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      Neurodegenerative Diseases: An Overview of Environmental Risk Factors

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          Abstract

          The population of the United States is aging, and an ever-increasing number of Americans are afflicted with neurodegenerative diseases. Because the pathogenesis of many of these diseases remains unknown, we must consider that environmental factors may play a causal role. This review provides an overview of the epidemiologic evidence for environmental etiologies for neurodegenerative diseases such as Alzheimer disease, Parkinson disease, parkinsonian syndromes (multiple system atrophy and progressive supranuclear palsy), and amyotrophic lateral sclerosis. Epidemiologic evidence for an association between environmental agents’ exposure and neurodegenerative diseases is not conclusive. However, there are indications that there may be causal links, and the need for more research is obvious.

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          Risk factors for Alzheimer's disease: a prospective analysis from the Canadian Study of Health and Aging.

          J. Lindsay (2002)
          A prospective analysis of risk factors for Alzheimer's disease was a major objective of the Canadian Study of Health and Aging, a nationwide, population-based study. Of 6,434 eligible subjects aged 65 years or older in 1991, 4,615 were alive in 1996 and participated in the follow-up study. All participants were cognitively normal in 1991 when they completed a risk factor questionnaire. Their cognitive status was reassessed 5 years later by using a similar two-phase procedure, including a screening interview, followed by a clinical examination when indicated. The analysis included 194 Alzheimer's disease cases and 3,894 cognitively normal controls. Increasing age, fewer years of education, and the apolipoprotein E epsilon4 allele were significantly associated with increased risk of Alzheimer's disease. Use of nonsteroidal anti-inflammatory drugs, wine consumption, coffee consumption, and regular physical activity were associated with a reduced risk of Alzheimer's disease. No statistically significant association was found for family history of dementia, sex, history of depression, estrogen replacement therapy, head trauma, antiperspirant or antacid use, smoking, high blood pressure, heart disease, or stroke. The protective associations warrant further study. In particular, regular physical activity could be an important component of a preventive strategy against Alzheimer's disease and many other conditions.
          Article 0 comments Cited 295 times – based on 0 reviews     Review now
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            Increased nigral iron content and alterations in other metal ions occurring in brain in Parkinson's disease.

            D T Dexter, F. R. Wells, A Lees … (1989)
            Levels of iron, copper, zinc, manganese, and lead were measured by inductively coupled plasma spectroscopy in parkinsonian and age-matched control brain tissue. There was 31-35% increase in the total iron content of the parkinsonian substantia nigra when compared to control tissue. In contrast, in the globus pallidus total iron levels were decreased by 29% in Parkinson's disease. There was no change in the total iron levels in any other region of the parkinsonian brain. Total copper levels were reduced by 34-45% in the substantia nigra in Parkinson's disease; no difference was found in the other brain areas examined. Zinc levels were increased in substantia nigra in Parkinson's disease by 50-54%, and the zinc content of the caudate nucleus and lateral putamen was also raised by 18-35%. Levels of manganese and lead were unchanged in all areas of the parkinsonian brain studied when compared to control brains, except for a small decrease (20%) in manganese content of the medial putamen. Increased levels of total iron in the substantia nigra may cause the excessive formation of toxic oxygen radicals, leading to dopamine cell death.
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              Transition metals, ferritin, glutathione, and ascorbic acid in parkinsonian brains.

              P Riederer, E Sofic, W Rausch … (1989)
              The regional distributions of iron, copper, zinc, magnesium, and calcium in parkinsonian brains were compared with those of matched controls. In mild Parkinson's disease (PD), there were no significant differences in the content of total iron between the two groups, whereas there was a significant increase in total iron and iron (III) in substantia nigra of severely affected patients. Although marked regional distributions of iron, magnesium, and calcium were present, there were no changes in magnesium, calcium, and copper in various brain areas of PD. The most notable finding was a shift in the iron (II)/iron (III) ratio in favor of iron (III) in substantia nigra and a significant increase in the iron (III)-binding, protein, ferritin. A significantly lower glutathione content was present in pooled samples of putamen, globus pallidus, substantia nigra, nucleus basalis of Meynert, amygdaloid nucleus, and frontal cortex of PD brains with severe damage to substantia nigra, whereas no significant changes were observed in clinicopathologically mild forms of PD. In all these regions, except the amygdaloid nucleus, ascorbic acid was not decreased. Reduced glutathione and the shift of the iron (II)/iron (III) ratio in favor of iron (III) suggest that these changes might contribute to pathophysiological processes underlying PD.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Environ Health Perspect
                Title: Environmental Health Perspectives
                Publisher: National Institute of Environmental Health Sciences
                ISSN (Print): 0091-6765
                Publication date (Print): September 2005
                Publication date (Electronic): 26 May 2005
                Volume: 113
                Issue: 9
                Pages: 1250-1256
                Affiliations
                [1 ] Association of Schools of Public Health, National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Washington, DC, USA
                [2 ] Departments of Neurology and Nuclear Medicine, Veterans Affairs Western New York Healthcare System and University at Buffalo, The State University of New York, Buffalo, New York, USA
                [3 ] National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Washington, DC, USA
                Author notes
                Address correspondence to R.C. Brown, U.S. EPA, NCEA, 1200 Pennsylvania Ave. NW, Mailcode 8623D, Washington, DC 20460 USA. Telephone: (202) 564-3293. Fax: (202) 565-0079. E-mail: brown.rebecca@epa.gov

                The authors declare they have no competing financial interests.

                Article
                Publisher ID: ehp0113-001250
                DOI: 10.1289/ehp.7567
                PMC ID: 1280411
                PubMed ID: 16140637
                SO-VID: 1f7d5ff2-71c5-495e-85d4-b2b968fd1655
                Copyright © This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                Date received : 1 September 2004
                Date accepted : 5 May 2005
                Categories
                Subject: Research
                Subject: Mini-Monograph

                ScienceOpen disciplines: Public health
                Keywords: parkinson disease,progressive supranuclear palsy,multiple system atrophy,amyotrophic lateral sclerosis,electromagnetic fields,pesticides,alzheimer disease,metals,solvents,neurodegeneration
                Data availability:
                ScienceOpen disciplines: Public health
                Keywords: parkinson disease, progressive supranuclear palsy, multiple system atrophy, amyotrophic lateral sclerosis, electromagnetic fields, pesticides, alzheimer disease, metals, solvents, neurodegeneration

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