Connections between Multiple Chemical Sensitivity (MCS) and Mechanisms of Neurodegenerative Diseases – Hints and References from Scientific Literature
Main Article Content
Abstract
This review focuses on pathologic mechanisms of neurodegenerative diseases and Multiple Chemical Sensitivity (MCS) in order to find out common properties that give hints to their common origin and mechanisms. Many epidemiologic studies already have proven that both, MCS and neurodegenerative diseases, especially Alzheimer’s and Parkinson’s Disease, are initiated by exposure to environmental chemicals. The mechanisms following these exposures show similar properties. They are initiated by binding to and activation of receptors located at cells of the brain immune system and at neurons, mainly the so called “transient receptor potential receptors” (TRP-receptors). As a consequence, the activation of N-methyl-D-aspartat-receptors (NMDA-receptors) in the Central Nervous System (CNS) plays a central role in the expression of neurotoxic mechanisms such as excitotoxicity, apoptose (programmed cell death) and chronic inflammation in the brain. The inflammation in brain is mainly performed by activated astrocytes and gliacells that are part of the inborn immune system. Under normal conditions these cells support the functions of neurons in the brain. Under pathologic conditions caused by different environmental chemicals these cells are activated and turn into a pathogenic state that supports inflammation. They then secrete cytokines as signal molecules that activate different inflammation mechanisms, leading to production of oxygen radicals (“oxidative stress”) and peroxynitrite (“nitrosative stress”). These pathogenic mechanisms constitute self enhancing vicious cycles that cause a risk of proceeding neurodegeneration. There are hints that some of these mechanisms also have been proven for Multiple Chemical Sensitivity (MCS).
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HILL, Hans-Ulrich; HUBER, Wolfgang.
Connections between Multiple Chemical Sensitivity (MCS) and Mechanisms of Neurodegenerative Diseases – Hints and References from Scientific Literature.
Medical Research Archives, [S.l.], v. 13, n. 5, may 2025.
ISSN 2375-1924.
Available at: <https://esmed.org/MRA/mra/article/view/6463>. Date accessed: 21 june 2025.
doi: https://doi.org/10.18103/mra.v13i5.6463.
Section
Review Articles
The Medical Research Archives grants authors the right to publish and reproduce the unrevised contribution in whole or in part at any time and in any form for any scholarly non-commercial purpose with the condition that all publications of the contribution include a full citation to the journal as published by the Medical Research Archives.
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9. Asherio A, Honglei C, Weisskopf MG, et al. Pesticide exposure and risk for Parkinson’s disease. Ann Neurol 2006;60(2):197-203
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12. Betarbet R, Sherer TB, MacKenzie G, Garcia-Osuna M, Panov AV, Greenamyre JT. Chronic systemic pesticide exposure reproduces features of Parkinson’s disease. 2012; Nat Neurosci. 2012;2000(3):1301–1306.
13. Moretto A, Colosio C. Biochemical and toxicological evidence of neurological effects of pesticides: the example of Parkinson’s disease. Neurotoxicology. 2011;32:383–391.
14. Thiruchelvam M, Brockel BJ, Richfield EK, Baggs RB, Cory-Slechta DA. Potentiated and preferential effects of combined paraquat and maneb on nigrostriatal dopamine systems: environmental risk factors for Parkinson’s disease? Brain Res. 2000;873:225–34.
15. Thiruchelvam M, Richfield EK, Baggs RB, Tank AW, Cory-Slechta DA. The nigrostriatal dopaminergic system as a preferential target of repeated exposures to combined paraquat and maneb: implications for Parkinson’s disease. J Neurosci. 2000; 20(24):9207–9214.
