Contributions of mitochondrial alterations, resulting from bad genes and a hostile environment, to the pathogenesis of Alzheimer's disease.
Mattson
Mark P
MP
Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. mattsonm@grc.nia.nih/gov
D000544:Alzheimer Disease / Q000209:etiology* / Q000235:genetics*; D016229:Amyloid beta-Peptides / Q000235:genetics; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D002149:Energy Intake; D004734:Energy Metabolism; D004777:Environment; D005492:Folic Acid / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics; D008928:Mitochondria / Q000235:genetics* / Q000378:metabolism / Q000648:ultrastructure; D009154:Mutation; D010809:Physical Fitness; D053764:Presenilin-1
D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D005609:Free Radicals; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1; D005492:Folic Acid; D002118:Calcium