Advances in the War on Alzheimer's   Cell  Volume 151, Issue 1, (September 2012) DOI: 10.1016/j.cell.2012.09.007 Copyright © 2012 Terms and Conditions

Medial surface projects of the brain demonstrate the absence of amyloid plaque in non-carriers of the gene (top left). In the pre-symptomatic phase of Alzheimer's in this cohort, amyloid plaques are wide spread, most notably in the medial parietal lobe (bright green area). Amyloid plaque burden continues to increase in participants with mild symptoms and in those with dementia. Amyloid plaque burden was measured using [11C]PiB PET imaging; images show quantitative standardized uptake value ratios (SUVRs). Image courtesy T. Benzinger and T. Blazey, DIAN Imaging Core. Cell 2012 151, DOI: (10.1016/j.cell.2012.09.007) Copyright © 2012 Terms and Conditions

Under conditions where expression levels of LDLR are increased (as shown here on a neuron and an astrocyte) and binding ApoE, Aβ is not retained in the brain interstitial fluid and more of the peptide is cleared from the brain to the blood. Image courtesy of Joseph Castellano. Cell 2012 151, DOI: (10.1016/j.cell.2012.09.007) Copyright © 2012 Terms and Conditions

Confocal microscopy of mitochondria-localized GFP reveals elongated mitochondria in neuronal cell bodies of human tau-expressing flies. Photo courtesy of Brian DuBoff. Cell 2012 151, DOI: (10.1016/j.cell.2012.09.007) Copyright © 2012 Terms and Conditions

Lipid droplets (bright green dots) are deposited in fibroblasts from Alzheimer disease patients, but not in normal cells. These droplets reflect one of the many aspects of deranged MAM function found in AD. Photo courtesy of Estela Area-Gomez, Columbia University. Cell 2012 151, DOI: (10.1016/j.cell.2012.09.007) Copyright © 2012 Terms and Conditions