16. Lee, Y., Chang-Hun Lee, C.H., and Oh, U. Painful Channels in Sensory Neurons. Mol Cells. 2005;20(3):315-324
17. Steenland HW, Shanelle W, Ko W, Wu LJ, Zhuo M. Hot receptors in the brain. Molecular Pain. 2006;2:34; doi:10.1186/1744-8069-2-34
18. Shi Z, El Obeid T, Riley M, et al. High chili intake and cognitive function among 4582 adults: An open cohort study over 15 years. Nutrients. 2019;11(5):1183,
1. online: https://doi.org/10.3390/nu11051183
19. Neves D, Salazar I.L, Almeida RD, Silva RM. Molecular mechanisms of ischemia and glutamate excitotoxicity. Life Sciences. Textbook Elsevier 2023; p. 328, https://doi.org/10.1016/j.lfs.2023/121814
20. Thiel G, Backes TM, Rössler OG. Chili und der Capsaicinrezeptor TRPV1. Biol Unserer Zeit. 2020;50(4):246-252
21. Spiegel, German press organ, No. 53 (2009)
22. Hargreaves AJ. Neurodegeneration induced by organophosphorous compounds. In: Ahmad SI (Ed.): Neurodegenerative Diseases. Springer Science + Business Media, LLC/Landes Bioscience, New York, 2012: Series: Advances in Experimental Medicine and Biology. 2012;724:189-204
23. Binz P. Zerstörung von familiären und sozialen Strukturen als Folge von Hirnschäden. Lecture at: Studientagung „Gewissenhafte Forschung. Diagnose und Handlungsmöglichkeiten bei Vergiftungen in der Arbeitswelt. Katholische Akademie Trier, 15.-17.5.2009
24. Binz P. (2010): 10 Fallberichte (Kasuistiken) von Patienten mit Chemikalienbelastungen (Organophosphat-Pestizide, Reinigungsmittel mit Chlorgehalt) aus der neurologischen Praxis. 2010; Personal letter communication and summary of medical status-reports of his patients as practising neurological physician.
25. Eicher T, Avery E. Toxic Encephalopathies. Neurol Clin. 2005;23:353-376
26. Okun E, and Mattson MP. Neuronal vulnerability to oxidative damage in aging. In: Veasey, S.C. (Ed.): Oxidative Neural Injury. Humana Press/ Springer, Dordrecht, Heidelberg, London, New York, 2009, p. 83-95
27. Bak LK, Schousboe A, Waagepetersen HS. Glutamate and glutamin in brain disorders. In: Blass, J.P. (Ed.): Neurochemical mechanisms in disease. Advances in Neurobiology 2011;1:196-209, Springer Science + Business Media
28. Chen G, Bunce NJ. Interaction between halogenated aromatic compounds in the Ah receptor signal transduction pathway. Environ Toxicol. 2004;19(5):480-489.
29. Denison MS, Nagy SR (2003): Activation of the aryl hydrocarbon receptor by structurally diverse exogenous and endogenous chemicals. Annu Rev Pharmacol Toxicol. 2003;43:309-334. Epub 2002 Jan 10.
30. Straub RH. Lehrbuch der klinischen Pathophysiologie komplexer chronischer Erkrankungen. (In English: Textbook of clinical pathophysiology of complex chronic diseases). Vandenhoek & Ruprecht 2007, Vol. II, p.20-21
31. Straub RH. Drei Gedächtnisse für den Körper (Textbook). Springer-Verlag, New York, Heidelberg, 2020, p. 214-217
32. Straub RH. Frühe Traumata als Ursprung von chronischer Entzündung. Textbook, Springer Verlag, New York, Heidelberg, 2022, p.173
33. Huber W, Prull KJ, Kochen W. Zu den Spätfolgen des Einsatzes chlororganischer Holzschutzmittel. (Longtime consequences of exposure to chloroorganic wood preservatives.) Umwelt, Medizin, Gesellschaft 2024;37(3):14-17
34. Vale C, Fonfria E, Bujons J, et al. The organochlorine pesticides γ-hexachlorocyclohexane (lindane), α-endosulfan and dieldrin differentially interact with GABAa and glycine-gated chloride channels in primary cultures of cerebellar granule cells. Neuroscience 2003;117:397-403
35. Suñol C, Vale C, Rodríguez-Farré E, et al. Polychlorocycloalkane insecticide action on GABA- and glycine-dependent chloride flux. Neurotoxicology 1998;19(4-5):573-580
36. Taghavi A, Heine K, Kalberlah F. Synopse zu Wirkungsmechanismen von Spurenstoffen im Säugerorganismus als Grundlage der Bewertung des Wirkungspotenzials von Stoffsummen und der Erkennung „neuer“ toxischer Endpunkte, Umweltbundesamt (UBA, Ed.), Brochure, 2014, p.88ff
37. Guzzi G, Grandi M, Cattaneo C, et al. Dental amalgam and mercury levels in autopsy tissues. Food for thought. Am J For Med Path. 2006;27:42-45
