Association between hypoglycemia and dementia in patients with type 2 diabetes

Sheen, Yi‐Jing; Sheu, Wayne H‐H

doi:10.1016/j.diabres.2016.04.004

Cited by 71 publications

(48 citation statements)

References 71 publications

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“…Compelling evidence suggests that insulin resistance and T2D worsen AD pathology and cognitive deficits (Haan, 2006; Ramos-Rodriguez et al, 2016; Saedi et al, 2016; Sena et al, 2015; Sheen and Sheu, 2016; Zilliox et al, 2016). To this end, central insulin signaling dysregulation has been demonstrated in post-mortem hippocampal and cortical samples from subjects with both mild cognitive impairment (MCI) and early AD (Talbot et al, 2012a; Watson and Craft, 2004).…”

Section: Introductionmentioning

confidence: 99%

Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer's disease

Velázquez

Tran

Ishimwe

et al. 2017

Neurobiology of Aging

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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder worldwide. While the causes of AD are not known, several risk factors have been identified. Among these, type 2 diabetes (T2D), a chronic metabolic disease, is one of the most prevalent risk factors for AD. Insulin resistance, which is associated with T2D, is defined as diminished or absent insulin signaling, and is reflected by peripheral blood hyperglycemia and impaired glucose clearance. In this study, we used complimentary approaches to probe for peripheral insulin resistance, central nervous system (CNS) insulin sensitivity and energy homeostasis in Tg2576 and 3xTg-AD mice, two widely used animal models of AD. We report that CNS insulin signaling abnormalities are evident months before peripheral insulin resistance. Additionally, we find that brain energy metabolism is differentially altered in both mouse models, with the 3xTg-AD mice showing more extensive changes. Collectively, our data suggest that early AD may reflect engagement of different signaling networks that influence CNS metabolism, which in-turn may alter peripheral insulin signaling.

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Section: Introductionmentioning

confidence: 99%

Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer's disease

Velázquez

Tran

Ishimwe

et al. 2017

Neurobiology of Aging

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show abstract

“…Evidence suggests that diabetes also affects the central nervous system, including the hippocampus, a part of the limbic system, which is associated with cognitive functions [3]. Several studies [4,5] have revealed the tight association of diabetes with cognitive impairment and dementia. It is estimated that 382 million adults had diabetes in 2013, and this number is predicted to reach 592 million in 2035 [6].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Improves Cognitive Impairment by Regulating Apoptosis and Synaptic Plasticity in Streptozotocin-Induced Diabetic Rats

Tian

Wang

et al. 2016

Cell Physiol Biochem

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Aims: To investigate the effects of resveratrol on cognitive impairment in streptozotocin (STZ)-induced diabetic rats and to explore the mechanisms of that phenomenon. Methods: Sixty healthy male Sprague Dawley rats were randomly divided into four groups: normal control group (Con group, n = 15), Res group (normal Sprague Dawley rats treated with resveratrol, n = 15), diabetes mellitus group (DM group, n = 15) and DM + Res group (diabetic rats treat with resveratrol, n = 15). Streptozotocin (STZ) was injected intraperitoneally to establish the diabetic model. One week after diabetic model induction, the animals in the Res group and the DM + Res group received resveratrol intraperitoneally once a day for consecutive 4 weeks. The Morris water maze test was applied to assess the effect of resveratrol on learning and memory. To explore the mechanisms of resveratrol on cognition, we detected the protein expression levels of Caspase-3, Bcl-2, Bax, NMDAR1 (N-Methyl-d-Aspartate receptor) and BDNF (Brain Derived Neurotrophic Factor) via western blotting analysis. Results: Resveratrol has no obvious effect on normal SD rats. Compared to Con group, cognitive ability was significantly impaired with increased expression of Caspase-3, Bax and down-regulation of Bcl-2, NMDAR1 and BDNF in diabetic rats. By contrast, resveratrol treatment improved the cognitive decline. Evidently, resveratrol treatment reversed diabetes-induced changes of protein expression. Conclusions: Resveratrol significantly ameliorates cognitive decline in STZ-induced diabetic model rats. The potential mechanism underlying the protective effect could be attributed to the inhibition of hippocampal apoptosis through the Bcl-2, Bax and Caspase-3 signaling pathways and improvement of synaptic dysfunction. BDNF may also play an indispensable role in this mechanism.

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“…Poor glycemic control is in most studies stipulated as the viscous circle of bidirectional associations between dementia and hypoglycaemia [2,5,16]. However, the effects of recurrent moderate hypoglycemia on cognitive decline and dementia remain largely uninvestigated [5].…”

Section: Introductionmentioning

confidence: 99%

“…Patients with Type 2 Diabetes Mellitus (T2DM) usually also are at increased risk for cognitive impairment and dementia [2,5]. In addition, elderly people with T2DM are more prone to develop cognitive impairment, for which several potential risk factors have been proposed.…”

Section: Introductionmentioning

confidence: 99%

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Type 3 Diabetes Reflects Disordered Lipid Metabolism in the Human Brain Related to Higher Degree of Unsaturated Fatty Acids Composition and is not Related to Body Mass Index

Ginneken¹,

Vries²,

Verheij³

et al. 2017

J Bioanal Biomed

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Association between hypoglycemia and dementia in patients with type 2 diabetes

Cited by 71 publications

References 71 publications

Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer's disease

Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer's disease

Resveratrol Improves Cognitive Impairment by Regulating Apoptosis and Synaptic Plasticity in Streptozotocin-Induced Diabetic Rats

Type 3 Diabetes Reflects Disordered Lipid Metabolism in the Human Brain Related to Higher Degree of Unsaturated Fatty Acids Composition and is not Related to Body Mass Index

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