Cargando…

Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford

(1) Introduction: Human exposure to aluminium is a burgeoning problem. In 1988, the population of the Cornish town of Camelford was exposed to exceedingly high levels of aluminium in their potable water supply. Herein we provide evidence that aluminium played a role in the death of a Camelford resid...

Descripción completa

Detalles Bibliográficos
Autores principales: Mold, Matthew, Cottle, Jason, Exley, Christopher
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6616903/
https://www.ncbi.nlm.nih.gov/pubmed/31208130
http://dx.doi.org/10.3390/ijerph16122129
_version_ 1783433568648691712
author Mold, Matthew
Cottle, Jason
Exley, Christopher
author_facet Mold, Matthew
Cottle, Jason
Exley, Christopher
author_sort Mold, Matthew
collection PubMed
description (1) Introduction: Human exposure to aluminium is a burgeoning problem. In 1988, the population of the Cornish town of Camelford was exposed to exceedingly high levels of aluminium in their potable water supply. Herein we provide evidence that aluminium played a role in the death of a Camelford resident following development of late-onset epilepsy. (2) Case summary: We have measured the aluminium content of brain tissue in this individual and demonstrated significant accumulations of aluminium in the hippocampus (4.35 (2.80) µg/g dry wt.) and the occipital lobe (2.22 (2.23) µg/g dry wt., mean, SD, n = 5), the latter being associated with abnormal calcifications. Aluminium-specific fluorescence microscopy confirmed the presence of aluminium in both of these tissues and made the consistent observation of aluminium-loaded glial cells in close proximity to aluminium-rich cell/neuronal debris. These observations support an inflammatory component in this case of late-onset epilepsy. Congo red failed to identify any amyloid deposits in any tissue while thioflavin S showed extensive extracellular and intracellular tau pathologies. (3) Discussion: We present the first data showing aluminium in brain tissue in epilepsy and suggest, in light of complementary evidence from scientific literature, the first evidence that aluminium played a role in the advent of this case of late-onset adult epilepsy.
format Online
Article
Text
id pubmed-6616903
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-66169032019-07-18 Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford Mold, Matthew Cottle, Jason Exley, Christopher Int J Environ Res Public Health Case Report (1) Introduction: Human exposure to aluminium is a burgeoning problem. In 1988, the population of the Cornish town of Camelford was exposed to exceedingly high levels of aluminium in their potable water supply. Herein we provide evidence that aluminium played a role in the death of a Camelford resident following development of late-onset epilepsy. (2) Case summary: We have measured the aluminium content of brain tissue in this individual and demonstrated significant accumulations of aluminium in the hippocampus (4.35 (2.80) µg/g dry wt.) and the occipital lobe (2.22 (2.23) µg/g dry wt., mean, SD, n = 5), the latter being associated with abnormal calcifications. Aluminium-specific fluorescence microscopy confirmed the presence of aluminium in both of these tissues and made the consistent observation of aluminium-loaded glial cells in close proximity to aluminium-rich cell/neuronal debris. These observations support an inflammatory component in this case of late-onset epilepsy. Congo red failed to identify any amyloid deposits in any tissue while thioflavin S showed extensive extracellular and intracellular tau pathologies. (3) Discussion: We present the first data showing aluminium in brain tissue in epilepsy and suggest, in light of complementary evidence from scientific literature, the first evidence that aluminium played a role in the advent of this case of late-onset adult epilepsy. MDPI 2019-06-16 2019-06 /pmc/articles/PMC6616903/ /pubmed/31208130 http://dx.doi.org/10.3390/ijerph16122129 Text en © 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/).
spellingShingle Case Report
Mold, Matthew
Cottle, Jason
Exley, Christopher
Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford
title Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford
title_full Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford
title_fullStr Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford
title_full_unstemmed Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford
title_short Aluminium in Brain Tissue in Epilepsy: A Case Report from Camelford
title_sort aluminium in brain tissue in epilepsy: a case report from camelford
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6616903/
https://www.ncbi.nlm.nih.gov/pubmed/31208130
http://dx.doi.org/10.3390/ijerph16122129
work_keys_str_mv AT moldmatthew aluminiuminbraintissueinepilepsyacasereportfromcamelford
AT cottlejason aluminiuminbraintissueinepilepsyacasereportfromcamelford
AT exleychristopher aluminiuminbraintissueinepilepsyacasereportfromcamelford