Non–cell autonomous toxicity in neurodegenerative disorders: ALS and beyond
By H. Ilieva, M. Polymenidou, D. Cleveland. Journal of Cell Biology, 2009
1,023 citations recorded by the source corpus.
Selective degeneration and death of one or more classes of neurons is the defining feature of human neurodegenerative disease. Although traditionally viewed as diseases mainly affecting the most vulnerable neurons, in most instances of inherited disease the causative genes are widely—usually ubiquitously—expressed. Focusing on amyotrophic lateral sclerosis (ALS), especially disease caused by dominant mutations in Cu/Zn superoxide dismutase (SOD1), we review here the evidence that it is the convergence of damage developed within multiple cell types, including within neighboring nonneuronal supporting cells, which is crucial to neuronal dysfunction. Damage to a specific set of key partner cells as well as to vulnerable neurons may account for the selective susceptibility of neuronal subtypes in many human neurodegenerative diseases, including Huntington's disease (HD), Parkinson's disease (PD), prion disease, the spinal cerebellar ataxias (SCAs), and Alzheimer's disease (AD).
Subfields: Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/a3f5d409999c242dd371e3abaf57ed23033f6974
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Citations in the corpus
- Glial Lipid Droplets and ROS Induced by Mitochondrial Defects Promote Neurodegeneration (2015, neutral): “[PubMed: 18400901] Ilieva H, Polymenidou M, Cleveland DW. Non-cell autonomous toxicity in neurodegenerative disorders: ALS and beyond.”
- A comprehensive review of amyotrophic lateral sclerosis (2015, background): “[167,297] Furthermore, this causes an excessive influx of calcium, excessive firing of motor neurons, and initiation of several destructive biochemical processes within the cell, which are all known as important pathophysiological processes in familial and sporadic forms of ALS.[126,313] Glutamate e”
- NG2+ CNS glial progenitors remain committed to the oligodendrocyte lineage in postnatal life and following neurodegeneration. (2010, background): “…in ALS mice, such as cell death, inflamma- tion, and gliosis, also occur in neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease (Ilieva et al., 2009), and following stroke and acute CNS trauma, it is possible that NG2+ cells exhibit greater lineage plasticity in response…”