Intracerebral Hemorrhage and Diabetes Mellitus: Blood-Brain Barrier Disruption, Pathophysiology, and Cognitive Impairments

被引:21
作者
Bahadar, Ghaith A. [1 ]
Shah, Zahoor A. [1 ]
机构
[1] Univ Toledo, Coll Pharm & Pharmaceut Sci, Dept Med & Biol Chem, Toledo, OH 43614 USA
基金
美国国家卫生研究院;
关键词
ICH; DM; blood-brain barrier; neuroinflammation; oxidative stress; brain edema; peripheral leukocytes; HMGB1; cognitive impairment; BDNF; TOLL-LIKE RECEPTOR; GLYCATION END-PRODUCTS; NF-KAPPA-B; INDUCED OXIDATIVE STRESS; HIPPOCAMPAL NEUROGENESIS; LYMPHOCYTE RATIO; FUNCTIONAL RECOVERY; ALZHEIMERS-DISEASE; NLRP3; INFLAMMASOME; NEUTROPHIL COUNT;
D O I
10.2174/1871527320666210223145112
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
There is a surge in diabetes incidence, with an estimated 463 million individuals been diagnosed worldwide. Diabetes Mellitus (DM) is a major stroke-related comorbid condition that increases the susceptibility of disabling post-stroke outcomes. Although less common, intracerebral hemorrhage (ICH) is the most dramatic subtype of stroke associated with higher mortality, particularly in the DM population. Previous studies have focused mainly on the impact of DM on ischemic stroke. Few studies have focused on the impact of DM on ICH and discussed the blood-brain barrier disruption, brain edema, and hematoma formation. However, more recently, investigating the role of oxidative damage and Reactive Oxygen Species (ROS) production in preclinical studies involving DM-ICH animal models has gained attention. But, little is known about the correlation between neuroinflammatory processes, glial cells activation, and peripheral immune cell invasion with DM-ICH injury. DM and ICH patients experience impaired abilities in multiple cognitive domains by relatively comparable mechanisms, which could get exacerbated in the setting of comorbidities. In this review, we discuss both the pathology of DM as a comorbid condition for ICH and the potential molecular therapeutic targets for the clinical management of the ICH and its recovery.
引用
收藏
页码:312 / 326
页数:15
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