RESUMO
Obesity and cognitive decline including dementia and Alzheimer's Disease (AD) affect millions worldwide. Several studies have shown that obese individuals suffer from cognitive decline. Here, we suggest that adiponectin and leptin, protein hormones secreted by white adipose tissue explain the relationship between obesity and cognitive decline. We systematically searched PubMed and World Health Organization (WHO) websites with the keywords obesity and dementia and compiled literature that explains how adiponectin and leptin impact obesity and cognitive decline. Full-text, free-access articles on PubMed published after 2009 have been included. Whereas articles published before 2009, books, and reports were excluded. We concentrated on mechanisms via which adiponectin and leptin affect energy expenditure, fatty acid catabolism, satiety, hunger, Body Mass Index (BMI), neurogenesis, and brain structures that lead to the development of cognitive dysfunction. Moreover, we hypothesized that adiponectin and leptin hormones explain how obesity and dementia are connected. After compiling the research studies, we summarized that adiponectin and leptin negatively correlate to BMI. Adiponectin arbitrates energy expenditure and fatty acid catabolism to prevent obesity. In the presence of adiponectin, hippocampal cells proliferate, whereas neurogenesis is reduced in its absence. However, leptin prevents obesity by promoting satiety, reducing hunger, and increasing insulin sensitivity. It also has neuroprotective effects thus reducing the risk of developing cognitive decline. So, physical exercise, diet alteration, weight reduction, adiponectin, and leptin supplementation should be carried out to protect against obesity-induced cognitive decline. Therefore, further research studies should be done in this area.
RESUMO
Stroke is found to be one of the global top causes of mortality and the major factor in years of life with a handicap (DALYs). Ischemic strokes contributed to nearly 70% of all strokes worldwide. For endovascular thrombectomy in acute ischemic stroke with large vessel obstruction (AIS-LVO), using stent retrievers and/or reperfusion catheters has become the gold standard of therapy. The methodology involved keyword-based search in databases like PubMed, Embase, and Google Scholar for recent publications on mechanical thrombectomy (MT), AIS, large vessel occlusion (Large Vessel Occlusion (LVO)), screening relevant articles, retrieving full texts, and synthesizing key findings on procedural advancements, patient selection, COVID-19 (coronavirus disease 2019) impact, delay effects, effectiveness, clinical outcomes, and future perspectives. Only people with substantial cerebral artery obstruction may do well from MT. This includes the distal carotid artery and the proximal middle cerebral artery (segment M1). The size of a blocked vessel and NIHSS (National Institute of Health Stroke Scale) score are directly connected. Both the 2018 and 2019 versions of the AHA/ASA (American Heart Association/American Stroke Association) Guidelines for the Early Management of Patients with Acute Ischemic Stroke contained the recommendations that cases with AIS-LVO get endovascular therapy when administered during the time frame of 0-6 h after onset (Grade IA evidence). It is questionable whether this group of patients can be managed without the need for intravenous tissue plasminogen activator at the onset. When functional independence [modified Rankin Scale (mRS) score 2] was present at long-term follow-up, the endovascular intervention was favored. Tenecteplase, which differs from alteplase in terms of genetic variation, has a greater half-life and a higher level of fibrin selectivity, enabling bolus infusion. Studies have also demonstrated its efficacy and safety, as well as its long-term cost-effectiveness.