Type 2 diabetes and risk of cognitive impairment and dementia

Kaiser Permanente Division of Research, Epidemiology Etiology & Prevention, 2000 Broadway, Oakland, CA 94612, USA.
Current Neurology and Neuroscience Reports (Impact Factor: 3.06). 10/2007; 7(5):373-80. DOI: 10.1007/s11910-007-0058-7
Source: PubMed


Diabetes is a major public health burden. Even a modest effect of diabetes on cognitive function has significant public health implications. Several lines of mechanistic evidence implicate a role of insulin and glucose metabolism on risk of developing dementia, including Alzheimer's disease. Population-based studies have shown that those with type 2 diabetes mellitus have an increased risk of cognitive impairment, dementia, and neurodegeneration. There are many mechanisms through which diabetes could increase risk of dementia, including glycemia, insulin resistance, oxidative stress, advanced glycation endproducts, inflammatory cytokines, and microvascular and macrovascular disease. This paper presents a review of the evidence on diabetes and increased risk of dementia and cognitive impairment, a discussion of different possible mechanisms, and remaining gaps in our knowledge.

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    • "In recent years it has been shown that the MS could affect the functioning of the CNS by inducing morphological, electrophysiological , and cognitive changes (Biessels et al., 2008; Wrighten et al., 2009). The MS has been suggested as a risk factor for Alzheimer's disease and vascular dementia, which are associated with cognitive dysfunction (Whitmer, 2007). There is also evidence of a relationship between hyperlipidemia and the increased risk of dementia (Etgen et al., 2011). "
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    ABSTRACT: A high calorie intake can induce the appearance of the metabolic syndrome (MS), which is a serious public health problem because it affects glucose levels and triglycerides in the blood. Recently, it has been suggested that MS can cause complications in the brain, since chronic hyperglycemia and insulin resistance are risk factors for triggering neuronal death by inducing a state of oxidative stress and inflammatory response that affect cognitive processes. This process, however, is not clear. In this study, we evaluated the effect of the consumption of a high-calorie diet (HCD) on both neurodegeneration and spatial memory impairment in rats. Our results demonstrated that HCD (90 day consumption) induces an alteration of the main energy metabolism markers, indicating the development of MS in rats. Moreover, an impairment of spatial memory was observed. Subsequently, the brains of these animals showed activation of an inflammatory response (increase in reactive astrocytes and interleukin1-β as well as tumor necrosis factor-α) and oxidative stress (reactive oxygen species and lipid peroxidation), causing a reduction in the number of neurons in the temporal cortex and hippocampus. Altogether, these results suggest that a HCD promotes the development of MS and contributes to the development of a neurodegenerative process and cognitive failure. In this regard, it is important to understand the relationship between MS and neuronal damage in order to prevent the onset of neurodegenerative disorders. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    Synapse 06/2015; 69(9). DOI:10.1002/syn.21832 · 2.13 Impact Factor
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    • "Our results suggest that acorns and leaves of Q. suber are endowed with molecules capable of inhibiting dietary carbohydrate digestive enzymes that might be useful for the control of glucose levels in T2DM patients. Since T2DM is considered as a significant risk factor for AD, probably due to chronic hyperglycaemia, among other factors, the potential anti-hyperglycaemic effects of the compounds present in Q. suber could also be beneficial for decreasing the risk of AD development in diabetics (Korf et al., 2006; Whitmer, 2007). "
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    ABSTRACT: This work reports the in vitro antioxidant and inhibitory activities of hexane, methanol and water extracts of cork oak (Quercus suber) against acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), α-amylase and α-glucosidase. The total content of phenolics (TPC), tannins (TTC) and flavonoids (TFC), and the HPLC profile of the main phenolic compounds present in the extracts, were also determined. In the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay the best results were obtained with the methanol and water extracts from both leaves and acorns (41–49%). In the 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) method the highest activity was observed with the methanol and leaf water extracts (63–71%). The most significant effects on cholinesterase activity were obtained with the methanol leaf extract at the concentration of 1 mg/mL, yielding inhibition values of 79 and 80% on AChE and BuChE, respectively. No relevant activity was detected against α-amylase, but samples significantly inhibited α-glucosidase from baker's yeast, and the best results were obtained with the water and methanol leaf extracts with values of 97 and 89%, respectively, higher than the positive controls used (acarbose and glucobay). The methanol leaf extract had the highest TPC (211 mg GAE/g, DW) and TFC (8.2 mg RE/g, DW), whereas the water extracts had the highest tannin levels (87 CE/g, DW). The main compound in the methanol leaf extract was gentisic acid (24.3 mg/g, DW). Our results suggest that leaves and acorns from cork oak contain compounds useful for alleviating symptoms associated with Alzheimer disease and other neurodegenerative ailments as well as diabetes.
    Industrial Crops and Products 02/2015; 64. DOI:10.1016/j.indcrop.2014.11.001 · 2.84 Impact Factor
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    • "These discrepancies may be due to differences in the cognitive stages of the T2DM patients studied. It has been hypothesized that cognitive dysfunction in T2DM patients may occur during a critical period, perhaps coinciding with the emergence of microvascular complications [1], [3], [63]. Progression of cognitive dysfunction associated with ALFF changes in the occipital lobe may also represent the transition from a compensated stage to a decompensated stage. "
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    ABSTRACT: Purpose To investigate correlations between altered spontaneous brain activity, diabetic vascular disease, and cognitive function for patients with type 2 diabetes mellitus (T2DM) using resting-state functional magnetic resonance imaging (rs-fMRI). Methods Rs-fMRI was performed for T2DM patients (n = 26) and age-, gender-, and education-matched non-diabetic control subjects (n = 26). Amplitude of low frequency fluctuations (ALFF) were computed from fMRI signals to measure spontaneous neuronal activity. Differences in the ALFF patterns between patients and controls, as well as their correlations with clinical variables, were evaluated. Results Compared with healthy controls, T2DM patients exhibited significantly decreased ALFF values mainly in the frontal and parietal lobes, the bilateral thalumi, the posterior lobe of the cerebellum, and increased ALFF values mainly in the visual cortices. Furthermore, lower ALFF values in the left subcallosal gyrus correlated with lower ankle-brachial index values (r = 0.481, p = 0.020), while lower ALFF values in the bilateral medial prefrontal gyri correlated with higher urinary albumin-creatinine ratio (r = −0.418, p = 0.047). In addition, most of the regions with increased ALFF values in the visual cortices were found to negatively correlate with MoCA scores. Conclusions These results confirm that ALFF are altered in many brain regions in T2DM patients, and this is associated with the presence of diabetic vascular disease and poor cognitive performance. These findings may provide additional insight into the neurophysiological mechanisms that mediate T2DM-related cognitive dysfunction, and may also serve as a reference for future research.
    PLoS ONE 10/2014; 9(10):e108883. DOI:10.1371/journal.pone.0108883 · 3.23 Impact Factor
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