabolism. Further research should be done on this matter.