Bacteriophages: Are they an overlooked driver of Parkinson's disease? | EurekAlert! Science News

In the first study of its kind, researchers from the New York-based
Human Microbiology Institute have discovered the role certain
bacteriophages may play in the onset of Parkinson's disease (PD). The
research is presented at ASM Microbe, the annual meeting of the American
Society for Microbiology, held from June 7th to June 11th in Atlanta,
Georgia.
The researchers, led by George, Tetz, M.D., Ph.D., Human Microbiology Institute, showed that the abundance of lytic Lactococcus phages was higher in PD patients when compared to healthy individuals.This abundance led to a 10-fold reduction in neurotransmitter-producing Lactococcus,
suggesting the possible role of phages in neurodegeneration.
Comparative analysis of the bacterial component also revealed
significant decreases in Streptococcus spp. and Lactobacillus spp. in PD.
Lactococcus are regulators of gut permeability and are
enteric dopamine producers, which plays a primary role in PD. "The
depletion of lactococcus due to high numbers of strictly lytic phages in
PD patients might be associated with PD development and directly linked
to dopamine decrease as well as the development of gastrointestinal
symptoms of PD," said Dr. Tetz.

Drugs that suppress immune system may protect against Parkinson's: People who take immunosuppressants less likely to develop the disease -- ScienceDaily

Racette and colleagues analyzed Medicare Part D prescription drug
data on 48,295 people diagnosed with Parkinson's in 2009 and 52,324
people never diagnosed with Parkinson's. They identified 26 commonly
prescribed immunosuppressant drugs, representing six classes of
medications. The researchers determined which people in the data set had
been prescribed any of the drugs a year or more before the date of
diagnosis or by a pre-set cutoff date. Prescriptions written in the 12
months before diagnosis or by the cutoff were excluded to rule out any
chance that the prescriptions might have been linked to early signs of
the disease.
The researchers found that people taking drugs in either of two
classes were significantly less likely to develop Parkinson's than those
taking no immunosuppressants. People taking corticosteroids such as
prednisone were 20 percent less likely to be diagnosed with Parkinson's,
while those on inosine monophosphate dehydrogenase (IMDH) inhibitors
were about one-third less likely.

Here's the paper:-

Immunosuppressants and Risk of Parkinson Disease. Annals of Clinical and Translational Neurology, May 31, 2018

Cause of pesticide exposure, Parkinson's link: Low-level exposure to the pesticides disrupts cells in a way that mimics the effects of mutations known to cause Parkinson's disease -- ScienceDaily

Previous studies have found an association between two commonly used
agrochemicals (paraquat and maneb) and Parkinson's disease. Now a
professor has determined that low-level exposure to the pesticides
disrupts cells in a way that mimics the effects of mutations known to
cause Parkinson's disease. Adding the effects of the chemicals to a
predisposition for Parkinson's disease drastically increases the risk of
disease onset.

From this Paper:-
Nitration of microtubules blocks axonal mitochondrial transport in a human pluripotent stem cell model of Parkinson’s disease. The FASEB Journal, 2018; fj.201700759RR DOI: 10.1096/fj.201700759RR

Toxoplasma Modulates Signature Pathways of Human Epilepsy, Neurodegeneration & Cancer | Scientific Reports

life cycle of Toxoplasma gondii (Photo credit: Wikipedia)

 One third of humans are infected lifelong with the brain-dwelling, protozoan parasite, Toxoplasma gondii. Approximately fifteen million of these have congenital toxoplasmosis. Although neurobehavioral disease is associated with seropositivity, causality is unproven. To better understand what this parasite does to human brains, we performed a comprehensive systems analysis of the infected brain: We identified susceptibility genes for congenital toxoplasmosis in our cohort of infected humans and found these genes are expressed in human brain. Transcriptomic and quantitative proteomic analyses of infected human, primary, neuronal stem and monocytic cells revealed effects on neurodevelopment and plasticity in neural, immune, and endocrine networks. These findings were supported by identification of protein and miRNA biomarkers in sera of ill children reflecting brain damage and T. gondii infection. These data were deconvoluted using three systems biology approaches: “Orbital-deconvolution” elucidated upstream, regulatory pathways interconnecting human susceptibility genes, biomarkers, proteomes, and transcriptomes. “Cluster-deconvolution” revealed visual protein-protein interaction clusters involved in processes affecting brain functions and circuitry, including lipid metabolism, leukocyte migration and olfaction. Finally, “disease-deconvolution” identified associations between the parasite-brain interactions and epilepsy, movement disorders, Alzheimer’s disease, and cancer. This “reconstruction-deconvolution” logic provides templates of progenitor cells’ potentiating effects, and components affecting human brain parasitism and diseases."


