[Vaccination therapy for Alzheimer's disease].
Since AN-1792 vaccine induced autoimmune encephalitis, several pharmaceutical companies are now concentrated in developing antibody therapy in Alzheimer's disease (AD). Each antibody has own characteristics. Thus, it is unpredictable at present which antibody is the most beneficial until we see the result of clinical trials. If disease modifying antibodies were found, they will be widely used for treatment of AD in near future. As a candidate of such antibodies, we have developed TAPIR-like antibody with much higher affinity to Abeta42 than Abeta40, and it effectively deleted senile plaque amyloid and Abeta oligomers without increasing microhemorrhages. Although passive immunization can avoid autoimmune encephalitis, it is expensive and it is not suitable for prevention. Thus, safe vaccines by active immunization would be better. Vaccines that induce Th2 type immune responses such as oral vaccine or per-nasal vaccine would be promising.
Tabira
Takeshi
T
Department of Diagnosis, Prevention and Treatment of Dementia, Graduate School of Juntendo University.
D000544:Alzheimer Disease / Q000628:therapy*; D023582:Alzheimer Vaccines / Q000627:therapeutic use; D016229:Amyloid beta-Peptides; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D061067:Antibodies, Monoclonal, Humanized; D002986:Clinical Trials as Topic; D000229:Dependovirus; D000068717:Glatiramer Acetate; D006801:Humans; D010446:Peptide Fragments; D010455:Peptides; D018418:Th2 Cells / Q000276:immunology; D014611:Vaccination
C437846:AN-1792; D023582:Alzheimer Vaccines; D016229:Amyloid beta-Peptides; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D010446:Peptide Fragments; D010455:Peptides; C075222:amyloid beta-protein (1-42); D000068717:Glatiramer Acetate; C545458:bapineuzumab