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(American Journal of Pathology. 2004;165:273-281.)
© 2004 American Society for Investigative Pathology

Mostly Separate Distributions of CLAC- versus Aß40- or Thioflavin S-Reactivities in Senile Plaques Reveal Two Distinct Subpopulations of ß-Amyloid Deposits

Hisatomo Kowa*{dagger}, Tomoko Sakakura*, Yusuke Matsuura*, Tomoko Wakabayashi*, David M.A. Mann{ddagger}, Karen Duff§, Shoji Tsuji{dagger}, Tadafumi Hashimoto* and Takeshi Iwatsubo*

From the Department of Neuropathology and Neuroscience,* Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan; the Department of Neurology,{dagger} Graduate School of Medicine, University of Tokyo, Tokyo, Japan; the Department of Pathological Sciences,{ddagger} University of Manchester, Manchester, United Kingdom; and the Nathan Kline Institute,§ New York University, Orangeburg, New York

Collagenous Alzheimer amyloid plaque component (CLAC) is a unique non-Aß amyloid component of senile plaques (SP) derived from a transmembrane collagen termed CLAC-precursor. Here we characterize the chronological and spatial relationship of CLAC with other features of SP amyloid in the brains of patients with Alzheimer’s disease (AD), Down syndrome (DS), and of PSAPP transgenic mice. In AD and DS cerebral cortex, CLAC invariably colocalized with Aß42 but often lacked Aß40- or thioflavin S (thioS)-reactivities. Immunoelectron microscopy of CLAC-positive SP showed labeling of fibrils that are more loosely dispersed compared to typical amyloid fibrils in CLAC-negative SP. In DS cerebral cortex, diffuse plaques in young patients were negative for CLAC, whereas a subset of SP became CLAC-positive in patients aged 35 to 50 years, before the appearance of Aß40. In DS cases over 50 years of age, Aß40-positive SP dramatically increased, whereas CLAC burden remained at a constant level. In PSAPP transgenic mice, CLAC was positive in the diffuse Aß deposits surrounding huge-cored plaques. Thus, CLAC and Aß40 or thioS exhibit mostly separate distribution patterns in SP, suggesting that CLAC is a relatively early component of SP in human brains that may have inhibitory effects against the maturation of SP into ß-sheet-rich amyloid deposits.




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