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Gene-environment interactions in Parkinson's disease: Specific evidence in humans and mammalian models

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TLDR
In this review, the most current data on gene-environment interactions in PD from human studies are critically discussed and goals and needs for the future of the field are proposed.
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This article is published in Neurobiology of Disease.The article was published on 2013-09-01 and is currently open access. It has received 146 citations till now.

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Oxidative damage to macromolecules in human Parkinson disease and the rotenone model.

TL;DR: The recent evidence for oxidative damage to nucleic acids, lipids, and proteins in both the brain and the peripheral tissues in human PD and in the rotenone model is reviewed.
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Parkinson's Disease and the Environment.

TL;DR: Environmental factors implicated in sporadic PD onset are presented and by understanding the mechanisms in which environmental factors interact with, and affect the brain the authors can stride toward finding the underlying cause(s) of PD.
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Genetics of Parkinson's disease: An introspection of its journey towards precision medicine.

TL;DR: The journey thus far of PD genetics is outlined, highlighting how significant advances have improved knowledge of the genetic basis of PD risk, onset and progression and foresee that genetic discoveries in PD will directly influence the ability to predict disease and aid in defining etiological subtypes, critical steps for the implementation of precision medicine for PD.
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Triggers, Facilitators, and Aggravators: Redefining Parkinson’s Disease Pathogenesis

TL;DR: It is hypothesized that Parkinson's disease pathogenesis can be divided into three temporal phases and clinical trials need to consider these three phases and target potential therapies at the appropriate stage of the disease process in order to be effective.
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Environmental enrichment and brain repair: harnessing the therapeutic effects of cognitive stimulation and physical activity to enhance experience-dependent plasticity.

TL;DR: The proposal that EE may act synergistically with other approaches, such as drug and cell therapies, to facilitate brain repair will be discussed, and the therapeutic potential of ‘enviromimetics’, drugs which mimic or enhance the therapeutic effects of cognitive activity and physical exercise, for both neuroprotection and brain repair are discussed.
References
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Journal ArticleDOI

Mutation in the α-synuclein gene identified in families with Parkinson's disease

TL;DR: A mutation was identified in the α-synuclein gene, which codes for a presynaptic protein thought to be involved in neuronal plasticity, in the Italian kindred and in three unrelated families of Greek origin with autosomal dominant inheritance for the PD phenotype.
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Alpha-synuclein in Lewy bodies.

TL;DR: Strong staining of Lewy bodies from idiopathic Parkinson's disease with antibodies for α-synuclein, a presynaptic protein of unknown function which is mutated in some familial cases of the disease, indicates that the LewY bodies from these two diseases may have identical compositions.
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Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

TL;DR: Mutations in the newly identified gene appear to be responsible for the pathogenesis of Autosomal recessive juvenile parkinsonism, and the protein product is named ‘Parkin’.
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Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis

TL;DR: It is proposed that this chemical selectively damages cells in the substantia nigra in patients who developed marked parkinsonism after using an illicit drug intravenously.
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Epidemiology of Parkinson's disease

TL;DR: This article reviews what is known about the prevalence, incidence, risk factors, and prognosis of PD from epidemiological studies and suggests that major gene mutations cause only a small proportion of all cases.
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