Axonal Self-Destruction and Neurodegeneration
By M. Raff, A. Whitmore, J. Finn. Science, 2002
666 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Physiology
View Paper: https://www.semanticscholar.org/paper/8ed7e1f3cfd56395ad3e42e9c44735528655c269
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In Cellular and Molecular Neuroscience
In Physiology
Citations in the corpus
- Molecular mechanisms of neurodegeneration in Alzheimer's disease. (2010, background): “Loss of synapses (7,51,52) and axonal pathology (53) are probably key neuropathological features leading to dementia in these neurodegenerative disorders; however, other factors may contribute.”
- Evaluation and management of peripheral nerve injury. (2008, background): “Loss of the axoplasmic cytoskeleton begins within about seven days in humans, accompanied by a caspase-independent program of autodestruction (Raff et al., 2002).”
- Axon degeneration mechanisms: commonality amid diversity (2005, background): “The delay in Wallerian degeneration by genetic mutation and the fact that it can be triggered by a wide range of insults suggest instead a regulated, proactive death programme akin to apoptosi”
- Selective vulnerability and pruning of phasic motoneuron axons in motoneuron disease alleviated by CNTF (2006, background): “pruning, the 'dying back' process in the FALS mode”
- Clinical Progression in Parkinson's Disease and the Neurobiology of Axons (2010, background): “This discrepancy was not unexpected, because there is substantial evidence that the canonical pathways of PCD seem to play a minor role in axon degeneration.(11,12) The concept that destruction of the neuron cell body, which is brought about by these pathways, is a separate and distinct process from”
- Oxidative stress in glaucomatous neurodegeneration: mechanisms and consequences. (2006, background): “Recent evidence supports that this active and regulated program of axonal self-destruction is molecularly distinct from somal apoptosis (Finn et al., 2000; Raff et al., 2002; Whitmore et al., 2003).”
- N-APP binds DR6 to cause axon pruning and neuron death via distinct caspases (2009, background): “Several properties of APP made it a candidate for a DR6 ligand: (1) it is highly expressed by developing spinal and sensory neurons and their axons (Fig.”
- Axon pruning: an essential step underlying the developmental plasticity of neuronal connections (2006, background): “…elimination have become synonymous with phenomena that are associated with this regressive phase of nervous system development (Purves & Lichtman 1980; Cowan et al. 1984; Burek & Oppenheim 1996; Lichtman & Colman 2000; Meier et al. 2000; Raff et al. 2002; Yuan et al. 2003; Luo & O'Leary 2005).”
- Classification of cell death (2005, neutral): “Additional less-characterized forms of cellular catabolism take place in the nervous system, such as Wallerian degeneration, in which part of a neuron or axon degenerates without affecting the main cell body.(69,70) This term does not describe a type of cell death sensu stricto, because neurons affe”
- Hallmarks of neurodegenerative diseases. (2023, neutral): “36,171,172 172, 176, 181 Notably, neurofilament aggregates are detected in several NDDs. 168,175 Neurofilament aggregates form a liquid crystal gel network in ALS, AD, PD, FTD, SMA, SCA1, and other NDDs. 168,175 Although the mechanism underlying protein aggregation in these situations remains largely…”