Figure 4From: In vivo modification of Abeta plaque toxicity as a novel neuroprotective lithium-mediated therapy for Alzheimer’s disease pathology Lithium treatment reduced the size and increased the compaction of the extracellular Abeta plaques. A) Lithium treatment reduced the size of Abeta deposits. Plaques were immunostained with anti-Abeta42 antibody. Representative images (a1 and a2) and quantitative analysis (a3 and a4) of Abeta plaque size from the CA1 subfield of control and lithium-treated PS1xAPP mice. (a3) The individual plaque size (μm2) was quantitatively assessed from 25 sections of 6 different control or lithium treated PS1xAPP mice. (a4) The plaque size distribution was determined by calculating the number of plaques falling into distinct area categories (ranging from <200 μm2 to >2000 μm2). For each category, the difference between control and lithium was determined by t-test. so, stratum oriens; sp, stratum pyramidale; sr, stratum radiatum. B) Lithium treatment increased the Abeta plaque compaction. Signal density of Abeta42 immunostained plaques from control (b1, b2) and lithium-treated (b3, b4) mice were measured in the CA1 subfield of hippocampus. Optical densities (pixel/μm2) of plaques from 5 sections/mouse and 5 mice per group was represented in the graph. C) Plaque oligomeric halo, considered as the difference between OC- and Thio-S-stained areas was reduced by lithium. Plaques were sequentially staining with Thio-S and the OC antibody. (c1-c6) Representative images of a similar size plaque in the CA1 region of control (c1-c3) or lithium-treated (c4-c6) mice showing the plaque halo. (c7) Similar size plaques (< 200 μm2) were analyzed (15 plaques per animal, n = 3 mice per group). Scale bars: a1, a2 200 μm; b1-b4 25 μm; c1-c6 20 μm.Back to article page