Neuroscience 2003 Abstract
| Presentation Number: | 133.8 |
|---|---|
| Abstract Title: | Antibodies against beta-amyloid slow cognitive decline in patients with Alzheimer's disease. |
| Authors: |
Nitsch, R. M.*1
; Konietzko, U.1
; Streffer, J. R.1
; Henke, K.1
; Wollmer, A. M.1
; Umbricht, D.1
; de Quervain, D. J. F.1
; Hofmann, M.1
; Maddalena, A.1
; Papassotiropoulos, A.1
; Hock, C.1
1Psychiatry Res, Univ. Zurich, Ch-8008 Zurich, Switzerland |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurodegenerative Disorders -- Alzheimer's Disease: APP, presenilin and Ab generation |
| Session: |
133. Alzheimer's Disease: Experimental Models & Therapies I Slide |
| Presentation Time: | Sunday, November 9, 2003 9:45 AM-9:45 AM |
| Location: | Morial Convention Center - Room 393 |
| Keywords: | vaccination, immunization, dementia, APP |
Immunization against beta-amyloid can reduce neuropathology and improve impaired behavior in transgenic mice. Whether antibodies against beta-amyloid are also effective in Alzheimer disease (AD) is unknown. We have previously described the generation of antibodies against beta-amyloid in AD patients who received a prime and a booster immunization of aggregated Abeta42 in a placebo-controlled randomized trial. We developed a tissue amyloid plaque immunoreactivity (TAPIR) assay to determine the ability of the antibodies to react with bona fide beta-amyloid plaques in brain tissue of transgenic mice expressing AD-causing mutations.
By following patients over a one-year period, we found that patients who generated TAPIR-positive antibodies showed significantly slower rates of decline of cognitive functions and activities of daily living, and scored better on hippocampus-dependent memory tests as compared to patients without such antibodies. The beneficial clinical effects were also present in patients who had experienced transient episodes of immunization-related aseptic meningoencephalitis as an unwanted side effect of immunization. Our results show that the generation antibodies against beta-amyloid in response to immunization can slow cognitive decline in patients with AD, suggesting that vaccination against beta-amyloid is a valuable option for the treatment of AD.
By following patients over a one-year period, we found that patients who generated TAPIR-positive antibodies showed significantly slower rates of decline of cognitive functions and activities of daily living, and scored better on hippocampus-dependent memory tests as compared to patients without such antibodies. The beneficial clinical effects were also present in patients who had experienced transient episodes of immunization-related aseptic meningoencephalitis as an unwanted side effect of immunization. Our results show that the generation antibodies against beta-amyloid in response to immunization can slow cognitive decline in patients with AD, suggesting that vaccination against beta-amyloid is a valuable option for the treatment of AD.
<B>Off-label Drug Use:</B> AN1792, a vaccine against Abeta42 developed by Elan and Wyeth/Ayerst.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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