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Immunotherapy of cerebrovascular amyloidosis in a transgenic mouse model

Lifshitz, Veronica, Weiss, Ronen, Benromano, Tali, Kfir, Einat, Blumenfeld-Katzir, Tamar, Tempel-Brami, Catherine, Assaf, Yaniv, Xia, Weiming, Wyss-Coray, Tony, Weiner, Howard L. and Frenkel, Dan 2012. Immunotherapy of cerebrovascular amyloidosis in a transgenic mouse model. Neurobiology of Aging 33 (2) , 432.e1-432.e13. 10.1016/j.neurobiolaging.2011.01.006

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Cerebrovascular amyloidosis is caused by amyloid accumulation in walls of blood vessel walls leading to hemorrhagic stroke and cognitive impairment. Transforming growth factor-β1 (TGF-β1) expression levels correlate with the degree of cerebrovascular amyloid deposition in Alzheimer's disease (AD) and TGF-β1 immunoreactivity in such cases is increased along the cerebral blood vessels. Here we show that a nasally administered proteosome-based adjuvant activates macrophages and decreases vascular amyloid in TGF-β1 mice. Animals were nasally treated with a proteosome-based adjuvant on a weekly basis for 3 months beginning at age 13 months. Using magnetic resonance imaging (MRI) we found that while control animals showed a significant cerebrovascular pathology, proteosome-based adjuvant prevents further brain damage and prevents pathological changes in the blood-brain barrier. Using an object recognition test and Y-maze, we found significant improvement in cognition in the treated group. Our findings support the potential use of a macrophage immunomodulator as a novel approach to reduce cerebrovascular amyloid, prevent microhemorrhage, and improve cognition.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Neuroscience and Mental Health Research Institute (NMHRI)
Publisher: Elsevier
ISSN: 0197-4580
Last Modified: 21 Aug 2019 02:21

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