Molecular Pathways of Neurodegeneration in Parkinson's Disease

By T. Dawson, Valina L. Dawson. Science, 2003

1,693 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/0ee0be5976ae3459621001484e05ec042b9d6435

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

In Neurology

Citations in the corpus

Cell biology of protein misfolding: The examples of Alzheimer's and Parkinson's diseases (2004, background): “This situation has begun to change in the last few years with the discovery of no less than five genes that predispose individuals to rare, familial forms of the diseas”
The scientific and clinical basis for the treatment of Parkinson disease (2009) (2009, background): “With the development of the Pittsburgh Compound-B ([(11)C]-PIB), which binds to -amyloid and can be used as a PET ligand for measuring plaque load in patients with Alzheimer disease (AD),62 an intense effort has been directed toward developing a similar ligand that binds to -synuclein and can be use”
Dopamine covalently modifies and functionally inactivates parkin (2005, background): “Given the number of cysteine residues in parkin (35), evidence of elevated oxidative stress in the midbrain of individuals with Parkinson diseas”
Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase (2006, background): “This has led to the discovery of common pathophysiological pathways such as enhanced oxidative stress, protein misfolding and aggregation and dysfunction of the ubiquitin-proteasome syste”
Inclusion formation and neuronal cell death through neuron-to-neuron transmission of α-synuclein (2009, background): “In PD, accumulation of -synuclein is associated with impairment in the protein quality control systems, such as proteasomal and autophagic degradation (17, 18).”
Role of cardiolipin alterations in mitochondrial dysfunction and disease. (2007, background): “These alterations were associated with a 15% reduction in linked complex I/III activity of the electron transport chain, which is thought to be a critical factor in the development of Parkinson’s disease (21).”
Aggregated α‐synuclein activates microglia: a process leading to disease progression in Parkinson's disease (2005, background): “UPS-mediated proteolysis, resulting in cell death (23, 24, 34).”
LRRK2 Mutant iPSC-Derived DA Neurons Demonstrate Increased Susceptibility to Oxidative Stress (2011, positive): “Although it is not well understood, the path- ogenesis of PD has been linked to both environmental and genetic factors (Dawson and Dawson, 2003).”
The mitochondrial energy transduction system and the aging process. (2007, background): “Inhibition of complex I creates an environment of mitochondrial oxidative damage and of nitration that may lead to opening of the permeability transition pore and to apoptotic cell death (72), or to aggregation of -synuclein with the subsequent death of dopaminergic neurons (46).”
Metals, oxidative stress and neurodegenerative disorders (2010, neutral): “In addition, other important factors, involving inflammation, toxic action of nitric oxide, defects in protein clearance, and mitochondrial dysfunction all contribute to the etiology of PD [13].”