Improved cognitive-cerebral function in older adults with chromium supplementation

ArticleinNutritional Neuroscience 13(3):116-22 · June 2010with15 Reads
DOI: 10.1179/147683010X12611460764084 · Source: PubMed
Abstract
Insulin resistance is implicated in the pathophysiological changes associated with Alzheimer's disease, and pharmaceutical treatments that overcome insulin resistance improve memory function in subjects with mild cognitive impairment (MCI) and early Alzheimer's disease. Chromium (Cr) supplementation improves glucose disposal in patients with insulin resistance and diabetes. We sought to assess whether supplementation with Cr might improve memory and neural function in older adults with cognitive decline. In a placebo-controlled, double-blind trial, we randomly assigned 26 older adults to receive either chromium picolinate (CrPic) or placebo for 12 weeks. Memory and depression were assessed prior to treatment initiation and during the final week of treatment. We also performed functional magnetic resonance imaging (fMRI) scans on a subset of subjects. Although learning rate and retention were not enhanced by CrPic supplementation, we observed reduced semantic interference on learning, recall, and recognition memory tasks. In addition, fMRI indicated comparatively increased activation for the CrPic subjects in right thalamic, right temporal, right posterior parietal, and bifrontal regions. These findings suggest that supplementation with CrPic can enhance cognitive inhibitory control and cerebral function in older adults at risk for neurodegeneration.
    • "In matured cultured cerebellar granule neuronal cells, Cr(VI) was shown to induce oxidative stress that further led to apoptosis and rosmarinic acid, an antioxidant , which was shown to rescue the exposed cells from death [14]. On a positive note, Cr(III) supplementation in early Alzheimer's disease has been shown to improve cognitive function in older humans [19]. Conversely, Cr(III) is reported to act as a genotoxic agent by forming DNA adducts and induces mutation in exposed organism/cells [10, 20]. "
    [Show abstract] [Hide abstract] ABSTRACT: A number of environmental chemicals are known to cause neurotoxicity to exposed organisms. Chromium (Cr), one of the major elements in earth’s crust, is a priority environmental chemical depending on its valence state, and limited information is available on its neurotoxic potential. We, therefore, explored the neurotoxic potential of environmentally present trivalent- (Cr(III)) and hexavalent-Cr (Cr(VI)) on tested brain cell types in a genetically tractable organism Drosophila melanogaster along with its organismal response. Third instar larvae of w 1118 were fed environmentally relevant concentrations (5.0–20.0 μg/ml) of Cr(III)- or Cr(VI)-salt-mixed food for 24 and 48 h, and their exposure effects were examined in different brain cells of exposed organism. A significant reduction in the number of neuronal cells was observed in organism that were fed Cr(VI)- but not Cr(III)-salt-mixed food. Interestingly, glial cells were not affected by Cr(III) or Cr(VI) exposure. The tested cholinergic and dopaminergic neuronal cells were affected by Cr(VI) only with the later by 20.0 μg/ml Cr(VI) exposure after 48 h. The locomotor activity was significantly affected by Cr(VI) in exposed organism. Concomitantly, a significant increase in the level of reactive oxygen species (ROS) coupled with increased oxidative stress led to apoptotic cell death in the tested brain cells of Cr(VI)-exposed Drosophila, which were reversed by vitamin C supplementation. Conclusively, the present study provides evidence of environmental Cr(VI)-induced adversities on the brain of exposed Drosophila along with behavioral deficit which would likely to have relevance in humans and recommends Drosophila as a model for neurotoxicity.
    Article · May 2016
    • "Over decades, it was hypothesized that neurodegeneration in AD is mainly caused by Aβ accumulation, phosphorylated tau aggregation, and/or neuroinflammation. However, recent human and preclinical studies have provided convincing evidence that AD is a degenerative metabolic disease, which is mediated by impairments in brain insulin responsiveness, glucose utilization, and energy metabolism leading to increased oxidative stress, inflammation, and worsening of insulin resistance (Hoyer, 2002Hoyer, , 2004 Schubert et al., 2004; Rivera et al., 2005; Steen et al., 2005; Watson and Craft, 2006; Craft, 2007; Neumann et al., 2008; Krikorian et al., 2010; Luchsinger, 2010; Baker et al., 2011; Talbot et al., 2012; Butterfield et al., 2014a,b; de La Monte, 2014). The accumulating evidence that reduced glucose utilization and deficient energy metabolism occur early in the course of disease, suggests a role for impaired insulin signaling in the pathogenesis of neurodegenerative diseases. "
    [Show abstract] [Hide abstract] ABSTRACT: Alzheimer's disease (AD) is the most common form of dementia affecting elderly people. AD is a multifaceted pathology characterized by accumulation of extracellular neuritic plaques, intracellular neurofibrillary tangles (NFTs) and neuronal loss mainly in the cortex and hippocampus. AD etiology appears to be linked to a multitude of mechanisms that have not been yet completely elucidated. For long time, it was considered that insulin signaling has only peripheral actions but now it is widely accepted that insulin has neuromodulatory actions in the brain. Insulin signaling is involved in numerous brain functions including cognition and memory that are impaired in AD. Recent studies suggest that AD may be linked to brain insulin resistance and patients with diabetes have an increased risk of developing AD compared to healthy individuals. Indeed insulin resistance, increased inflammation and impaired metabolism are key pathological features of both AD and diabetes. However, the precise mechanisms involved in the development of AD in patients with diabetes are not yet fully understood. In this review we will discuss the role played by aberrant brain insulin signaling in AD. In detail, we will focus on the role of insulin signaling in the deposition of neuritic plaques and intracellular NFTs. Considering that insulin mitigates beta-amyloid deposition and phosphorylation of tau, pharmacological strategies restoring brain insulin signaling, such as intranasal delivery of insulin, could have significant therapeutic potential in AD treatment.
    Full-text · Article · Jun 2015
    • "In adults with mild cognitive impairment, chromium supplementation increased cerebral activation and enhanced performance during various learning, recall, and recognition memory tasks, independent of any changes in peripheral glucose or insulin concentration [80]. Cognitive deficits that contribute to the development and maintenance of obesity and eating disorders are especially pronounced among obese persons with co-morbid binge eating disorder [81] [82]. "
    [Show abstract] [Hide abstract] ABSTRACT: Dietary chromium supplementation for the treatment of diabetes remains controversial. The prevailing view that chromium supplementation for glucose regulation is unjustified has been based upon prior studies showing mixed, modest-sized effects in patients with type 2 diabetes (T2DM). Based on chromium's potential to improve insulin, dopamine, and serotonin function, we hypothesize that chromium has a greater glucoregulatory effect in individuals who have concurrent disturbances in dopamine and serotonin function - that is, complex patients with comorbid diabetes, depression, and binge eating. We propose, as suggested by the collective data to date, the need to go beyond the "one size fits all" approach to chromium supplementation and put forth a series of experiments designed to link physiological and neurobehavioral processes in the chromium response phenotype. Copyright © 2015. Published by Elsevier Ltd.
    Article · Mar 2015
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