CLINICAL NEUROSCIENCE AND NEUROPATHOLOGYGangliosides determine the amyloid pathology of Alzheimer's diseaseOikawa, Naotoa; Yamaguchi, Haruyasub; Ogino, Koichic; Taki, Takaoc; Yuyama, Koheia; Yamamoto, Naokia; Shin, Ryong-Woond; Furukawa, Koichie; Yanagisawa, KatsuhikoaAuthor Information aDepartment of Alzheimer's Disease Research, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Obu bGunma University School of Health Sciences, Maebashi cMolecular Medical Science Institute, Otsuka Pharmaceutical Co. Ltd., Tokushima dDepartment of Neurological Science, Tohoku University Graduate School of Medicine, Sendai eDepartment of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya, Japan Correspondence to Katsuhiko Yanagisawa, Vice Director, National Institute for Longevity Sciences, NCGG, 36-3 Gengo, Morioka, Obu, Aichi 474-8522, Japan Tel/fax: +81 562 44 6594; e-mail: firstname.lastname@example.org Present affiliation of Naoki Yamamoto, Department of Pharmacy, College of Pharmaceutical Sciences, Ritsumeikan University, Shiga, Japan Received 25 December 2008 accepted 5 February 2009 NeuroReport: August 5th, 2009 - Volume 20 - Issue 12 - p 1043-1046 doi: 10.1097/WNR.0b013e32832e4b9d Buy SDC Metrics Abstract Gangliosides, GM3 and GM1, are suggested to accelerate the deposition of the amyloid β-protein as amyloid angiopathy and senile plaques, respectively, in the Alzheimer brain. We investigated the profile of amyloid deposition in the brains of transgenic mice expressing a mutant amyloid precursor protein with a disrupted GM2 synthase gene, in which GM3 accumulates whereas GM1 is lacking. These mice showed a significantly increased level of deposited amyloid β-protein in the vascular tissues. Furthermore, formation of severe dyshoric-form amyloid angiopathy, in which amyloid extended from the blood vessel walls deeply into the surrounding parenchyma was observed. Our results indicate that the expression of gangliosides is a critical determinant for the amyloid pathology in the Alzheimer brain. © 2009 Lippincott Williams & Wilkins, Inc.