期刊
MEDICAL SCIENCE MONITOR BASIC RESEARCH
卷 20, 期 -, 页码 118-129出版社
INT SCIENTIFIC LITERATURE, INC
DOI: 10.12659/MSMBR.891278
关键词
Nitric Oxide; Diabetes Mellitus; Type 2; Free Radicals; Endothelial Cells; Etiology; Alzheimer Disease
资金
- National Natural Scientific Foundation of China (NSFC) [30901397, 81271242, 81371248]
- Nanjing Municipal Outstanding Young Scientist Grant in Medical Science Development [JQX12009]
- MitoGenetics, Corp (Sioux Falls, South Dakota)
The endothelium performs a crucial role in maintaining vascular integrity leading to whole organ metabolic homeostasis. Endothelial dysfunction represents a key etiological factor leading to moderate to severe vasculopathies observed in both Type 2 diabetic and Alzheimer's Disease (AD) patients. Accordingly, evidence-based epidemiological factors support a compelling hypothesis stating that metabolic rundown encountered in Type 2 diabetes engenders severe cerebral vascular insufficiencies that are causally linked to long term neural degenerative processes in AD. Of mechanistic importance, Type 2 diabetes engenders an immunologically mediated chronic pro-inflammatory state involving interactive deleterious effects of leukocyte-derived cytokines and endothelial-derived chemotactic agents leading to vascular and whole organ dysfunction. The long term negative consequences of vascular pro-inflammatory processes on the integrity of CNS basal forebrain neuronal populations mediating complex cognitive functions establish a striking temporal comorbidity of AD with Type 2 diabetes. Extensive biomedical evidence supports the pivotal multi-functional role of constitutive nitric oxide (NO) production and release as a critical vasodilatory, anti-inflammatory, and anti-oxidant, mechanism within the vascular endothelium. Within this context, we currently review the functional contributions of dysregulated endothelial NO expression to the etiology and persistence of Type 2 diabetes-related and co morbid ADrelated vasculopathies. Additionally, we provide up-to-date perspectives on critical areas of AD research with special reference to common NO-related etiological factors linking Type 2 diabetes to the pathogenesis of AD.
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