Apoptosis and caspases in neurodegenerative diseases.
By R. Friedlander. New England Journal of Medicine, 2003
888 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/26c41f11dadc97cf386fcbc83e656d5b8cc6f39d
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 Molecular Biology
- R. Youle
- J. Martinou
- P. Whitton
- J. Morillas-Ruiz
- J. M. Rubio-Pérez
- G. Perkins
- P. Mehlen
- E. Bossy‐Wetzel
Citations in the corpus
- Cell death in the nervous system (2006, background): “Minocycline, a second-generation tetracycline that inhibits mitochondrial cytochrome c release, effected neuroprotection in mouse models of HD, PD and AL”
- Complexity of dopamine metabolism (2013, background): “Due to ROS overload, injurious effects such as lipid oxidation, uncoupling of the electron transport chain or DNA damage occur, which finally leads to cell death [181-184].”
- A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines (2012, background): “Supplementation of these natural compounds may provide a new therapeutic line of approach to this brain disorder.”
- Melatonin: a multitasking molecule. (2010, background): “The intrinsic apoptotic pathway (the mitochondrial pathway) involves the release of proapoptotic molecules from the mitochondria (Friedlander, 2003).”
- Nitric oxide‐induced mitochondrial fission is regulated by dynamin‐related GTPases in neurons (2006, background): “Both caspase-dependent and independent pathways appear to operate in the neuronal loss in neurodegenerative disorders (Li et al, 2000; Leist and Jaattela, 2001; Friedlander, 2003; Cregan et al, 2004).”
- Histone Deacetylase Inhibition by Sodium Butyrate Chemotherapy Ameliorates the Neurodegenerative Phenotype in Huntington's Disease Mice (2003, neutral): “Early molecular events likely trigger cascades of damage and compensatory responses, leading to dysfunctional neurons that are susceptible to other insults, such as oxidative injury, excitotoxic stress, inflammatory and proapoptotic signals, and energy depletion (Beal, 2000; Friedlander, 2003).”
- Inflammation as a causative factor in the aetiology of Parkinson's disease (2007, background): “It has also been recognized that oxidative stress leading to caspase activation and consequent apoptosis are clearly evident in PD (Friedlander, 2003).”