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Extending the work from the PLoS ONE study, Michael Agadjanyan proposes a new preventive vaccination scheme for Alzheimer disease (see Movsesyan et al., 2008). This multivalent DNA epitope vaccine would contain currently known T helper (Th) cell epitopes of various conventional vaccines (e.g., tetanus, diphtheria, pertussis, HBV, etc.) fused with three copies of the Aβ42 B cell epitope, Aβ1-11, and a strong Th2-type molecular adjuvant (e.g., MDC as reported in the PLoS ONE paper). People immunized with the conventional vaccines should develop long-lasting memory Th cells to those pathogens. Those later diagnosed with early AD or pre-AD pathology can receive the DNA vaccine (e.g., mTh-Abeta1-11 fused with any potent molecular adjuvant), which should induce activation of pre-existing memory Th cells specific to the various pathogen epitopes on the multivalent vaccine and, subsequently, rapid and robust antibody production through activation of B cells specific to the Aβ component of the same vaccine. To demonstrate the feasibility of this strategy, Agadjanyan is collaborating with flu vaccine researcher Adolfo Garcia-Sastre, Mount Sinai School of Medicine, New York. They plan to use APP/Tg mice to test the potency of pre-existing memory Th cells generated in response to a conventional flu vaccine by immunizing these animals with a chimeric recombinant influenza virus expressing the immunodominant B-cell epitope of Aβ42, Aβ1-10, in the HA peptide, flu-Aβ1-10. Image credit: Michael Agadjanyan
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Comment by: M. Paul Murphy
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Submitted 12 May 2008
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Posted 14 May 2008
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I'd be willing to bet that this would likely work. However, although a nice idea in principle, it would be cripplingly expensive and beyond the financial reach of most people. I suspect that even the best health care plans would balk at paying for this, especially since it would need to go on for many years. Although as researchers we put a lot of thought into how to advance treatments for AD, maybe it's time we started to give equal time to how much they might cost. This should be especially important now, as several forms of potential therapy get closer to becoming a reality.  View all comments by M. Paul Murphy |
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Comment by: Emory Hill (Disclosure)
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Submitted 12 May 2008
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Posted 14 May 2008
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Why not focus the early "diagnosis" earlier than the stage that PIB-PET scans and CSF ratios can detect? Aβ accumulation would only be a useful measure (and, even then, how often can people afford it?) when it is known to affect actual cognitive abilities. (Disclosure: We developed an MCI screen for the need to administer such expensive diagnostic tests.) References: Tornatore JB, Hill E, Laboff JA, McGann ME. Self-administered screening for mild cognitive impairment: initial validation of a computerized test battery. J Neuropsychiatry Clin Neurosci. 2005 Winter;17(1):98-105. Abstract
Tornatore JB, Hill E, Laboff JA, Fogel B. Preliminary Screening for Mild Cognitive Impairment: Using the CANS-MCI to Determine Need for Imaging. 9th International Conference on Alzheimer's Disease, Philadelphia, PA, July 2004.
Hill E, Ross J, Tornatore JB, Reid M. Longitudinal Validity of a Mild Cognitive Impairment Screen: The CANS-MCI Study. American Journal of Geriatric Psychiatry, Volume 16, No. 3, Supplement 1, A96-A97, March 2008. (Abstract)
View all comments by Emory Hill |
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