T. Gondii interactome 



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Immune system may mount an attack in Parkinson’s disease | National Institutes of Health (NIH)

Immune system may mount an attack in Parkinson’s disease | National Institutes of Health (NIH): "A research team led by David Sulzer, Ph.D., professor of neurology at Columbia University in New York City and Alessandro Sette, Dr.Biol.Sci., professor of infectious diseases at the La Jolla Institute for Allergy and Immunology in California, examined the role of T cells in PD.

Drs. Sulzer and Sette, along with their colleagues, collected blood samples from 67 individuals with Parkinson’s disease and 36 healthy controls. Immune cells were extracted from the samples and mixed with portions of the alpha-synuclein protein, which accumulates in the brains of people with PD and can result in cell death.

They found that T cells from people with PD responded to the presence of alpha-synuclein to a much greater degree than those gathered from the control group.

In particular, two regions of alpha-synuclein evoked reactions from T cells: a section that often contains mutations linked with PD, and a portion undergoing a chemical change that can lead to accumulation of the protein in the brain.  "

Related articles:

Human serum antibodies against EBV latent membrane protein 1 cross-react with α-synuclein.

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Study finds link between upper GI infections and protein (synuclein) implicated in Parkinson’s disease

 "Acute and chronic infections in a person's upper gastrointestinal tract appear to be linked to Parkinson's disease, say scientists at Georgetown University Medical Center and their collaborators at the National Institutes of Health and other institutions.

Their study, published in the Journal of Innate Immunity, finds that alpha-Synuclein (αS), the protein implicated in Parkinson's disease and other forms of neurodegenerative diseases, is released when an infection occurs in the upper GI tract (the esophagus, stomach, and duodenum) inducing an immune response as part of the body's innate immune system. The researchers say that these findings suggest that frequent or chronic upper GI infections could overwhelm the body's capacity to clear αS, leading to disease."



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Related articles

• Could "Advanced Probiotics" Soon Treat Parkinson's Disease?

Synergistic effects of influenza and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can be eliminated by the use of influenza therapeutics: experimental evidence for the multi-hit hypothesis | npj Parkinson's Disease

H1N1 virus (Photo credit: Wikipedia)

"Central Nervous System inflammation has been implicated in neurodegenerative disorders including Parkinson’s disease (Ransohoff, Science 353: 777–783, 2016; Kannarkat et al. J. Parkinsons Dis. 3: 493–514, 2013). Here, we examined if the H1N1 influenza virus (Studahl et al. Drugs 73: 131–158, 2013) could synergize with the parkinsonian toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (Jackson-Lewis et al. in Mark LeDoux (ed) Movement Disorders: Genetics and Models: 287–306, Elsevier, 2015) to induce a greater microglial activation and loss of substantia nigra pars compacta dopaminergic neurons than either insult alone. H1N1-infected animals administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine exhibit a 20% greater loss of substantia nigra pars compacta dopaminergic neurons than occurs from the additive effects of H1N1 or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine alone (p < 0.001). No synergistic effects were found in microglial activation. The synergistic dopaminergic neuron loss is eliminated by influenza vaccination or treatment with oseltamivir carboxylate. This work shows that multiple insults can induce synergistic effects; and even these small changes can be significant as it might allow one to cross a phenotypic disease threshold that would not occur from individual non-interacting exposures. Our observations also have important implications for public health, providing impetus for influenza vaccination or prompt treatment with anti-viral medications upon influenza diagnosis."



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Could Parkinson's disease start in the gut? -- ScienceDaily

 Parkinson's disease may start in the gut and spread to the brain via the vagus nerve, according to a study published in the April 26, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. The vagus nerve extends from the brainstem to the abdomen and controls unconscious body processes like heart rate and food digestion.

