Immunotherapy might provide an effective treatment for
Alzheimer disease (AD). A unique feature of AD
immunotherapies is that an immune response against a
self antigen needs to be elicited without causing adverse autoimmune reactions. Current research is focussed on two possible targets in this regard: One is the inhibition of accumulation and deposition of
Amyloid beta 1-42 (Aβ42), which is one of the major
peptides found in
senile plaques and the second target is hyperphosphorylated tau, which forms neurofibrillary tangles inside the nerve cell and shows association with the progression of
dementia. Mouse models have shown that
immunotherapy targeting Aβ42 as well as tau with the respective anti-Aβ or anti-tau
antibodies can provide significant improvements in these mice. While anti-Aβ immunotherapy (active and passive immunizations) is already in several stages of clinical trials, tau based immunizations have been analyzed only in mouse models. Recently, as a significant correlation of progression of
dementia and levels of phoshorylated tau was found, high interest has again focussed on further development of tau based
therapies. While Aβ
immunotherapy might delay the onset of AD,
immunotherapy targeting tau might provide benefits in later stages of this disease. And last but not least, targeting Aβ and tau simultaneously with
immunotherapy might provide additional
therapeutic effects as these two pathologies are likely synergistic; an approach which has not been tested yet. In this review, we will summarize animal models used to test possible
therapies for AD, some of the facts about Aβ42 and tau biology, present on overview on halted, ongoing and upcoming clinical trials together with ongoing preclinical studies targeting tau or Aβ42.