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.
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 -