Vacina para combater a Doença de Alzheimer

Vacina desenvolvida em laboratório espanhol, com bons resultados, em cobaias, na redução da concentração de proteína B amilóide.

International Journal of Alzheimer's Disease
Volume 2012 (2012), Article ID 376138, 17 pages
doi:10.1155/2012/376138

Research Article

Vaccine Development to Treat Alzheimer’s Disease Neuropathology in APP/PS1 Transgenic Mice

Iván Carrera,¹ Ignacio Etcheverría,¹ Lucía Fernández-Novoa,¹ Valter Lombardi,¹ Ramón Cacabelos,² and Carmen Vigo³

¹Department of Neurosciences, EuroEspes Biotechnology, Polígono de Bergondo, Nave F, 15165 A Coruña, Spain
²EuroEspes Biomedical Research Center, Institute for CNS Disorders and Genomic Medicine and EuroEspes Foundation, 15166 La Coruña, Spain
³Neuroscience Division, Atlas Pharmaceuticals, Sunnyvale, CA 94089, USA

Abstract

A novel vaccine addressing the major hallmarks of Alzheimer’s disease (AD), senile plaque-like deposits of amyloid beta-protein (Aβ), neurofibrillary tangle-like structures, and glial proinflammatory cytokines, has been developed. The present vaccine takes a new approach to circumvent failures of previous ones tested in mice and humans, including the Elan-Wyeth vaccine (AN1792), which caused massive T-cell activation, resulting in a meningoencephalitis-like reaction. The EB101 vaccine consists of  𝛽1-4 2delivered in a novel immunogen-adjuvant composed of liposomes-containing sphingosine-1-phosphate (S1P). EB101 was administered to APPswe/PS1dE9 transgenic mice before and after AD-like pathological symptoms were detectable. Treatment with EB101 results in a marked reduction of Aβplaque burden, decrease of neurofibrillary tangle-like structure density, and attenuation of astrocytosis. In this transgenic mouse model, EB101 reduces the basal immunological interaction between the T cells and immune activation markers in the affected hippocampal/cortical areas, consistent with decreased amyloidosis-induced inflammation. Therefore, immunization with EB101 prevents and reverses AD-like neuropathology in a significant manner by halting disease progression without developing behavioral spatial deficits in transgenic mice.