Here's the paper:

Vagotomy and Parkinson disease

A Swedish register–based matched-cohort study

Parkinson's disease and Parkinson's disease medications have distinct signatures of the gut microbiome - Hill-Burns - 2017 - Movement Disorders - Wiley Online Library

Background

There is mounting evidence for a connection between the gut and Parkinson's disease (PD). Dysbiosis of gut microbiota could explain several features of PD.

Objective

The objective of this study was to determine if PD involves dysbiosis of gut microbiome, disentangle effects of confounders, and identify candidate taxa and functional pathways to guide research.
Methods 


A total of 197 PD cases and 130 controls were studied. Microbial composition was determined by 16S rRNA gene sequencing of DNA extracted from stool. Metadata were collected on 39 potential confounders including medications, diet, gastrointestinal symptoms, and demographics. Statistical analyses were conducted while controlling for potential confounders and correcting for multiple testing. We tested differences in the overall microbial composition, taxa abundance, and functional pathways.

Results

Independent microbial signatures were detected for PD (P = 4E-5), participants' region of residence within the United States (P = 3E-3), age (P = 0.03), sex (P = 1E-3), and dietary fruits/vegetables (P = 0.01). Among patients, independent signals were detected for catechol-O-methyltransferase-inhibitors (P = 4E-4), anticholinergics (P = 5E-3), and possibly carbidopa/levodopa (P = 0.05). We found significantly altered abundances of the Bifidobacteriaceae, Christensenellaceae, [Tissierellaceae], Lachnospiraceae, Lactobacillaceae, Pasteurellaceae, and Verrucomicrobiaceae families. Functional predictions revealed changes in numerous pathways, including the metabolism of plant-derived compounds and xenobiotics degradation.

Conclusion

 PD is accompanied by dysbiosis of gut microbiome. Results coalesce divergent findings of prior studies, reveal altered abundance of several taxa, nominate functional pathways, and demonstrate independent effects of PD medications on the microbiome. The findings provide new leads and testable hypotheses on the pathophysiology and treatment of PD. "



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Related articles

• Colonic bacterial composition in Parkinson's disease. - PubMed - NCBI

Effects of titanium dioxide nanoparticles exposure on parkinsonism in zebrafish larvae and PC12. - PubMed - NCBI

Nanomaterials hold significant potential for industrial and biomedical application these years. Therefore, the relationship between nanoparticles and neurodegenerative disease is of enormous interest. In this contribution, zebrafish embryos and PC12 cell lines were selected for studying neurotoxicity of titanium dioxide nanoparticles (TiO2 NPs). After exposure of different concentrations of TiO2 NPs to embryos from fertilization to 96 hpf, the hatching time of zebrafish was decreased, accompanied by an increase in malformation rate. However, no significant increases in mortality relative to control were observed. These results indicated that TiO2 NPs exposure hold a risk for premature of zebrafish embryos, but not fatal. The further investigation confirmed that TiO2 NPs could accumulate in the brain of zebrafish larvae, resulting in reactive oxygen species (ROS) generation and cell death of hypothalamus. Meanwhile, q-PCR analysis showed that TiO2 NPs exposure increased the pink1, parkin, α-syn and uchl1 gene expression, which are related with the formation of Lewy bodies. We also observed loss of dopaminergic neurons in zebrafish and in vitro. These remarkable hallmarks are all linked to these Parkinson's disease (PD) symptoms. Our results indicate that TiO2NPs exposure induces neurotoxicity in vivo and in vitro, which poses a significant risk factor for the development of PD.

Effects of titanium dioxide nanoparticles on α-synuclein aggregation and the ubiquitin-proteasome system in dopaminergic neurons. - PubMed - NCBI

Dopaminergic neurons (PC12 cells) were treated with different doses of titanium dioxide nanoparticles (TiO2-NPs), to investigate their effects on α-Synuclein (α-Syn) aggregation and their mechanism of action. Western blotting and immunofluorescent staining were performed. Exposure to TiO2-NPs increased α-Syn expression (p < 0.05) and induced dose-dependent α-Syn aggregation. Pretreatment with N-acetylcysteine partially inhibited α-Syn expression induced by a 200 μg/ml dose of TiO2-NPs. TiO2-NPs reduced the expressions of parkin and ubiquitin C-terminal hydrolase protein, and were associated with oxidative stress in PC12 cells. Dysfunction of the ubiquitin-proteasome system also contributed to α-Syn aggregation. The potentially neurotoxic TiO2-NPs may cause Parkinson's disease



