The gestational environment and Parkinson's disease: Evidence for neurodevelopmental origins of a neurodegenerative disorder

• Published in: Reproductive toxicology (Elmsford, N.Y.) Vol. 23; no. 3; pp. 457 - 470
• Main Authors: Barlow, Brian K., Cory-Slechta, Deborah A., Richfield, Eric K., Thiruchelvam, Mona
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-04-2007
• Subjects: ( n = 8) Fetal basis of adult disease; Animals; Dopamine; Dopamine - metabolism; Environmental Exposure - adverse effects; Female; Humans; Maneb; Multiple hit hypothesis; Neurodegenerative Diseases - etiology; Neurodegenerative Diseases - metabolism; Neurodegenerative Diseases - pathology; Nigrostriatal system; Paraquat; Parkinson Disease - etiology; Parkinson Disease - metabolism; Parkinson Disease - pathology; Parkinson's disease; Pregnancy; Prenatal Exposure Delayed Effects; Silent toxicity; Parkinson's disease; Dopamine; Multiple hit hypothesis; ( n = 8) Fetal basis of adult disease; Paraquat; Silent toxicity; Maneb; Nigrostriatal system
• ISSN: 0890-6238; 1873-1708
• DOI: 10.1016/j.reprotox.2007.01.007

Parkinson's Disease (PD) is a degenerative neurological disorder that typically manifests symptoms in late adulthood, after loss of dopaminergic neurons in the nigrostriatal system. A lack of heritability for idiopathic PD has implicated adulthood environmental factors in the etiology of the disease. However, compelling evidence from animal models published within the past few years has shown that a range of environmental factors occurring during the perinatal period (including exposure to the common pesticides paraquat and maneb, organochlorine pesticides, and iron-enriched diet) and the prenatal period (including the pesticide maneb, cocaine, and the bacterial product LPS) can either directly cause a reduction in the number of dopamine neurons, or cause an increased susceptibility to degeneration of these neurons with subsequent environmental insults or with aging alone. In this review, these models are described for potential relevance in linking PD with the Fetal Basis of Adult Disease (FeBAD) hypothesis. Additionally, challenges in studying the neurodevelopmental basis of neurodegeneration experimentally and epidemiologically are presented.