Parkinson’s disease
                                      # 14. cause of death in 2005

Men are more likely to develop Parkinson's disease than women are. Exposure to an environmental toxin, such as a
pesticide, that inhibits dopamine production and produces free radicals and oxidation damage may be involved. Direct
contact with herbicides and pesticides puts you at increased risk of Parkinson's. You also have a higher risk if you're
involved in farming, live in a rural area or drink well water. Reduced estrogen levels. Reduced estrogen levels may
increase the risk of Parkinson's disease.

Also see cerebrovascular

Nervous system diseases ; Central nervous system disease ; Degenerative disease ; Extrapyramidal syndrome ;
Cerebral disorder ; Viral disease ; Human ; Pathogenesis ; Virus ; Influenza A ; Parkinson disease ; Infection

Parkinson's disease linked to H. pylori infection
Parkinson's disease may be associated with the peptic ulcer causing bacterium Helicobacter pylori, say researchers
who found that eradication of the bacterium significantly improves certain physical abilities in people with the
neurological condition.

Parkinson's disease is a
degenerative brain disorder in which neurons in a specific area of the brain become
dysfunctional. Symptoms of Parkinson's disease include tremors, muscular rigidity or stiffness, slowness of movement,
balance problems and difficulties with handwriting and other forms of communication such as speech and facial

1: Jpn J Infect Dis. 1999 Jun;52(3):89-98
Viral etiology for Parkinson's disease--a possible role of influenza A virus infection.Takahashi M, Yamada T.
Department of Internal Medicine and Health Care, School of Medicine, Fukuoka University, Japan. mm039012@msat.

Some clinical reports and epidemiological data suggest that a virus may play a role in the etiology of Parkinson's
disease (PD). Once a certain strain of influenza A virus has adapted to the central nervous system, it will gain infectivity
to neurons, especially in the substantia nigra, cerebellum and hippocampus, both in human cases and experimental
models. Although efforts to detect virus particles in the brains, or antibodies in the serum or cerebrospinal fluid of
patients with PD have been generally unsuccessful, recent immunohistochemical work has revealed the presence of
complement proteins and the interferon-induced MxA in association with Lewy bodies and swollen neuronal process.
We propose a hypothesis that neurovirulent influenza A virus and other potent viruses may be responsible for the
formation of Lewy bodies and the later death of nigral neurons, to constitute a viral etiology for PD.

Nature Neuroscience  3, 1301 - 1306 (2000)

Chronic systemic pesticide exposure reproduces features of Parkinson's disease
Ranjita Betarbet1, 2, Todd B. Sherer1, 2, Gillian MacKenzie1, Monica Garcia-Osuna1, Alexander V. Panov1 & J.
Timothy Greenamyre1
1  Department of Neurology, Emory University, 1639 Pierce Drive, WMB 6000, Atlanta, Georgia 30322, USA

2  The first two authors contributed equally to this work

Correspondence should be addressed to J. Timothy Greenamyre

The cause of Parkinson's disease (PD) is unknown, but epidemiological studies suggest an association with pesticides
and other environmental toxins, and biochemical studies implicate a systemic defect in mitochondrial complex I. We
report that chronic, systemic inhibition of complex I by the lipophilic pesticide, rotenone, causes highly selective
nigrostriatal dopaminergic degeneration that is associated behaviorally with hypokinesia and rigidity. Nigral neurons in
rotenone-treated rats accumulate fibrillar cytoplasmic inclusions that contain ubiquitin and -synuclein. These results
indicate that chronic exposure to a common pesticide can reproduce the anatomical, neurochemical, behavioral and
neuropathological features of PD.

NEUROLOGY 1992;42:1328
© 1992 American Academy of Neurology

Parkinson's disease and exposure to agricultural work and pesticide chemicals
Karen M. Semchuk, PhD, Edgar J. Love, MD, PhD and Robert G. Lee, MD, FRCP(C)
Departments of Community Health Sciences (Drs. Semchuk and Love) and Clinical Neurosciences (Dr. Lee), Faculty of
Medicine, The University of Calgary, Calgary, AB, Canada; and the Centre for Agricultural Medicine, Department of
Medicine (Dr. Semchnk), College of Medicine and the College of Nursing (Dr. Semchuk), University of Saskatchewan,
Saskatoon, SK, Canada.

This population-based case-control study of 130 Calgary residents with neurologist-confirmed idiopathic Parkinson's
disease (PD) and 260 randomly selected age- and sex-matched community controls attempted to determine whether
agricultural work or the occupational use of pesticide chemicals is associated with an increased risk for PD. We
obtained by personal interviews lifetime occupational histories, including chemical exposure data, and analyzed the
data using conditional logistic regression for matched sets. In the univariate analysis, a history of field crop farming,
grain farming, herbicide use, or insecticide use resulted in a significantly increased crude estimate of the PD risk, and
the data suggested a dose-response relation between the PD risk and the cumulative lifetime exposure to field crop
farming and to grain farming. However, in the multivariate analysis, which controlled for potential confounding or
interaction between the exposure variables, previous occupational herbicide use was consistently the only significant
predictor of PD risk. These results support the hypothesis that the occupational use of herbicides is associated with an
increased risk for PD.