Amyloid beta deposition is related to decreased glucose transporter-1 levels and hippocampal atrophy in brains of aged APP/PS1 mice

Hooijmans, Carlijn R.; Graven, C.; Dederen, Pieter J.; Tanila, Heikki; Groen, Thomas van; Kiliaan, Amanda J.

doi:10.1016/j.brainres.2007.08.063

Cited by 108 publications

(75 citation statements)

References 53 publications

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“…The expression of GLUT-1 protein has been found to be decreased in the brains (hippocampus, cerebral cortex) of AD Tg mice and humans (7,27). These findings are in accordance with the results of this and previous studies (38,39).…”

Section: Discussionsupporting

confidence: 92%

“…Thus, the elevated circulating metabolic parameters may be directly connected to the elevation of Aß-42 levels, possibly via inhibition of glucose utilization, glucose transport or insulin signaling (7,50). We also confirmed the results of other studies (13,16,24) that found that reductions in metabolic parameters (TC, glucose and insulin) could be elicited by treating AD Tg-mice or diabetic rats with ET or LA alone.…”

Section: Discussionmentioning

confidence: 99%

“…These phenotypes are also known to be involved in impaired cellular glucose transport activity (7), deranged expression of heat-shock proteins (8), hypercholesterolemia and hyperinsulinemia (9,10). Taken together, the results of these studies suggest that therapeutic strategies for human chronic degenerative disease can be simultaneously applied against pathogenic phenotypes of AD.…”

Section: Introductionmentioning

confidence: 92%

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The combination of exercise training and α-lipoic acid treatment has therapeutic effects on the pathogenic phenotypes of Alzheimer's disease in NSE/APPsw-transgenic mice

Cho¹

2010

Int J Mol Med

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Abstract. Exercise training was suggested as a practical therapeutic strategy for human subjects suffering from Alzheimer's disease (AD) in our previous study. Therefore, the purpose of this study was to investigate the effects of combining exercise training with the administration of antioxidants on the pathological phenotype of AD. To accomplish this, non-transgenic mice (Non-Tg) and NSE/ APPsw Tg mice were treated with ·-lipoic acid and treadmill exercised for 16 weeks, after which their brains were evaluated to determine whether any changes in the pathological phenotype-related factors occurred. The results indicated that (i) the combination-applied (COMA) Tg group with exercise training (ET) and ·-lipoic acid administration (LA) showed ameliorated spatial learning and memory compared to the sedentary (SED)-Tg and single-treatment groups; (ii) there were no differences in the level of Aß-42 peptides across groups; (iii) the level of glucose transporter-1 and brain-derived neurotrophic factor proteins were highly increased in the COMA group, (iv) ET and LA did not induce a synergistic effect on the expression of heat shock protein-70 and apoptotic proteins including Bax and caspase-3; (v) the levels of SOD-1 and CAT suppressing oxidative stress were extensively higher in the COMA than in the singletreated groups and (vi) there were no significant differences across groups regarding these serum characteristics, although these levels were lower than the SED-Tg group. Taken together, these results suggest that the combination with ET and LA may contribute to protect the neuron injury induced by Aß peptides and may be considered an effective therapeutic strategy for human subjects suffering from AD.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

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The combination of exercise training and α-lipoic acid treatment has therapeutic effects on the pathogenic phenotypes of Alzheimer's disease in NSE/APPsw-transgenic mice

Cho¹

2010

Int J Mol Med

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“…APP/PS1 transgenic mice expressing mutant human APP and PS1 genes are a useful research tool to study Aβ-related pathogenesis. There are several studies characterizing cognitive as well as noncognitive abnormality in APP/PS1 mice at 15-24 months of age (Morgan et al 2000;Arendash et al 2001;Sadowski et al 2004;Wilcock et al 2004;Hooijmans et al 2007;Minkeviciene et al 2008;Pistell et al 2008;Mei et al 2010;Ke et al 2011;Gengler et al 2012;Manczak and Reddy 2012;Wang et al 2012;Duffy and Hölscher 2013;Do et al 2014;Huang et al 2015;Janus et al 2015;Sahlholm et al 2015;Yousefi et al 2015) (A detailed summary is available in Table 2). However, the majority of experiments utilize young or adult APP/PS1 mice, which does not replicate typical hallmarks of AD, such as severe hippocampal atrophy and extensive neuronal loss (Bales 2012;Bilkei-Gorzo 2014).…”

