Consistently, the overexpression of PGC-1α via adeno-associated virus in the brain of the AD murine transgenic model APP23 is sufficient to enhance the transcription of growth factors and to blunt Aβ-mediated neuroinflammation and neuronal death, leading to reduced-amyloid production and neuronal loss [179], together with decreased mitochondrial damage, thus restoring AD cognitive deficits [180]. The gene discussed is PPARGC1A; the disease is Alzheimer disease.