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Posted on Apr 18, 2005, 7 p.m.
By Bill Freeman
Lifelong immunization with human beta-amyloid (1-42) protects Alzheimer transgenic mice against cognitive impairment throughout aging. According to recent research from the United States, "Although both active and passive beta-amyloid (A-beta) immunotherapy have been shown to protect against or lessen cognitive impairment in various Alzheimer transgenic mouse lines, these studies have focused on a single task and involved standard statistical analysis.
Lifelong immunization with human beta-amyloid (1-42) protects Alzheimer transgenic mice against cognitive impairment throughout aging.
According to recent research from the United States, "Although both active and passive beta-amyloid (A-beta) immunotherapy have been shown to protect against or lessen cognitive impairment in various Alzheimer transgenic mouse lines, these studies have focused on a single task and involved standard statistical analysis. Because Alzheimer disease impacts multiple cognitive domains, the current study employed an extensive behavioral battery and multimetric analysis therein to determine the impact of A-beta immunization given throughout most of adult life (from 2-16 1/2 months of age) to APP PS1 transgenic mice. At both adult (4 1/2-6 month) and aged (15-16 1/2 month) test points, the same 6-week behavioral battery was administered."
"Results indicate that A-beta immunotherapy partially or completely protected APP PS1 mice at both test points from otherwise impaired performance in a variety of tasks spanning multiple cognitive domains (reference learning/memory, working memory, search/recognition)," reported M. T. Jensen and collaborators at the Johnnie B. Byrd Alzheimer's Center and Research Institute and University of South Florida. "At both adult and aged test points, the cognitive benefits of A-beta immunotherapy were evident even when behavioral measures were analyzed collectively (as 'overall' performance) through discriminant function analysis."
"Since behavioral protection at the 15- to 16 1/2-month test point occurred without a decrease in (or correlation to) A-beta deposition, the mechanism of A-beta immunotherapy's action most likely involves neutralization/removal of small A-beta oligomers from the brain," reported the scientists. "However, in factor analysis performed at this aged test point, brain A-beta deposition measures loaded heavily with key cognitive measures. Collectively, our results suggest that the entire process of A-beta deposition deleteriously impacts cognitive performance and that A-beta-based preventative strategies can provide long-term cognitive benefits extending well into older age."
Jensen and associates published their study in Neuroscience (Lifelong immunization with human beta-amyloid (1-42) protects Alzheimer's transgenic mice against cognitive impairment throughout aging. Neuroscience, 2005;130(3):667-684).
For additional information, contact Gary W. Arendash, University of South Florida, Memory and Aging Research Laboratory, SCA 110, Tampa, FL 33620, USA. E-mail: arendash@cas.usf.edu.
Publisher contact information for the journal Neuroscience is: Pergamon-Elsevier Science Ltd., The Boulevard, Langford Lane, Kidlington, Oxford OX5 1GB, England.
The information in this article comes under the major subject areas of Alzheimer Disease Vaccine, Vaccine Development, Immunology, Immunotherapy, Cognition, Geriatrics, Neurodegeneration, Neurology, Neuroscience, and Proteomics. This article was prepared by Biotech Week editors from staff and other reports. Copyright 2005, Biotech Week via NewsRx.com.
According to recent research from the United States, "Although both active and passive beta-amyloid (A-beta) immunotherapy have been shown to protect against or lessen cognitive impairment in various Alzheimer transgenic mouse lines, these studies have focused on a single task and involved standard statistical analysis. Because Alzheimer disease impacts multiple cognitive domains, the current study employed an extensive behavioral battery and multimetric analysis therein to determine the impact of A-beta immunization given throughout most of adult life (from 2-16 1/2 months of age) to APP PS1 transgenic mice. At both adult (4 1/2-6 month) and aged (15-16 1/2 month) test points, the same 6-week behavioral battery was administered."
"Results indicate that A-beta immunotherapy partially or completely protected APP PS1 mice at both test points from otherwise impaired performance in a variety of tasks spanning multiple cognitive domains (reference learning/memory, working memory, search/recognition)," reported M. T. Jensen and collaborators at the Johnnie B. Byrd Alzheimer's Center and Research Institute and University of South Florida. "At both adult and aged test points, the cognitive benefits of A-beta immunotherapy were evident even when behavioral measures were analyzed collectively (as 'overall' performance) through discriminant function analysis."
"Since behavioral protection at the 15- to 16 1/2-month test point occurred without a decrease in (or correlation to) A-beta deposition, the mechanism of A-beta immunotherapy's action most likely involves neutralization/removal of small A-beta oligomers from the brain," reported the scientists. "However, in factor analysis performed at this aged test point, brain A-beta deposition measures loaded heavily with key cognitive measures. Collectively, our results suggest that the entire process of A-beta deposition deleteriously impacts cognitive performance and that A-beta-based preventative strategies can provide long-term cognitive benefits extending well into older age."
Jensen and associates published their study in Neuroscience (Lifelong immunization with human beta-amyloid (1-42) protects Alzheimer's transgenic mice against cognitive impairment throughout aging. Neuroscience, 2005;130(3):667-684).
For additional information, contact Gary W. Arendash, University of South Florida, Memory and Aging Research Laboratory, SCA 110, Tampa, FL 33620, USA. E-mail: arendash@cas.usf.edu.
Publisher contact information for the journal Neuroscience is: Pergamon-Elsevier Science Ltd., The Boulevard, Langford Lane, Kidlington, Oxford OX5 1GB, England.
The information in this article comes under the major subject areas of Alzheimer Disease Vaccine, Vaccine Development, Immunology, Immunotherapy, Cognition, Geriatrics, Neurodegeneration, Neurology, Neuroscience, and Proteomics. This article was prepared by Biotech Week editors from staff and other reports. Copyright 2005, Biotech Week via NewsRx.com.
