Burden of Cardiometabolic Risk Factors on Cerebrovascular Events in a Southern Italian Population

Background: Stroke is the second leading cause of death in the world and the third due to disability. However, there are few data available that identify the risk factors associated with it and their weight in different populations (population risk). Aim: Contribute to the knowledge of burden risk factors in stroke in a large cohort of Southern Italy. Methods: The data refer to a randomized Campania cohort of 1200 subjects (35 - 74 years) enrolled in 2008-09. Ten years later (2018-19) they were re-evaluated. We analyzed data from 32 patients who reported a cerebrovascular event (stroke or TIA) with the event-free group of subjects (804 subjects: 378 men and 426 women). We evaluated: absolute risk, Odds Ratio (OR), Additional Risk (AR), Risk Attributable to the Population (PAR) and, finally, the Population Attributable risk Fraction (FAP). Results: In the comparison between the two groups (patients with events and patients without events) the risk factors with statistically significant differences were: age, Systolic Blood Pressure (SBP), BMI, cholesterol, triglycerides, glycemia and hyperinsulinemia. The ORs with the greatest impact were: blood glucose (5.1), BMI (3.3) and BPS (2.9). Linear regression analysis identified Glycemia and BMI as the only independent variables. The FAPs with the greatest impact were SBP (47.4%) and BMI (42.6%). Discussion and Conclusions: Our data confirm that the high incidence of stroke in Campania is particularly related to the high prevalence of obesity and hypertension. In the single patient, however, the risk factors with the greatest impact are: glycaemia BMI an SBP.

Buyanghuanwu decoction promotes angiogenesis after cerebral ischemia/reperfusion injury：mechanisms of brain tissue repair

Buyanghuanwu decoction has been shown to protect against cerebral ischemia/reperfusion injury,but the underlying mechanisms remain unclear.In this study,rats were intragastrically given Buyanghuanwu decoction,15 m L/kg,for 3 days.A rat model of cerebral ischemia/reperfusion injury was established by middle cerebral artery occlusion.In rats administered Buyanghuanwu decoction,infarct volume was reduced,serum vascular endothelial growth factor and integrin αvβ3 levels were increased,and brain tissue vascular endothelial growth factor and CD34 expression levels were increased compared with untreated animals.These effects of Buyanghuanwu decoction were partially suppressed by an angiogenesis inhibitor（administered through the lateral ventricle for 7 consecutive days）.These data suggest that Buyanghuanwu decoction promotes angiogenesis,improves cerebral circulation,and enhances brain tissue repair after cerebral ischemia/reperfusion injury.

S-adenosylmethionine Administration Attenuates Low Brain-Derived Neurotrophic Factor Expression Induced by Chronic Cerebrovascular Hypoperfusion or Beta Amyloid Treatment

Chronic cerebrovascular hypoperfusion is a high-risk factor for Alzheimer＇s disease（AD） as it is conducive to beta amyloid（Ab） over-production. Brainderived neurotrophic factor（BDNF） is a member of the neurotrophin family widely expressed in the central nervous system. The structure of the rat BDNF gene is complex, consisting of eight non-coding exons（I–VIII） and one coding exon（IX）. The BDNF gene is transcribed from multiple promoters located upstream of different 50 noncoding exons to produce a heterogeneous population of BDNF m RNAs. S-adenosylmethionine（SAM） produced in the methionine cycle is the primary methyl donor and the precursor of glutathione. In this study, a cerebrovascular hypoperfusion rat model and an Ab intrahippocampal injection rat model were used to explore the expression profiles of all BDNF transcripts in the hippocampus with chronic cerebrovascular hypoperfusion or Ab injection as well as with SAM treatment. We found that the BDNF m RNAs and protein were down-regulated in the hippocampus undergoing chronic cerebrovascular hypoperfusion as well as Ab treatment, and BDNF exons IV and VI played key roles. SAM improved the low BDNF expression following these insults mainly through exons IV and VI.These results suggest that SAM plays a neuroprotective role by increasing the expression of endogenous BDNF and could be a potential target for AD therapy.