Abstract
Recent advances in our understanding of the neurobiology of Alzheimer's disease (AD) have led to the development of putative disease-modifying treatments. The most revolutionary of these approaches consists in the removal of brain β-amyloid (Aβ) via anti-Aβ antibodies. Brain imaging and neuropathological studies have shown the ability of both active and passive anti-Aβ immunotherapies of clearing Aβ deposits from the brain of the AD patients. An active anti-Aβ vaccine preparation, AN1792, has been used in AD patients with some clues of clinical efficacy but causing meningoencephalitis in about 6% of patients and it has been abandoned. Several second-generation active Aβ vaccines and passive Aβ immunotherapies have been developed and are under clinical investigation with the aim of accelerating Aβ clearance from the brain of the AD patients. The most advanced of these immunological approaches is bapineuzumab, composed of humanized anti-Aβ monoclonal antibodies, that has been tested in two Phase II trials, demonstrating to reduce Aβ burden in the brain of AD patients. However, the preliminary cognitive efficacy of bapineuzumab appears uncertain. The occurrence of vasogenic edema, especially in apolipoprotein E E{open}4 carriers, may limit its clinical use and have led to abandon the highest dose of the drug (2 mg/kg). The results of four ongoing large Phase III trials on bapineuzumab will tell us if passive anti-Aβ immunization is able to alter the course if this devastating disease.
| Original language | English |
|---|---|
| Pages (from-to) | 808-817 |
| Number of pages | 10 |
| Journal | Current Alzheimer Research |
| Volume | 8 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - Dec 2011 |
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Keywords
- β-amyloid
- Active immunotherapy
- Alzheimer's disease
- Bapineuzumab
- Passive immunotherapy
ASJC Scopus subject areas
- Neurology
- Clinical Neurology
Cite this
Anti-β -amyloid immunotherapy for alzheimer's disease : Focus on Bapineuzumab. / Panza, Francesco; Frisardi, Vincenza; Imbimbo, Bruno P.; Seripa, Davide; Paris, Francesco; Santamato, Andrea; D'Onofrio, Grazia; Logroscino, Giancarlo; Pilotto, Alberto; Solfrizzi, Vincenzo.
In: Current Alzheimer Research, Vol. 8, No. 8, 12.2011, p. 808-817.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Anti-β -amyloid immunotherapy for alzheimer's disease
T2 - Focus on Bapineuzumab
AU - Panza, Francesco
AU - Frisardi, Vincenza
AU - Imbimbo, Bruno P.
AU - Seripa, Davide
AU - Paris, Francesco
AU - Santamato, Andrea
AU - D'Onofrio, Grazia
AU - Logroscino, Giancarlo
AU - Pilotto, Alberto
AU - Solfrizzi, Vincenzo
PY - 2011/12
Y1 - 2011/12
N2 - Recent advances in our understanding of the neurobiology of Alzheimer's disease (AD) have led to the development of putative disease-modifying treatments. The most revolutionary of these approaches consists in the removal of brain β-amyloid (Aβ) via anti-Aβ antibodies. Brain imaging and neuropathological studies have shown the ability of both active and passive anti-Aβ immunotherapies of clearing Aβ deposits from the brain of the AD patients. An active anti-Aβ vaccine preparation, AN1792, has been used in AD patients with some clues of clinical efficacy but causing meningoencephalitis in about 6% of patients and it has been abandoned. Several second-generation active Aβ vaccines and passive Aβ immunotherapies have been developed and are under clinical investigation with the aim of accelerating Aβ clearance from the brain of the AD patients. The most advanced of these immunological approaches is bapineuzumab, composed of humanized anti-Aβ monoclonal antibodies, that has been tested in two Phase II trials, demonstrating to reduce Aβ burden in the brain of AD patients. However, the preliminary cognitive efficacy of bapineuzumab appears uncertain. The occurrence of vasogenic edema, especially in apolipoprotein E E{open}4 carriers, may limit its clinical use and have led to abandon the highest dose of the drug (2 mg/kg). The results of four ongoing large Phase III trials on bapineuzumab will tell us if passive anti-Aβ immunization is able to alter the course if this devastating disease.
AB - Recent advances in our understanding of the neurobiology of Alzheimer's disease (AD) have led to the development of putative disease-modifying treatments. The most revolutionary of these approaches consists in the removal of brain β-amyloid (Aβ) via anti-Aβ antibodies. Brain imaging and neuropathological studies have shown the ability of both active and passive anti-Aβ immunotherapies of clearing Aβ deposits from the brain of the AD patients. An active anti-Aβ vaccine preparation, AN1792, has been used in AD patients with some clues of clinical efficacy but causing meningoencephalitis in about 6% of patients and it has been abandoned. Several second-generation active Aβ vaccines and passive Aβ immunotherapies have been developed and are under clinical investigation with the aim of accelerating Aβ clearance from the brain of the AD patients. The most advanced of these immunological approaches is bapineuzumab, composed of humanized anti-Aβ monoclonal antibodies, that has been tested in two Phase II trials, demonstrating to reduce Aβ burden in the brain of AD patients. However, the preliminary cognitive efficacy of bapineuzumab appears uncertain. The occurrence of vasogenic edema, especially in apolipoprotein E E{open}4 carriers, may limit its clinical use and have led to abandon the highest dose of the drug (2 mg/kg). The results of four ongoing large Phase III trials on bapineuzumab will tell us if passive anti-Aβ immunization is able to alter the course if this devastating disease.
KW - β-amyloid
KW - Active immunotherapy
KW - Alzheimer's disease
KW - Bapineuzumab
KW - Passive immunotherapy
UR - http://www.scopus.com/inward/record.url?scp=80053385682&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80053385682&partnerID=8YFLogxK
U2 - 10.2174/156720511798192718
DO - 10.2174/156720511798192718
M3 - Article
C2 - 21592055
AN - SCOPUS:80053385682
VL - 8
SP - 808
EP - 817
JO - Current Alzheimer Research
JF - Current Alzheimer Research
SN - 1567-2050
IS - 8
ER -