Vol.64

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.63

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.62

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.61

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.60

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.59

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.58

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.57

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.56

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.55

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.54

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.53

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.52

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.51

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.50

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.49

• No.1
• No.2/3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.48

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

• Vol.47 to 1
  (Members Only)

• HOME
• Vol.52 No.11
• CLINICA NEUROL, 52: 1168−1170, 2012
• Vol.52 No.11 contents

Symposium 2

Development of antibodies for immunotherapy of Alzheimer's disease

Shin-ei Matsumoto, Ph.D.¹⁾, Haifeng Jin, Ph.D.¹⁾, Kazuya Takeda, Ph.D.¹⁾, Yukako Hasegawa¹⁾, Yumiko Motoi, M.D., Ph.D.¹⁾²⁾, Nobutaka Hattori, M.D., Ph.D.¹⁾²⁾ and Takeshi Tabira, M.D., Ph.D.¹⁾

¹⁾Department of Diagnosis, Prevention and Treatment of Dementia, Graduate School of Medicine, Juntendo University
²⁾Department of Neurology, Juntendo University School of Medicine

Based on the amyloid cascade hypothesis, immunotherapy targeting amyloid β (Aβ) for Alzheimer's disease (AD) has been developed. It was reported that active immunization using Aβ peptide attenuates amyloid deposits and memory impairment in AD model mice. However, active immunization of patients with AD (AN-1792) was halted due to adverse effects in which a subset of patients developed meningoencephalitis. In order to avoid autoimmune encephalitis, passive immunotherapy using humanized monoclonal antibodies with specificity to Aβ are in clinical trials. We also developed an anti-Aβ monoclonal antibody 3.4A10, which react with AD brain-specific Aβ oligomers. On the other hand, some studies showed that immunotherapy approach targeting tau could attenuate pathology in AD model mouse. Here we introduce a current trend of immunotherapy for AD.
Full Text of this Article in Japanese PDF (210K)

(CLINICA NEUROL, 52: 1168−1170, 2012)
key words: Alzheimer's disease, vaccine, antibody, amyloid β, tau

(Received: 24-May-12)