Molecular pathophysiology of Parkinson's disease.

By D. Moore, A. West, Valina L. Dawson, T. Dawson. Annual Review of Neuroscience, 2005

1,280 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/150549acc3717695fa0e1dbb73c05a508bc78b75

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Citations in the corpus

A Review of the Common Neurodegenerative Disorders: Current Therapeutic Approaches and the Potential Role of Nanotherapeutics (2022, background): “Several mechanisms have been identified to play key roles in PD disease progression, and these include α-synuclein misfolding and aggregation, mitochondrial dysfunction, dysfunctional protein clearance systems, the ubiquitin–proteasome system, and autophagy– lysosome system, and neuroinflammation [3”
Oxidative stress and neurodegeneration: where are we now? (2006, background): “Thus, in some studies, treatment of rats or monkeys with low-dose rotenone over long periods produces PD-like symptoms and neurodegeneration accompanied by oxidative damage, nitrotyrosine formation, and generation of protein aggregates containing a-synuclein (Moore et al. 2005).”
Calcium and neurodegeneration (2007, background): “Mutations in several different genes have been linked to earlyonset inherited PD; they include α-synuclein, Parkin, and DJ-1 (Moore et al., 2005).”
EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers (2008, background): “The protein consists of an amphiphatic Nterminal domain, a hydrophobic core domain, also known as the NAC (non-Aβ component) region, and an acidic, proline-rich C-terminal domain [34, 43 ].”
Diagnosis and treatment of Parkinson disease: molecules to medicine. (2006, background): “org Volume 116 Number 7 July 2006 have been identified (75).”
Genetic Animal Models of Parkinson’s Disease (2010, neutral): “Several excellent reviews on these animal and cellular models exist (see Bové et al., 2005; Chesselet et al., 2008; Gupta et al., 2008; Lim and Ng, 2009; Moore et al., 2005; Pallanck and Whitworth, 2007; Wong, 2007).”
RING domain E3 ubiquitin ligases. (2009, background): “Courtesy of Ted Dawson, John Hopkins University (189).”
Parkinson's disease-associated mutations in LRRK2 link enhanced GTP-binding and kinase activities to neuronal toxicity. (2007, background): “Numerous reports suggest that proteins associated with PD respond to oxidative stress, either functioning in a neuroprotective manner in the case of parkin and DJ-1, or through potentiating aggregation and toxicity in the case of a-synuclein (26,27).”
Ageing and neuronal vulnerability (2006, background): “Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calciumdependent apoptosis.”
A Nurr1/CoREST transrepression pathway attenuates neurotoxic inflammation in activated microglia and astrocytes (2009, neutral): “Nurr1 Exerts Anti-Inflammatory and Neuroprotective Effects in Glia Although a number of genes have been identified as causes of familial PD, the majority of cases are sporadic and of unknown etiology (Farrer, 2006; Moore et al., 2005).”
PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy (2010, background): “The major ity of PD cases are sporadic; however, the discovery of genes linked to rare familial forms of this disease has provided important insight into the molecular mechanisms of disease pathogenesis (Moore et al., 2005; Hardy et al., 2006).”
Studies on free radicals, antioxidants, and co-factors (2007, background): “This is a progressive neurodegenerative movement disorder and is the most common form of motor system degeneration affecting approximately 1% of the population over the age of 65 (Moore et al 2005).”