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Parkinson's Disease Linked to Microbiome | Caltech

Caltech scientists have discovered for the first time a functional link between bacteria in the intestines and Parkinson's disease (PD). The researchers show that changes in the composition of gut bacterial populations—or possibly gut bacteria themselves—are actively contributing to and may even cause the deterioration of motor skills that is the hallmark of this disease.
When gut bacteria break down dietary fiber, they produce molecules called short-chain fatty acids (SCFAs), such as acetate and butyrate. Previous research has shown that these molecules also can activate immune responses in the brain. Thus, Mazmanian's group hypothesized that an imbalance in the levels of SCFAs regulates brain inflammation and other symptoms of PD. Indeed, when germ-free mice were fed SCFAs, cells called microglia—which are immune cells residing in the brain—became activated. Such inflammatory processes can cause neurons to malfunction or even die. In fact, germ-free mice fed SCFAs now showed motor disabilities and alpha=synuclein aggregation in regions of the brain linked to PD.

Cerebrospinal Fluid Biomarkers in Highly Exposed PM2.5 Urbanites: The Risk of Alzheimer’s and Parkinson’s Diseases in Young Mexico City Residents - IOS Press

Exposure to fine particulate matter (PM2.5) and ozone (O3) above US EPA standards is associated with Alzheimer’s disease (AD) risk, while Mn toxicity induces parkinsonism. Mexico City Metropolitan Area (MCMA) children have pre- and postnatal sustained and high exposures to PM2.5, O3, polycyclic aromatic hydrocarbons, and metals. Young MCMA residents exhibit frontal tau hyperphosphorylation and amyloid-β (Aβ)1 - 42 diffuse plaques, and aggregated and hyperphosphorylated α-synuclein in olfactory nerves and key brainstem nuclei. We measured total prion protein (TPrP), total tau (T-tau), tau phosphorylated at threonine 181 (P-Tau), Aβ1–42, α-synuclein (t-α-syn and d-α-synuclein), BDNF, insulin, leptin, and/or inflammatory mediators, in 129 normal CSF samples from MCMA and clean air controls. Aβ1–42 and BDNF concentrations were significantly lower in MCMA children versus controls (p = 0.005 and 0.02, respectively). TPrP increased with cumulative PM2.5 up to 5 μg/m3 and then decreased, regardless of cumulative value or age (R2 = 0.56). TPrP strongly correlated with T-Tau and P-Tau, while d-α-synuclein showed a significant correlation with TNFα, IL10, and IL6 in MCMA children. Total synuclein showed an increment in childhood years related to cumulated PM2.5, followed by a decrease after age 12 years (R2 = 0.47), while d-α-synuclein exhibited a tendency to increase with cumulated PM2.5 (R2 = 0.30). CSF Aβ1–42, BDNF, α-synuclein, and TPrP changes are evolving in young MCMA urbanites historically showing underperformance in cognitive processes, odor identification deficits, downregulation of frontal cellular PrP, and neuropathological AD and PD hallmarks. Neuroprotection of young MCMA residents ought to be a public health priority."

Functional characterization of alpha-synuclein protein with antimicrobial activity.

Alpha-synuclein (α-Syn), a small (14 kDa) protein associated with Parkinson's disease, is abundant in human neural tissues. α-Syn plays an important role in maintaining a supply of synaptic vesicles in presynaptic terminals; however, the mechanism by which it performs this function are not well understood. In addition, there is a correlation between α-Syn over-expression and upregulation of an innate immune response. Given the growing body of literature surrounding antimicrobial peptides (AMPs) in the brain, and the similarities between α-Syn and a previously characterized AMP, Amyloid-β, we set out to investigate if α-Syn shares AMP-like properties. Here we demonstrate that α-Syn exhibits antibacterial activity against Escherichia coli and Staphylococcus aureus. In addition, we demonstrate a role for α-Syn in inhibiting various pathogenic fungal strains such as Aspergillus flavus, Aspergillus fumigatus and Rhizoctonia solani. We also analyzed localizations of recombinant α-Syn protein in E. coli and Candida albicans. These results suggest that in addition to α-Syn's role in neurotransmitter release, it appears to be a natural AMP.

