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The Journal of Neuroscience, 1999:RC10:1-5

RAPID COMMUNICATION
Histochemically Reactive Zinc in Plaques of the Swedish Mutant -Amyloid Precursor Protein Transgenic Mice

Joo-Yong Lee, Inhee Mook-Jung, and Jae-Young Koh

National Creative Research Initiative Center for the Study of CNS Zinc and Department of Neurology, University of Ulsan College of Medicine, Seoul 138-736, Korea

Endogenous metals such as zinc may contribute to -amyloid (A) aggregation and hence the plaque formation. In the present study, we examined brains of four Swedish mutant amyloid precursor protein (APP) transgenic mice at 12 months of age for histochemically reactive zinc in the plaques. Here, we report that all the Congo red (+) mature plaques contained chelatable zinc, as demonstrated by staining with the zinc-specific fluorescent dye 6-methoxy-8-quinolyl-para-toluenesulfonamide (TSQ). On the other hand, Congo red () preamyloid A deposits were not stained with TSQ. Interestingly, although cerebellum contained similar degree of preamyloid A deposits as cerebral cortex, it was completely devoid of Congo red- or TSQ-stained mature plaques. Although zinc from plaques was only slowly and partially removed by a specific zinc remover, dithizone, treatment of brain sections with heparinase-III, which degrades heparan sulfate proteoglycan (HSPG), another major constituent of plaques, greatly fastened the zinc removal with dithizone.

The present study has demonstrated the presence of histochemically reactive zinc in plaques, but not preamyloid A deposits, of the Swedish mutant APP transgenic mice. Because preamyloid A deposits fail to develop into congophilic plaques in cerebellum where synaptic vesicle zinc is deficient, the synaptic zinc may be a necessary element in the plaque formation. In holding zinc inside plaques, HSPG may contribute in addition to A.

Key words: -amyloid; Alzheimer's disease; heparan sulfate proteoglycan; metal; cortex; cerebellum

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Copyright © 1999 Society for Neuroscience  0270-6474/99/$05.00/0

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