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KMID : 1100220050040020076
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Dementia and Neurocognitive Disorders
2005 Volume.4 No. 2 p.76 ~ p.80
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Disease Modifying Strategies for the Treatment of Alzheimer’s Disease: A Newer Concept of AD Vaccine
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Tabira Takeshi
Hara Hideo
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Abstract
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Alzheimer’s disease (AD) is characterized by progressive loss of cognitive function due to β amyloid deposits in the central nervous system[1]. Immunization of amyloid precursor protein (APP)-transgenic mice with synthetic Aβ in complete and subsequently incomplete Freund’s adjuvant showed a marked reduction of amyloid burden in the brain[2]. Repetitive passive transfer of Aβ antibodies[3] was also effective for reducing the amyloid deposits. Although Aβ is not an infectious agent, this treatment is now widely accepted as “vaccination” from its analogy in mechanism. Since vaccinated mice showed an improvement of memory loss in mice[4, 5], clinical trials were performed in humans in the States and Europe. The phase II trial of AN-1792 vaccine composed of synthetic Aβ1-42 and adjuvant QS21 was halted because of complication, subacute meningoencephalitis which appeared in 6% of patients[6]. However autopsy cases with or without the complication suggested effective clearance of β amyloid by vaccination[7-9], and patients who produced antibodies against senile plaque amyloid showed better cognitive functions or less cognitive decline than those who did not produce such antibodies[10, 11]. Therefore, Aβ vaccination seems to be a promising way to delay the onset or to slow progression of AD, if the complication is minimized. We have developed an oral Aβ vaccine using the recombinant adeno-associated virus vector (AAV), which successfully reduced amyloid burden in Tg2576 APP transgenic mice without any complications[12].
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