Groundwater pesticide levels and the association with Parkinson disease. - PubMed - NCBI

It is unclear whether exposure to environmentally relevant levels of pesticides in groundwater is associated with an increased risk of Parkinson disease (PD). The purpose of this study was to examine the relationship between PD and pesticide levels in groundwater. This cross-sectional study included 332 971 Medicare beneficiaries, including 4207 prevalent cases of PD from the 2007 Colorado Medicare Beneficiary Database. Residential pesticide levels were estimated from a spatial model based on 286 well water samples with atrazine, simazine, alachlor, and metolachlor measurements. A logistic regression model with known PD risk factors was used to assess the association between residential groundwater pesticide levels and prevalent PD. We found that for every 1.0 µg/L of pesticide in groundwater, the risk of PD increases by 3% (odds ratio = 1.03; 95% confidence interval: 1.02-1.04) while adjusting for age, race/ethnicity, and gender suggesting that higher age-standardized PD prevalence ratios are associated with increasing levels of pesticides in groundwater.



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Alpha-synuclein expression restricts RNA viral infections in the brain. - PubMed - NCBI

We have discovered that native, neuronal expression of alpha-synuclein (Asyn) inhibits viral infection, injury, and disease in the central nervous system. Enveloped RNA viruses such as West Nile virus (WNV) invade the central nervous system (CNS) and cause encephalitis; yet, little is known about the innate neuron-specific inhibitors of viral infections in the CNS. Following WNV-infection of primary neurons, we found that Asyn protein expression is increased. Infectious viral titer of WNV and Venezuelan equine encephalitis virus (VEEV) TC83 in the brains of Asyn knockout mice exhibited a mean increase of 10(4.5) infectious viral particles compared to wild-type and heterozygote littermates. Asyn knockout mice also exhibited significantly increased virus-induced mortality compared to Asyn heterozygote or homozygote control mice. Viral-induced Asyn localized to perinuclear, neuronal regions expressing viral envelope protein and the ER-associated trafficking protein, Rab1. In Asyn knockout primary neuronal cultures, ER signaling pathways known to support WNV replication are significantly elevated before and during viral infection compared to neurons expressing Asyn. We propose a model in which virus-induced Asyn localizes to ER-derived membranes, modulates virus-induced ER-stress signaling, and inhibits viral replication, growth, and injury in the CNS. These data provide a novel and important functional role for native

alpha-synuclein expression, a protein that is closely associated with the development of Parkinson's disease.

IMPORTANCE: Neuroinvasive viruses such as West Nile
virus are able to infect neurons and cause severe disease such as

encephalitis, infection of brain tissue. Following viral infection in the central nervous system only select neurons are infected, implying that neurons exhibit innate resistance to viral infections. We discovered that native neuronal expression of alpha-synuclein inhibited viral infection in the central nervous system.

When the gene for alpha-synuclein was deleted, mice exhibited significantly decreased survival, markedly increased viral growth in the brain, and evidence

of increased neuron injury. Virus-induced alpha-synuclein localized to

intracellular neuron membranes, and in the absence of alpha-synuclein expression, specific endoplasmic reticulum stress signaling events were significantly

increased. We describe a new neuron-specific inhibitor of viral infections in the central nervous system. Given the importance of alpha-synuclein as a cause of

Parkinson's disease, these data also ascribe a novel functional role for native

expression of alpha-synuclein in the CNS.

Hepatitis C virus infection as a risk factor for Parkinson disease: A nationwide cohort study.

OBJECTIVE: To determine whether hepatitis C virus (HCV) infection is a risk factor for developing Parkinson disease (PD).
METHODS: This nationwide population-based cohort study was based on data obtained from a dataset of the Taiwan National Health Insurance Research Database for the period 2000 to 2010. A total of 49,967 patients with viral hepatitis were included for analysis. Furthermore, 199,868 people without viral hepatitis were
included for comparisons. Patients with viral hepatitis were further grouped into 3 cohorts: hepatitis B virus (HBV) infection, HCV infection, and HBV-HCV coinfection. In each cohort, we calculated the incidence of developing PD. A Cox  proportional hazards model was applied to estimate the risk of developing PD in terms of hazard ratios (HRs) and 95% confidence intervals (CIs).
RESULTS: The crude HRs for developing PD was 0.66 (95% CI = 0.55-0.80) for HBV infection, 2.50 (95% CI = 2.07-3.02) for HCV infection, and 1.28 (95% CI = 0.88-1.85) for HBV-HCV coinfection. The association between HCV and PD remained statistically significant after adjustments for age, sex, and comorbidities (adjusted HR = 1.29, 95% CI = 1.06-1.56).
CONCLUSIONS:We conducted a large nationwide population-based study and found that patients with HCV exhibit a significantly increased risk of developing PD.