Section: Discussionmentioning

confidence: 99%

Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice

Huang

Nie

Cao

et al. 2016

AGE

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Transgenic APPSwe/PS1dE9 (APP/PS1) mice that overproduce amyloid beta (Aβ) are extensively used in the studies of pathogenesis and experimental therapeutics and new drug screening for Alzheimer's disease (AD). However, most of the current literature uses young or adult APP/PS1 mice. In order to provide a broader view of AD-like phenotype of this animal model, in this study, we systematically analyzed behavioral and pathological profiles of 24-month-old male APP/ PS1 mice. Aged APP/PS1 mice had reference memory deficits as well as anxiety, hyperactivity, and social interaction impairment. Consistently, there was obvious deposition of amyloid plaques in the dorsal hippocampus with decreased expression of insulin-degrading enzyme, a proteolytic enzyme responsible for degradation of intracellular Aβ. Furthermore, decreases in hippocampal volume, neuronal number and synaptophysin expression, and astrocyte atrophy were also observed in aged APP/PS1 mice. This finding suggests that aged APP/PS1 mice can well replicate cognitive and noncognitive behavioral abnormalities, hippocampal atrophy, and neuronal and astrocyte degeneration in AD patients, to enable more objective and refined preclinical evaluation of therapeutic drugs and strategies for AD treatment.

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“…[39]. In another transgenic AD mice model (APP/PS1 transgenic mice) reduced levels of GLUT1 were found in the hippocampus (highest in the dentate gyrus) at age of 18 months with no differences in capillary density; while at 8 months, no differences were observed [40]. The authors concluded that the GLUT-1 amount and capillary density in both wild type and transgenic mice decreased due to ageing and that β-amyloid load in the hippocampus preceded the reduction of GLUT- …”

Section: Brain Glucose Transporters and Alzheimer's Diseasementioning

confidence: 93%

Brain glucose transporter protein 2 and sporadic Alzheimer’s disease

Šalković‐Petrišić

Riederer

2010

Translational Neuroscience

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Sporadic Alzheimer’s disease (sAD) is associated with decreased glucose/energy metabolism in the brain. The majority of glucose utilization in the brain appears to be mediated through glucose transporter protein 1 and 3 (GLUT1 and GLUT3). Deficiency of GLUT1 and GLUT3 in the brain has been found in sAD patients post mortem; however this is not unique to the disease as it is associated with different clinical syndromes as well. In line with recent findings that insulin resistant brain state precedes and may possibly cause sAD, an experimental sAD model based on the central application of the streptozotocin (STZ-icv rat model), which is a selective GLUT2 substrate, has drawn attention to the possible significance of the brain GLUT2 in sAD etiopathogenesis. Important steps in the GLUT2 and sAD interplay are reviewed and discussed. It is concluded that increased vulnerability of GLUT2 expressing neurons may be involved in development of sAD.

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Amyloid beta deposition is related to decreased glucose transporter-1 levels and hippocampal atrophy in brains of aged APP/PS1 mice

Cited by 108 publications

References 53 publications

The combination of exercise training and α-lipoic acid treatment has therapeutic effects on the pathogenic phenotypes of Alzheimer's disease in NSE/APPsw-transgenic mice

The combination of exercise training and α-lipoic acid treatment has therapeutic effects on the pathogenic phenotypes of Alzheimer's disease in NSE/APPsw-transgenic mice

Characterization of AD-like phenotype in aged APPSwe/PS1dE9 mice

Brain glucose transporter protein 2 and sporadic Alzheimer’s disease

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