Despite being the subject of intense study, the pathogenesis of Parkinson's disease still remains unclear. In recent years, however, there has been increasing evidence to support a role for genetic factors in its cause. This has come from twin and family studies, the mapping and cloning of PARK genes that are associated with the development of PD, and analysis of potential susceptibility genes. There is also evidence indicating that environmental factors may play a role in the disease process. It is likely that for most cases, there is a complex interplay between these genetic and environmental influences in the causation of Parkinson's disease. This article reviews the evidence in support of genetic and environmental factors in the cause of PD.
"Parkinson’s disease (PD) is the second most common and progressive neurodegenerative disorder worldwide with a prevalence of approximately 1% in people over age 60. Clinically, the disease is characterized by resting tremor, rigidity, bradykinesia and postural instability [1-3]. Progression of these symptoms is secondary to the selective loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) . "
[Show abstract][Hide abstract] ABSTRACT: Neuroinflammation and oxidative stress has been shown to be associated with the development of Parkinson disease (PD). In the present study, we investigated the effect of intraperitoneal (i.p) administration of silymarin, on 6-OHDA-induced motor-impairment, brain lipid per-oxidation and cerebrospinal fluid (CSF) levels of inflammatory cytokine in the rats.
The results showed that silymarin is able to improve motor coordination significantly (p < 0.001) in a dose dependent manner. There was a significant (p < 0.001) increase in MDA levels of 6-OHDA-lesioned rats whereas; in silymarin (100, 200 and 300 mg/kg, i.p. for 5 days) pre-treated hemi-parkinsonian rats MDA levels was decreased markedly (p < 0.001). Furthermore the CSF levels of IL-1beta was decreased (p < 0.001) in silymarin (100, 200 and 300 mg/kg) pre-treated rats up to the range of normal non-parkinsonian animals.
We found that pre-treatment with silymarin could improve 6-OHDA-induced motor imbalance by attenuating brain lipid per-oxidation as well as CSF level of IL-1beta as a pro-inflammatory cytokine. We suggest a potential prophylactic effect for silymarin in PD. However, further clinical trial studies should be carried out to prove this hypothesis.
DARU-JOURNAL OF FACULTY OF PHARMACY 04/2014; 22(1):38. DOI:10.1186/2008-2231-22-38 · 1.64 Impact Factor
"Most cases of Parkinson's disease (PD) are idiopathic since their cause is unknown. Genetic susceptibility and environmental factors (Warner and Schapira, 2003) that mediate mitochondrial dysfunction, inflammation, abrogation of the autosomal-lysomal autophagy system (Beal, 2003), and endoplasmic reticulum stress (Ryu et al., 2002) play a role in disease development. A growing body of evidence suggests that nutrition may play an important role in PD. "
[Show abstract][Hide abstract] ABSTRACT: Parkinson's disease (PD) is the second most prevalent neurodegenerative disease in ageing individuals. It is now clear that genetic susceptibility and environmental factors play a role in disease etiology and progression. Because environmental factors are involved with the majority of the cases of PD, it is important to understand the role nutrition plays in both neuroprotection and neurodegeneration. Recent epidemiological studies have revealed the promise of some nutrients in reducing the risk of PD. In contrast, other nutrients may be involved with the etiology of neurodegeneration or exacerbate disease progression. This review summarizes the studies that have addressed these issues and describes in detail the nutrients and their putative mechanisms of action in PD.
"Several genes have been identified in the rare familial cases (about 5%), whereas the majority of cases are sporadic, thus underlying a critical interplay between genetic susceptibility and environmental factors (Di Monte et al., 2002; Warner and Schapira, 2003; Gao and Hong, 2011; Gao et al., 2012; Cannon and Greenamyre, 2013) (Table 1). Aging and exposure to neurotoxic agents, in particular, represent critical contributing risk 2011; Desplats et al., 2012). "
[Show abstract][Hide abstract] ABSTRACT: During the past three decades, the Wingless-type MMTV integration site (Wnt) signaling cascade has emerged as an essential system regulating multiple processes in developing and adult brain. Accumulating evidence points to a dysregulation of Wnt signaling in major neurodegenerative pathologies including Parkinson's disease (PD), a common neurodegenerative disorder characterized by the progressive loss of midbrain dopaminergic (mDA) neurons and deregulated activation of astrocyte and microglial. This review highlights the emerging link between Wnt signaling and key inflammatory pathways during mDA neuron damage/repair in PD progression. In particular, we summarize recent evidence documenting that aging and neurotoxicant exposure strongly antagonize Wnt/¦Â-catenin signaling in mDA neurons and subventricular zone (SVZ) neuroprogenitors via astrocyte-microglial interactions. Dysregulation of the crosstalk between Wnt/¦Â-catenin signaling and anti-oxidant/anti-inflammatory pathways delineate novel mechanisms driving the decline of SVZ plasticity with age and the limited nigrostrial dopaminergic self-repair in PD. These findings hold a promise in developing therapies that target Wnt/¦Â-catenin signaling to enhance endogenous restoration and neuronal outcome in age-dependent diseases, such as PD.
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