Abstract

Alzheimer’s disease (AD) is a neuropathology characterized by progressive cognitive impairment and dementia. The disease is attributed to senile plaques, which are aggregates of amyloid beta (Aβ) outside nerve cells; neurofibrillary tangles, which are filamentous accumulations of phosphorylated tau in nerve cells; and loss of neurons in the brain tissue. Immunization of an AD mouse model with Aβ-eliminated pre-existing senile plaque amyloids and prevented new accumulation. Furthermore, its effect showed that cognitive function can be improved by passive immunity without side effects, such as lymphocyte infiltration in AD model mice treated with vaccine therapy, indicating the possibility of vaccine therapy for AD. Further, considering the possibility of side effects due to direct administration of Aβ, the practical use of the safe oral vaccine, which expressed Aβ in plants, is expected. Indeed, administration of this oral vaccine to Alzheimer’s model mice reduced Aβ accumulation in the brain. Moreover, almost no expression of inflammatory IgG was observed. Therefore, vaccination prior to Aβ accumulation or at an early stage of accumulation may prevent Aβ from causing AD.

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