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    Parkinson disease and Alzheimer disease: environmental risk factors.

    Abstract

    INTRODUCTION

    The purpose of this review is to update and summarise available evidence on environmental risk factors that have been associated with risk of Parkinson disease (PD) or Alzheimer disease (AD) and discuss their potential mechanisms.

    DEVELOPMENT

    Evidence consistently suggests that a higher risk of PD is associated with pesticides and that a higher risk of AD is associated with pesticides, hypertension and high cholesterol levels in middle age, hyperhomocysteinaemia, smoking, traumatic brain injury and depression. There is weak evidence suggesting that higher risk of PD is associated with high milk consumption in men, high iron intake, chronic anaemia and traumatic brain injury. Weak evidence also suggests that a higher risk of AD is associated with high aluminium intake through drinking water, excessive exposure to electromagnetic fields from electrical grids, DM and hyperinsulinaemia, obesity in middle age, excessive alcohol consumption and chronic anaemia. Evidence consistently suggests that a lower risk of PD is associated with hyperuricaemia, tobacco and coffee use, while a lower risk of AD is associated with moderate alcohol consumption, physical exercise, perimenopausal hormone replacement therapy and good cognitive reserve. Weak evidence suggests that lower risk of PD is associated with increased vitamin E intake, alcohol, tea, NSAIDs, and vigorous physical exercise, and that lower risk of AD is associated with the Mediterranean diet, coffee and habitual NSAID consumption.

    CONCLUSIONS

    Several environmental factors contribute significantly to risk of PD and AD. Some may already be active in the early stages of life, and some may interact with other genetic factors. Population-based strategies to modify such factors could potentially result in fewer cases of PD or AD.

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    Authors+Show Affiliations

    Campdelacreu J

    Servicio de Neurología, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, España. Electronic address: 33357jcf@Comb.Cat.

    Source

    MeSH

    Alzheimer Disease
    Animals
    Environmental Exposure
    Female
    Humans
    Male
    Meta-Analysis as Topic
    Parkinson Disease
    Risk Factors
    Risk Reduction Behavior

    Pub Type(s)

    Journal Article
    Review

    Language

    eng spa

    PubMed ID

    22703631

    Citation

    Campdelacreu, J. "Parkinson Disease and Alzheimer Disease: Environmental Risk Factors." Neurologia (Barcelona, Spain), vol. 29, no. 9, 2014, pp. 541-9.
    Campdelacreu J. Parkinson disease and Alzheimer disease: environmental risk factors. Neurologia. 2014;29(9):541-9.
    Campdelacreu, J. (2014). Parkinson disease and Alzheimer disease: environmental risk factors. Neurologia (Barcelona, Spain), 29(9), pp. 541-9. doi:10.1016/j.nrl.2012.04.001.
    Campdelacreu J. Parkinson Disease and Alzheimer Disease: Environmental Risk Factors. Neurologia. 2014;29(9):541-9. PubMed PMID: 22703631.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Parkinson disease and Alzheimer disease: environmental risk factors. A1 - Campdelacreu,J, Y1 - 2012/06/14/ PY - 2012/01/23/received PY - 2012/04/06/revised PY - 2012/04/15/accepted PY - 2012/6/19/entrez PY - 2012/6/19/pubmed PY - 2015/8/19/medline KW - Alzheimer disease KW - Enfermedad de Alzheimer KW - Enfermedad de Parkinson KW - Environmental risk factors KW - Environmental toxins. Parkinson disease KW - Factores de riesgo ambientales KW - Factores protectores KW - Interacción KW - Interaction KW - Protective factors KW - Tóxicos ambientales SP - 541 EP - 9 JF - Neurologia (Barcelona, Spain) JO - Neurologia VL - 29 IS - 9 N2 - INTRODUCTION: The purpose of this review is to update and summarise available evidence on environmental risk factors that have been associated with risk of Parkinson disease (PD) or Alzheimer disease (AD) and discuss their potential mechanisms. DEVELOPMENT: Evidence consistently suggests that a higher risk of PD is associated with pesticides and that a higher risk of AD is associated with pesticides, hypertension and high cholesterol levels in middle age, hyperhomocysteinaemia, smoking, traumatic brain injury and depression. There is weak evidence suggesting that higher risk of PD is associated with high milk consumption in men, high iron intake, chronic anaemia and traumatic brain injury. Weak evidence also suggests that a higher risk of AD is associated with high aluminium intake through drinking water, excessive exposure to electromagnetic fields from electrical grids, DM and hyperinsulinaemia, obesity in middle age, excessive alcohol consumption and chronic anaemia. Evidence consistently suggests that a lower risk of PD is associated with hyperuricaemia, tobacco and coffee use, while a lower risk of AD is associated with moderate alcohol consumption, physical exercise, perimenopausal hormone replacement therapy and good cognitive reserve. Weak evidence suggests that lower risk of PD is associated with increased vitamin E intake, alcohol, tea, NSAIDs, and vigorous physical exercise, and that lower risk of AD is associated with the Mediterranean diet, coffee and habitual NSAID consumption. CONCLUSIONS: Several environmental factors contribute significantly to risk of PD and AD. Some may already be active in the early stages of life, and some may interact with other genetic factors. Population-based strategies to modify such factors could potentially result in fewer cases of PD or AD. SN - 1578-1968 UR - https://www.unboundmedicine.com/medline/citation/22703631/full_citation L2 - http://www.elsevier.es/en/linksolver/ft/pii/S0213-4853(12)00109-0 DB - PRIME DP - Unbound Medicine ER -