Fas ligand-mediated apoptosis in degenerative disorders of the brain.
While defective apoptosis predisposes to neoplasia, inappropriate apoptosis in the brain leads to permanent neurological deficits. Disregulated apoptosis has been implicated in several neurodegenerative disorders including Alzheimer's, Parkinson's, and Huntington's diseases. Recent reports have suggested that the key apoptosis regulator Fas ligand (FasL) may participate in both neuronal and immune cell apoptosis in Alzheimer's disease. FasL has also been implicated as a negative regulator for the inflammatory component of the demyelinating brain disorder multiple sclerosis (MS). Here, we discuss how FasL-mediated apoptosis may balance immune cell access to the brain with Alzheimer's disease and MS representing extremes of too little and too much immune access, respectively.
Division of Biomedical Sciences, University of California-Riverside, 900 University Avenue, Riverside, California 92521-0121, USA. doug.ethell@ucr.edu
Douglas W
DW
Ethell
Lillian A
LA
Buhler
D016229:Amyloid beta-Peptides / Q000378:metabolism / Q000633:toxicity; D000818:Animals; D017209:Apoptosis; D053222:Fas Ligand Protein; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism*; D019636:Neurodegenerative Diseases / Q000378:metabolism* / Q000473:pathology*; D009474:Neurons / Q000378:metabolism / Q000473:pathology
D016229:Amyloid beta-Peptides; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins