7
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Increased Aluminum Content in Certain Brain Structures is Correlated with Higher Silicon Concentration in Alcoholic Use Disorder

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Introduction: Alcohol overuse may be related to increased aluminum (Al) exposure, the brain accumulation of which contributes to dementia. However, some reports indicate that silicon (Si) may have a protective role over Al-induced toxicity. Still, no study has ever explored the brain content of Al and Si in alcoholic use disorder (AUD). Materials and methods: To fill this gap, the present study employed inductively coupled plasma optical emission spectrometry to investigate levels of Al and Si in 10 brain regions and in the liver of AUD patients ( n = 31) and control ( n = 32) post-mortem. Results: Al content was detected only in AUD patients at mean ± SD total brain content of 1.59 ± 1.19 mg/kg, with the highest levels in the thalamus (4.05 ± 12.7 mg/kg, FTH), inferior longitudinal fasciculus (3.48 ± 9.67 mg/kg, ILF), insula (2.41 ± 4.10 mg/kg) and superior longitudinal fasciculus (1.08 ± 2.30 mg/kg). Si content displayed no difference between AUD and control, except for FTH. Positive inter-region correlations between the content of both elements were identified in the cingulate cortex, hippocampus, and ILF. Conclusions: The findings of this study suggest that AUD patients may potentially be prone to Al-induced neurodegeneration in their brain—although this hypothesis requires further exploration.

          Related collections

          Most cited references54

          • Record: found
          • Abstract: found
          • Article: not found

          Aluminium as a risk factor in Alzheimer's disease, with emphasis on drinking water.

          Aluminium (Al) is clearly a powerful neurotoxicant. Considerable evidence exists that Al may play a role in the aetiology or pathogenesis of Alzheimer's disease (AD), but whether the link is causal is still open to debate. This paper reviews the epidemiological evidence linking Al and AD. Nine out of 13 published epidemiological studies of Al in drinking water and AD have shown statistically significant positive relations. Given the difficulty in producing high-quality data for the occurrence of AD and also for Al exposure, with the resulting unavoidable misclassification errors biasing any true association towards the null value, these studies are remarkably consistent. A major problem in their interpretation is that drinking water, even at high Al concentrations, only contributes a fraction of the total dietary intake of Al. In particular, regular consumers of antacids ingest gram amounts of Al daily, thousands of times the amounts taken in through drinking water, and epidemiological studies of antacid exposure and AD have been largely negative. However, Al is very poorly absorbed in the gastrointestinal tract, and the possibility that some Al fractions present in drinking water may be particularly bioavailable cannot be dismissed at present. The combined evidence linking Al and AD warrants substantial research efforts. Such efforts should focus on clarification of the cellular and molecular mechanisms in Al toxicity and of the basic metabolism and kinetics of Al in the human body, and on further epidemiological studies including diverse routes of Al exposure and also variables that are known or suspected to influence the individuals' susceptibility to AD, such as apolipoprotein E allele status and family history of AD.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Aluminum: impacts and disease.

            Aluminum is the most widely distributed metal in the environment and is extensively used in modern daily life. Aluminum enters into the body from the environment and from diet and medication. However, there is no known physiological role for aluminum within the body and hence this metal may produce adverse physiological effects. The impact of aluminum on neural tissues is well reported but studies on extraneural tissues are not well summarized. In this review, the impacts of aluminum on humans and its impact on major physiological systems are summarized and discussed. The neuropathologies associated with high brain aluminum levels, including structural, biochemical, and neurobehavioral changes, have been summarized. In addition, the impact of aluminum on the musculoskeletal system, respiratory system, cardiovascular system, hepatobiliary system, endocrine system, urinary system, and reproductive system are discussed.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Human exposure to aluminium.

              Human activities have circumvented the efficient geochemical cycling of aluminium within the lithosphere and therewith opened a door, which was previously only ajar, onto the biotic cycle to instigate and promote the accumulation of aluminium in biota and especially humans. Neither these relatively recent activities nor the entry of aluminium into the living cycle are showing any signs of abating and it is thus now imperative that we understand as fully as possible how humans are exposed to aluminium and the future consequences of a burgeoning exposure and body burden. The aluminium age is upon us and there is now an urgent need to understand how to live safely and effectively with aluminium.
                Bookmark

                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Molecules
                Molecules
                molecules
                Molecules
                MDPI
                1420-3049
                03 May 2019
                May 2019
                : 24
                : 9
                : 1721
                Affiliations
                [1 ]Department of Anatomy, Medical University of Lublin, Jaczewskiego 4, 20-090 Lublin, Poland; jacek.baj@ 123456me.com (J.B.); maciejewski.r@ 123456gmail.com (R.M.)
                [2 ]Department of Neurosurgery and Pediatric Neurosurgery, Medical University of Lublin, Jaczewskiego 8, 20-954 Lublin, Poland; jakub.litak@ 123456gmail.com (J.L.); apodkowinski@ 123456wp.pl (A.P.)
                [3 ]Department of Analytical Chemistry, Medical University of Lublin, Chodźki 4a, 20-093 Lublin, Poland; bayrena@ 123456o2.pl (E.B.); jolanta.flieger@ 123456umlub.pl (J.F.)
                [4 ]Department of Clinical Genetics, Medical University of Lublin, Radziwiłłowska 11, 20-080 Lublin, Poland; jacekbogucki@ 123456wp.pl
                [5 ]Faculty of Chemistry, Department of Analytical Chemistry, Adam Mickiewicz University in Poznań, 89B Umultowska Street, 61-614 Poznan, Poland; jed.proch@ 123456gmail.com (J.P.); pnied@ 123456amu.edu.pl (P.N.)
                [6 ]Department of Forensic Medicine, Medical University of Lublin, 8b Jaczewskiego St, 20-090 Lublin, Poland; mierzwinska.aa@ 123456gmail.com (A.M.); grzegorz.teresinski@ 123456umlub.pl (G.T.)
                [7 ]Department of Environmental Medicine, Poznan University of Medical Sciences, 61-701 Poznan, Poland; rzymskipiotr@ 123456ump.edu.pl
                Author notes
                [* ]Correspondence: cezary.grochowski@ 123456o2.pl ; Tel.: +48-81448-6020
                Author information
                https://orcid.org/0000-0002-2938-885X
                https://orcid.org/0000-0003-0023-044X
                https://orcid.org/0000-0002-1372-8987
                https://orcid.org/0000-0001-6881-3161
                https://orcid.org/0000-0002-4184-9305
                https://orcid.org/0000-0002-4713-0801
                Article
                molecules-24-01721
                10.3390/molecules24091721
                6539762
                31058813
                ab486597-fe90-488e-912f-1fc38279c773
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 08 April 2019
                : 01 May 2019
                Categories
                Article

                aluminum,silicon,icp-oes,trace elements,brain trace element concentration,brain toxicity

                Comments

                Comment on this article