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An Astrocyte Model Looking Toward Understanding Neurodeneration
Author(s) -
Corcoran Ellen,
Hemkin Sheryl
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.533.88
Subject(s) - astrocyte , neurodegeneration , neuroscience , neurochemical , biology , glutamate receptor , intracellular , central nervous system , nervous system , neuroinflammation , microbiology and biotechnology , disease , medicine , immunology , inflammation , pathology , receptor , biochemistry
Astrocytes, the most numerous subtype of glial cell in the central nervous system, have been previously identified as key regulators of neural systems due to their ability to maintain neurochemical homeostasis in the central nervous system. There is growing evidence that astrocytes not only have a supportive role in regulation, but are active partners in the information transfer processes within the brain. A healthy astrocyte can, under unknown circumstances, be transformed to a pathogenic or “reactive” astrocyte. This astrocyte form has been linked to neurodegeneration and enigmatic diseases such as Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis. It is postulated that intercellular signals shuttled through the astrocyte may be at least partially responsible for this neural degeneration, and extracellular stimuli to the astrocyte, such as by glutamate, ATP or TNFα, may cause changes in the oscillatory behavior of the cytosolic calcium and thus cause the downstream signaling. This work proposes a new model to help gain insight as to neuroinflammatory signals alter intracellular calcium dynamics, disrupt astrocyte metabolism, and ultimately facilitate neurodegeneration. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .