There have been several reports over the years that the AD brain exhibits deficits in energy metabolism. In 1994, Yankner's group reported that sodium azide treatment increased the processing of APP to potentially amyloidogenic fragments in culture. Paul Jantzen and colleagues report (Abstract 592.7) on the effects of NaAz administrationin PS1/APP (Duff/Hsiao) mice. Following four weeks of administration of NaAz (via subcutaneous infusion pump), they found that cytochrome oxidase activity was reduced by 22 percent. In untreated double Tg mice, they see relatively few activated microglia (detected with F480) associated with Aβ deposits, but in the NaAz treated animals, there is an extensive upregulation of microglia around Aβ deposits. The group did not report an increase in microglia associated with Aβ deposits in untreated Tg animals, in contrast to other studies. However, the association of activated microglia in the NaAz-treated animals mirrored that typically seen in moderately severe AD cases, and was more extensive than I've seen in any transgenic model. Also, they reported the presence of TUNEL-positive nuclei in the NaAz-treated Tg mice, while infusion of NaAz into non-Aβ depositing littermates did not active microglia nor result in significant numbers of TUNEL positive nuclei. Presumably, these littermates were nontransgenic, but this was not clear from the presentation. Jantzen did not present data addressing whether NaAz treatment actually leads to greater deposition of Aβ itself, as one might predict. It is encouraging that many labs are now moving to phases where different systems within these Tg models are challenged (e.g., see also Abstract 592.6).—Brian J. Cummings


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