Impaired Insulin Signaling and Mechanisms of Memory Loss

被引:45
作者
Bloemer, Jenna [1 ]
Bhattacharya, Subhrajit [1 ]
Amin, Rajesh [1 ]
Suppiramaniam, Vishnu [1 ]
机构
[1] Auburn Univ, Dept Pharmacal Sci, Harrison Sch Pharm, Auburn, AL 36849 USA
来源
GLUCOSE HOMEOSTATIS AND THE PATHOGENESIS OF DIABETES MELLITUS | 2014年 / 121卷
关键词
BLOOD-BRAIN-BARRIER; GROWTH-FACTOR-I; LONG-TERM POTENTIATION; AMYLOID-BETA-PEPTIDE; HIPPOCAMPAL SYNAPTIC PLASTICITY; CENTRAL-NERVOUS-SYSTEM; FACTOR-KAPPA-B; STREPTOZOTOCIN-DIABETIC RATS; CEREBRAL GLUCOSE-METABOLISM; GLYCATION END-PRODUCTS;
D O I
10.1016/B978-0-12-800101-1.00013-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Insulin is secreted from the beta-cells of the pancreas and helps maintain glucose homeostasis. Although secreted peripherally, insulin also plays a profound role in cognitive function. Increasing evidence suggests that insulin signaling in the brain is necessary to maintain health of neuronal cells, promote learning and memory, decrease oxidative stress, and ultimately increase neuronal survival. This chapter summarizes the different facets of insulin signaling necessary for learning and memory and additionally explores the association between cognitive impairment and central insulin resistance. The role of impaired insulin signaling in the advancement of cognitive dysfunction is relevant to the current debate of whether the shared pathophysiological mechanisms between diabetes and cognitive impairment implicate a direct relationship. Here, we summarize a vast amount of literature that suggests a strong association between impaired brain insulin signaling and cognitive impairment.
引用
收藏
页码:413 / 449
页数:37
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