Beyond Aβ deposition, emerging evidence strongly suggested that neuroinflammation and mitochondrial dysfunction are prerequisites for AD pathogenesis.443,444 Sheng and colleagues showed that expression levels of PGC-1α, NRF-1, and NRF-2 are significantly decreased in both AD hippocampal tissues and APPswe M17 cells. Here, PPARGC1A is linked to Alzheimer disease.