38. Mutter J, Naumann J, Sadaghiani C, et al. Alzheimer Disease: Mercury as pathogenic factor and apolipoprotein E as a moderator. Neuroendocrinology Letters. 2004;25(5):331-339
39. Jirau-Colon, H., Gonzalez-Parrilla, L., Martinez-Jimenez, J., Adam, W., Jimenez-Velez, B. Rethinking the dental amalgam dilemma: an integrated toxicological approach. Int J Environ Res Public Health. 2019;16(6):1036, online under: https://www.ncbi.nlm.nih.gov/pmcarticles/PMC6446133/ )
40. Olivieri G, Novakovic M, Savaskan E, et al. (2002): The effects of ß-estradiol on SHSY5Y neuroblastoma cells during heavy metal induced oxidative stress, neurotoxicity and ß-amyloid secretion. Neurosci. 2002;113:849-855
41. Leong, C., Syed, N., Lorscheider, F., et al. (2001): Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neur Rep. 2001;12:733-737
42. Takeuchi H. Glial communication via gap junction in neuroinflammation. In: Suzumura A., Ikenaka K.: Neuron-glia interaction in neuroinflammation. Springer, New York, Heidelberg, 2013, p.119-134
43. Farina C. Neuron-glia-interaction via neurotrophins. In: Suzumura A, Ikenaka K. Neuron-glia interaction in neuroinflammation. Springer, New York, Heidelberg, 2013, p.101-118
44. Reinisch VM, Krause DL, Müller N. Neuroinflammation in Alzheimer’s Disease. In Peterson PK, Toborek M (Ed.): Neuroinflammation and Neurodegeneration. Springer, New York, 2014, p.161-177.
45. Pall, M.L. (2007): Explaining Unexplained Illnesses. Disease paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, Gulf War Syndrome, and Others. Harrington Park Press, New York, London, 2007, doi: 10.1300/5139-a.
46. Pall, M.L. (2009): Multiple Chemical Sensitivity: Toxicological Questions and Mechanisms. In: Timothy C. Marrs, Tore Syversen (Eds.): General and Applied Toxicology. Chapter XX John Wiley & Sons, London, 2009
47. Acarin L, Peluffo H, Gonzalez B, Castellano B (2002): Expression of inducible nitric oxide synthase and cyclooxygenase-2 after excitotoxic damage to the immature rat brain. J Neurosci Res. 2002;68:745-754
48. Schnakenberg, E., Fabig, K.R., Stanulla, M., et al. (2007): A cross sectional study of self reported chemical-related sensitivity is associated with gene variants of drug metabolizing enzymes. Environ. Health. 2007;6(1):6 http://www.ehjournal.net/content/6/1/6
49. Suzumura A (2013): Interactions between neurons and microglia during neuroinflammation. In: Suzumura A., Ikenaka K. Neuron-glia interaction in neuroinflammation. Springer, New York, Heidelberg, 2013, p. 63-73.
50. Lee, SJ. Toll-like receptors and neuroinflammation. In: Suzumura A., Ikenaka K. Neuron-glia interaction in neuroinflammation. Springer, New York, Heidelberg, 2013, p. 135-156.
51. Godbout JP, Chen J, Abraham J, Richwine AF, Berg BM, Kelley KW, Johnson RW. Exaggerated neuroinflammation and sickness behaviour in aged mice following activation of the peripheral innate immune system. FASEB J. 2005;19:1329-1331
52. Chang, Q., Szegedi, S.S., O’Connor, J.C., Dantzer, R., Kelley, K.W. Cytokine induced sickness behavior and depression. In: Siegel, A., und Zalcman, S.S. (Ed.): The neuroimmunological basis of behaviour and mental disorders. Springer, New York, 2009, p. 145-181
53. Opitz CA, Litzenburger UM, Sahm F, et al. An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor. Nature. 2011;478(7368):197-203
54. Lajtha, A. (Ed.): Handbook of Neurochemistry and Molecular Neurobiology: Degenerative Diseases of the Nervous System. Springer Science +Business Media, 2007
55. Ahmad SI (Ed.): Neurodegenerative Diseases. Springer Science +Business Media, Landes Bioscience, 2012
56. Genuis, S.J. Sensitivity-related illness: the escalating pandemic of allergy, food intolerance and chemical sensitivity. Sci Total Environ. 2010;408:6047-6061.
57. Pacher, P, Beckman, JS and Liaudet, L. Nitric oxide and peroxynitrite in health and disease. Physiol Rev. 2007;87:315-424.
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