Amyloid-β Immunotherapy on Alzheimer disease: Prevention and Therapeutic Target

Abstract

Alzheimer disease (AD) is the most common neurodegenerative disease and form of dementia. The peptide amyloid-β (Aβ) is a most therapeutic target in AD on the basis of pathological and genetic suffices that supports a role for this molecule in the disease process. Studies show that Aβ immunotherapies (Active and passive) have been revealed to alleviate cerebral Aβ levels and improve cognition in animal models of AD. In humans, clinical trial phase 2 AN1792 conducted by Elan et al stated that Aβ vaccine was stopped when ~6% of the immunized patients developed meningoencephalitis. However, some plaque clearance and modest clinical improvements were observed in patients following immunization. In this study, Aβ immunotherapies will be discussed. Passive and active method of treatment in human and non-human primate with AD will also be review. Preclinical studies and the limited data from clinical trials and non-human primates’ evidence suggest Aβ immunotherapy as the most effective in preventing or slowing the progression of AD when patients are immunized before or in the very earliest stages of disease onset. AD Biomarkers and imaging technology have improved greatly over the past 11 years and, in the future, can be used to identify pre-symptomatic, at-risk individuals who might benefit from Aβ immunotherapy

Immunotherapies for Alzheimer’s Disease—A Review

“…To prevent the accumulation of plaques, novel and safer plant-based vaccine strategies have been suggested [84]. In 2002, the first active AD vaccine (AN1792) developed by ELAN in Ireland and Wyeth in the USA went through a phase IIa clinical trial but was suspended due to the development of meningoencephalitis in ~6% of the individuals [10,80]. The exact mechanism of this was unknown and determined to have no clear relation to serum anti-Aβ 42 antibody titers but may have been an autoimmune response rising from T cell interactions [85,86].…”