© 2015 American Academy of Neurology.

Pesticide found in milk decades ago may be associated with signs of Parkinson's

For the study, 449 Japanese-American men with an average age of 54 who participated in the Honolulu-Asia Aging Study were followed for more than 30 years and until death, after which autopsies were performed. Tests looked at whether participants had lost brain cells in the substantia nigra area of the brain, which occurs in Parkinson's disease and can start decades before any symptoms begin. Researchers also measured in 116 brains the amount of residue of a pesticide called heptachlor epoxide. The pesticide was found at very high levels in the milk supply in the early 1980s in Hawaii, where it was used in the pineapple industry. It was used to kill insects and was removed from use in the US around that time. The pesticide may also be found in well water.

Methylmercury can induce Parkinson's-like neurotoxicity similar to 1-methyl-4- phenylpyridinium: a genomic and proteomic analysis on MN9D dopaminergic neurones

"Exposure to environmental chemicals has been implicated as a possible risk factor for the development of neurodegenerative diseases. Our previous study showed that methylmercury (MeHg) exposure can disrupt synthesis, uptake and metabolism of dopamine similar to 1-methyl-4-phenylpyridinium (MPP(+)). The objective of this study was to investigate the effects of MeHg exposure on gene and protein profiles in a dopaminergic MN9D cell line. MN9D cells were treated with MeHg (1-5 μM) and MPP(+) (10-40 μM) for 48 hr. Real-time PCR Parkinson's disease (PD) arrays and high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS) were performed for the analysis. PD PCR array results showed that 19% genes were significantly changed in the 2.5 μM MeHg treated cells, and 39% genes were changed in the 5 μM MeHg treated cells. In comparison, MPP(+) treatment (40 µM) resulted in significant changes in 25% genes. A total of 15 common genes were altered by both MeHg and MPP(+), and dopaminergic signaling transduction was the most affected pathway. Proteomic analysis identified a total of 2496 proteins, of which 188, 233 and 395 proteins were differentially changed by 1 μM and 2.5 μM MeHg, and MPP(+) respectively. A total of 61 common proteins were changed by both MeHg and MPP(+) treatment. The changed proteins were mainly involved in energetic generation-related metabolism pathway (propanoate metabolism, pyruvate metabolism and fatty acid metabolism), oxidative phosphorylation, proteasome, PD and other neurodegenerative disorders. A total of 7 genes/proteins including Ube2l3 (Ubiquitin-conjugating enzyme E2 L3) and Th (Tyrosine 3-monooxygenase) were changed in both genomic and proteomic analysis. These results suggest that MeHg and MPP(+) share many similar signaling pathways leading to the pathogenesis of PD and other neurodegenerative diseases."



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Parkinson's Disease and Pesticides Exposure: New Findings From a Comprehensive Study in Nebraska, USA. - PubMed - NCBI

"The association between exposure to agricultural pesticides and Parkinson's Disease (PD) has long been a topic of study in the field of environmental health. This research takes advantage of the unique Nebraska PD registry and state-level crop classification data to investigate the PD-pesticides exposure relationship.

METHODS:
First, Geographic Information System and satellite remote sensing data were adopted to calculate exposure to different pesticides for Nebraska residents. An integrated spatial exploratory framework was then adopted to explore the association between PD incidence and exposure to specific pesticide ingredients at the county level.

RESULTS:
Our results reveal similarities in geographic patterns of pesticide exposure and PD incidence. The regression analyses indicate that, for most Nebraska counties, PD incidence was significantly associated with exposure to certain pesticide ingredients such as alachlor and broxomy. However, the results also suggest that factors other than pesticide exposure may help further explain the risk of PD at the county level.

CONCLUSIONS:
We found significant associations between PD incidence and exposure to different pesticide ingredients. These results have useful implications for PD prevention in Nebraska and other agricultural states in the United States."



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