Diabetes mellitus and cognitive impairments

Saedi, Elham; Gheini, Mohammad Reza; Faiz, Firoozeh; Arami, Mohammad Ali

doi:10.4239/wjd.v7.i17.412

Cited by 215 publications

(146 citation statements)

References 76 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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“…Both types of diabetes have been reported to be associated with the risk of dementia, although the odds of developing dementia remain modest again and causal-effect being not necessarily direct or independent [56]. For instance, an analysis of 28 studies showed a relative risk of dementia from insulin-dependent diabetes (IDD) of 1.7 (95% CI 1.6–1.8) which was lower for Alzheimer (1.5, 95% CI 1.4–1.7) [57].…”

Section: Discussionmentioning

confidence: 99%

Incidence and Risk Profile of Dementia in the Regions of Middle East and North Africa

et al. 2018

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Background: The risk of dementia is reported as “epidemic” and “looming” over the Middle East and North Africa (MENA) region. For this, we performed a multi-language review and feasible analysis on the incidence of dementia to offer apt conclusions. Methods: Totally, 3 databases (Magiran, Scientific Information Database, and PubMed) and 1 non-database source (Google) were searched in French, English, and Persian by using specific keywords and their combinations. All searches were independent and had no restriction for the year or type of publication. We also calculated cumulative incidence of dementia for Egypt and Israel-Palestine from relevant prevalence estimates by using standard formula. Results: Little information on incidence was available, sparing Israel (2.4/100,000/year; pre-senile). Ten (48.0%) countries had none-to-little information (of any kind) on dementia, indicating considerable awareness deficit in this region. Cumulative incidence of dementia in Egypt and Israel-Palestine was 2.7% over 20 years (55 new cases) and 14.7% (130 new cases) over 6 years, respectively. In Lebanon, cumulative incidence was 7.5% over 20 years. Data looked across dementia-related factors (i.e., fertility rate, polygamy, violence, hypovitaminosis D, diabetes, hypertension, life expectancy, age structure) did not seem to support epidemic proportions of dementia for MENA. Conclusions: MENA is youthful and dementia here is neither likely to be an epidemic nor looming over. The only possible exception might be Arab pocket in Israel. To us, previous attributions on dementia do not seem to be based on the realities of this region and, therefore, may prevent pragmatic addressal of dementia. Lastly, values-based collaborations are invited to jointly fill the awareness deficit in a unique low-cost manner.

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“…The resolution of the inflammatory process ends with an increase in the number of glial cells, microglia, and astrocytes, leading to dendritic atrophy and neuronal death (for a review see Flores, Flores-Gómez, et al, 2016), a process known as neurodegeneration (for review see Deleidi et al, 2015;Rawji et al, 2016). Accordingly, the anatomical and histological changes in the prefrontal cortex (PFC) and the hippocampus caused by chronic blood hyperglycemia lead to deficits in the cognitive process (for review see Hamed, 2017;Saedi et al, 2016), and reduced memory processing as a consequence of neurodegeneration (for review see Rojas-Gutierrez, et al, 2017).…”

Section: Animal Model In Dm S T Z-induced Hyperg Lycemia In R Atsmentioning

confidence: 99%

Consequences of diabetes mellitus on neuronal connectivity in limbic regions

Flores-Gómez

Gómez-Villalobos

Flores

2018

Synapse

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Diabetes mellitus (DM) is characterized by high levels of blood glucose. In recent years, its prevalence has increased, which was 422 million in the world in 2014. In elderly patients, DM is associated with deficits in memory and learning processes. The cognitive deficits lead to dementia. With the development of animal models in DM, it has been possible to better understand quantitative morphological changes in numerous neuronal structures belonging to the limbic system, such as the prefrontal cortex (PFC), the hippocampus and basolateral amygdala (BLA). These structures are in close relationship with processes of memory and learning. Several reports have demonstrated that chronic hyperglycemia reduces spinogenesis and dendritic arborization in the aforementioned regions along with a decline in memory and learning processes, especially in streptozotocin (STZ)‐induced diabetic rats. In the present review, we discuss animal models, the effects of chronic hyperglycemia on dendritic morphology of limbic regions and memory and learning processes, the effect on neural transmission in these regions, the pathologic mechanisms involved, and the relevance of dendritic morphology in diabetes. All of this information can help us to have a better understanding of dementia in diabetes mellitus and propose strategies for its prevention and treatment.

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Diabetes mellitus and cognitive impairments

Cited by 215 publications

References 76 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

Incidence and Risk Profile of Dementia in the Regions of Middle East and North Africa

Consequences of diabetes mellitus on neuronal connectivity in limbic regions

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