期刊
NEUROTHERAPEUTICS
卷 7, 期 4, 页码 471-481出版社
SPRINGER
DOI: 10.1016/j.nurt.2010.05.012
关键词
Astrogliosis; amyotrophic lateral sclerosis; excitotoxicity; oxidative stress; death receptors; glutathione
资金
- Amyotrophic Lateral Sclerosis (ALS) Association
- National Institute of Environmental Health Sciences (NIEHS) [ES08089]
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R29ES008089, R01ES008089] Funding Source: NIH RePORTER
Amyotrophic lateral sclerosis (ALS) is a fatal disorder characterized by the progressive loss of motor neurons. Although the molecular mechanism underlying motor neuron degeneration remains unknown; non-neuronal cells (including astrocytes) shape motor neuron survival in ALS. Astrocytes closely interact with neurons to provide an optimized environment for neuronal function and respond to all forms of injury in a typical manner known as reactive astrogliosis. A strong reactive astrogliosis surrounds degenerating motor neurons in ALS patients and ALS-animal models. Although reactive astrogliosis in ALS is probably both primary and secondary to motor neuron degeneration; astrocytes are not passive observers and they can influence motor neuron fate. Due to the important functions that astrocytes perform in the central nervous system; it is of key importance to understand how these functions are altered when astrocytes become reactive in ALS. Here; we review the current evidences supporting a potential toxic role of astrocytes and their viability as therapeutic targets to alter motor neuron degeneration in ALS.
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