Diabetic cognitive dysfunction: a long and strenuous way from bench to clinical

来源 :中国药理学会第十三次全国学术大会 | 被引量 : 0次 | 上传用户:deadhorse
下载到本地 , 更方便阅读
声明 : 本文档内容版权归属内容提供方 , 如果您对本文有版权争议 , 可与客服联系进行内容授权或下架
论文部分内容阅读
  Type 2 diabetes increase the risk of development of cognitive dysfunction in the elderly, in the form of shortterm memory and executive function deficits.Genetic and dietinduced models of type 2 diabetes further support this link displaying deficits in working memory, learning, and memory performance.The risk factors for diabetic cognitive dysfunction include vascular disease, hypoglycemia, hyperlipidemia, adiposity, lifestyle factors,and genetic factors.Using neuronimage technologies, diabetic patients with cognitive dysfunction shows whole brain atrophy, gray matter atrophy, hippocampal atrophy, and amygdala atrophy, increased ventricular volume and white matter volume, brain infarcts, impaired network integrity, microstructural abnormality, reduced cerebral blood flow and amplitude of lowfrequency fluctuations.The pathogenesis mechanisms of type 2 diabetes with cognitive dysfunction involve hyperglycemia, macrovascular and microvascular diseases, insulin resistance, inflammation, apoptosis, impaired neurogenesis, impaired bloodbrain barrier, and disorder neurotransmitters.Some antidiabetic drugs and Traditional Chinese Medicine partly improve diabetic cognitive dysfunction, but more clinical investigations are demanded to verify their efficiencies and novel drugs are urgent need to develop.Large clinical studies will provide further evidences of risks factors and biomarkers for diabetic cognitive dysfunction.Both novel disease animal models and advanced neuronimage technologies will help to investigate the exact pathogenesis mechanisms and to develop better therapeutic interventions and treatment.
其他文献
Background and Aim Vascular smooth muscle cell (SMC) phenotype change is a hallmark of vascular remodeling, which can be regulated via MicroRNAs (miRNAs)dependent mechanism.We recently identified Asym
TP53, encoding a wellknown tumor suppressor p53, plays essential roles in tumor initiation and progression, and is frequently mutated in lung cancer.However, pharmacological stabilization and reactiva
Aim It is well known that menopause could worsen agerelated ventricular concentric remodeling and increased incidence of arrhythmias following estrogen (E2) deficiency.However, the underlying mechanis
Aim Autosomal dominant polycystic kidney disease (ADPKD) affects between 1 in 400 to 1000 individuals and is characterized by massive enlargement of fluidfilled cysts of renal tubular origin that comp
Progressive beta cell apoptosis is a major cause leading to a decline in beta cell mass in type 2 diabetes.While it has been discovered that mitochondrial protein Sirtuin 5 (SIRT5) functions as the pr
Currently, accumulating studies indicated that upregulation of glycogen synthase kinase3β (GSK3β)played an important role in depression pathogenesis.Our previous study demonstrated that ammoxetine, a
Aim Aging is the dominant risk factor for cardiovascular disease.Recently, we have shown that genomic instability, a causative mechanism of aging in general, induced by functional mutation of the ERCC
会议
Aim DL08052 is a novel Rhokinases inhibitor which has been found to have potent cardiovascular effects.In the present research, we aimed to study the potential of DL08052 in the treatment of pulmonary
Danshen has been used in stroke treatment for thousands of years in China.However, the underlying mechanism still remains elusive.Neuron loss is the cardinal feature of stroke.Stimulating endogenous n
P2X7 receptor (P2X7r) is important in inflammation and fibrosis.The aim of the present study was to investigate the effect of P2X7r inhibition, using a specific inhibitor (A438079) to prevent the deve