Inflammation as a causative factor in the aetiology of Parkinson's disease

By P. Whitton. British Journal of Pharmacology, 2007

629 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/1e4bc957179eda7003096ab0fb0ff7e3908ecc6d

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In Cellular and Molecular Neuroscience

In Neurology

Citations in the corpus

The role of exercise and PGC1α in inflammation and chronic disease (2008, background): “These cytokines are thought to promote the death of dopamine-containing neurons in the substantia nigra region of the brain, thereby contributing to the pathology of Parkinson's diseas”
Selective Neuronal Vulnerability to Oxidative Stress in the Brain (2010, positive): “While infl ammatory responses may protect neurons by removing injured cells or neuronal processes from the vulnerable regions, there is evidence showing that chronic infl ammation can be a causative factor for SNV (Herrera et al., 2005; Whitton, 2007).”
A Nurr1/CoREST transrepression pathway attenuates neurotoxic inflammation in activated microglia and astrocytes (2009, positive): “Several lines of evidence suggest that inflammatory mediators such as tumor necrosis factor (TNF)a, nitric oxide (NO) and Interleukin (IL)-1b derived from nonneuronal cells, including microglia, modulate the progression of PD (Brown, 2007; Hartmann et al., 2003; Teismann and Schulz, 2004; Whitton, 2”
The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, neutral): “…appears to be a ubiquitous finding in PD patients and experimental models of PD. Phagocyte activation, increased synthesis and release of proinflammatory cytokines, complement activation, activation of microglia, and release of reactiveoxygenspecies (ROS) havebeendescribed (Whitton,2007).”
Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease. (2008, background): “In addition to these well established pathomechanisms, there is mounting evidence from epidemiological, postmortem and animal studies to suggest that innate neuroinflammatory processes associated with glial cell activation participate in the progression of DN cell death (2-6).”
Increased Intestinal Permeability Correlates with Sigmoid Mucosa alpha-Synuclein Staining and Endotoxin Exposure Markers in Early Parkinson's Disease (2011, background): “It should also be noted that endotoxins might be directly involved in initiation and/or progression of neuroinflammatory injury in both the ENS and CNS in PD without systemic endotoxemia [36].”
Complexity of dopamine metabolism (2013, background): “Therefore, we refer to other reviews that nicely summarize this topic [175-178].”
Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress (2008, neutral): “Inflammation is a common feature of neurodegeneration, and is known to be present in PD patients and animal models (26).”
Neuroinflammation in Parkinson’s disease: its role in neuronal death and implications for therapeutic intervention (2009, background): “An important feature of the oxidative stress hypothesis of PD is that a transient initiation factor (i.e., toxins, bacterial, or viral infections, particulate matter, pesticides, etc.) may trigger an active, self-perpetuating cycle of chronic neuroinflammation (i.e., increased production of chemokin”
Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease (2011, methodology): “, 2003b) is consistent with the inflammatory features found in idiopathic PD (Gerhard et al., 2006; Whitton, 2007; Tansey and Goldberg, 2010), lending support to the construct validity of this model.”