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.