April 18, 2008
Startling New Evidence Suggests IVIg May Help Alzheimer's Patients
Analysis of:
Study Suggests Gammagard Liquid May Target the Primary Pathway Involved in Alzheimer's Disease | biz.yahoo.com
This analysis is solely the work of the author. It has not been edited or endorsed by GLG.
Implications: Three presentations at this week's AAN meeting in Chicago are adding in a big way to accumulating evidence that intravenous immunoglobulin (IVIg) may slow, halt or even PREVENT accumulation of toxic beta-amyloid -- a prime culprit in the development of Alzheimer's disease (AD) in millions of aging individuals. Antibody-binding, serology and preclinical findings powerfully suggest that progression to AD has something to do with a failure to mount an adequate humoral (antibody) immune response to beta-amyloid oligomers, which then deposit in brain tissues. New lab, PET scan imaging, clinical and lookback study results now offer important new evidence that frequent infusions with low doses of IVIg may restore the "missing link" in immunity and allow the patient's cellular immune function to more effectively kick in and clear the toxic beta-amyloid. Whether monoclonal antibody preparations now in development can mimic an array of natural human antibodies remains an open question.
Analysis: Back in August 2006, Cornell doctors reported encouraging results with IVIg in a small 8-patient AD study, echoing similar findings by a German team.
A year later, Cornell announced "favorable" outcomes in a 24-subject Phase II trial of Baxter's GAMMAGARD. Separately, a large lookback study found that non-demented patients who got IVIg for other reasons had an astonishing 42% lower risk for subsequently developing AD and related dementias.
Lab, imaging and clinical findings presented at this week's AAN meeting are adding credibility to the assertion that failure of natural immune-mediated clearance of beta-amyloid oligomers is key to understanding why AD occurs as people age.
Many indicators now suggest a therapeutic role for anti-beta-amyloid antibodies, in early-stage AD possibly even in at-risk individuals. Answers from Phase III trials are 3 years away. In the meantime, the temptation for patients and the "worried well" to give IVIg a try will be significant.
Analysis: Back in August 2006, Cornell doctors reported encouraging results with IVIg in a small 8-patient AD study, echoing similar findings by a German team.
A year later, Cornell announced "favorable" outcomes in a 24-subject Phase II trial of Baxter's GAMMAGARD. Separately, a large lookback study found that non-demented patients who got IVIg for other reasons had an astonishing 42% lower risk for subsequently developing AD and related dementias.
Lab, imaging and clinical findings presented at this week's AAN meeting are adding credibility to the assertion that failure of natural immune-mediated clearance of beta-amyloid oligomers is key to understanding why AD occurs as people age.
Many indicators now suggest a therapeutic role for anti-beta-amyloid antibodies, in early-stage AD possibly even in at-risk individuals. Answers from Phase III trials are 3 years away. In the meantime, the temptation for patients and the "worried well" to give IVIg a try will be significant.
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