The role of cerebral amyloid β accumulation in common forms of Alzheimer disease
J. Clin. Invest. Sam Gandy, et al. 115:1121 doi:10.1172/JCI25100 [Go to this article.]

Figure 3
Amyloid plaque–forming transgenic mice and positron emission tomography (PET) scans of amyloid plaque load in normal human subjects and subjects with AD. (A) Thioflavin staining of subiculum of control mouse, aged 14 months. Fluorescence is nonspecific and cellular. Magnification, ×20. (B) Thioflavin staining of littermate, mutant APP X mutant PS mouse, demonstrating thioflavin-positive amyloid plaques. Magnification, ×20. (C) Immunostaining of amyloid plaque from cortex from same mouse as in B. Magnification, ×40. Figures courtesy of Michelle Ehrlich (Thomas Jefferson University). (D) [¹⁸F]FDDNP PET scan (to examine amyloid plaque and NFT load), MRI, and fluoro-deoxy-glucose (FDG) PET (to examine glucose metabolism) images of a subject with AD and a control normal subject. The [¹⁸F]FDDNP and FDG (summed) images are coregistered to their respective MRI images. Areas of FDG hypometabolism (blue) are matched with the localization of amyloid plaques and NFTs as visualized by [¹⁸F]FDDNP binding. The color bar represents the scaling of the [¹⁸F]FDDNP and FDG images. FDDNP, 2-(1-[6-[(2-[¹⁸F]fluoroethyl)(methyl)amino]-2-naphthyl]ethylidene)malononitrile; max, maximum; min, minimum. Figure reproduced with permission from the American Journal of Geriatric Psychiatry (62).