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(American Journal of Pathology. 2006;168:898-906.)
© 2006 American Society for Investigative Pathology

Transmission of Amyloidosis in Offspring of Mice with AApoAII Amyloidosis

Tatsumi Korenaga^*, Jingmin Yan^*, Jinko Sawashita^*, Takatoshi Matsushita, Hironobu Naiki, Masanori Hosokawa, Masayuki Mori^*, Keiichi Higuchi^*¶ and Xiaoying Fu^*¶

From the Department of Aging Biology,^* Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, Matsumoto; the Field of Regeneration Control, Institute for Frontier Medical Science, Kyoto University, Kyoto; the Department of Pathology, Fukui Medical University, Matsuoka; the Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, Kasugai; and The Core Research for Evolutional Science and Technology,^¶ Japan Science and Technology Corporation, Tokyo, Japan

Pre-existing amyloid fibrils can induce further polymerization of endogenous precursor proteins in vivo. Thus, transmission of amyloid fibrils (AApoAII) may induce a conformational change in endogenous apolipoprotein A-II and accelerate amyloid deposition in mouse senile amyloidosis. To characterize transmissibility, we examined amyloidosis in the offspring of AApoAII-injected mother mice that possessed the amyloidogenic Apoa2^c allele of the apolipoprotein A-II gene. At 4 months of age, amyloid deposits were detected in the intestines of offspring born from and nursed by amyloid fibril-injected mothers, with intensity of deposition increasing thereafter. No amyloid deposits were detected in the offspring of noninjected control mothers. Accelerated amyloidosis was also observed in offspring born from mothers without injection but nursed by amyloid fibril-injected mothers. However, this was not observed in offspring born from amyloid fibril-injected mothers but nursed by control mothers. This fostering excluded vertical transmission through the placenta, suggesting the presence of factors that accelerate amyloidosis during the nursing period. In addition, milk obtained from amyloid fibril-injected mothers induced AApoAII amyloidosis in young mice, and transmission electron microscopy detected noodle-like amyloid fibrils in milk of amyloid fibril-injected mothers. These results provide important insight into the etiology and pathogenesis of amyloid diseases.

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