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CpG DNA Therapy For Alzheimer Disease

Oct. 22, 2009 — Dr. Yukiko Doi and colleagues at Nagoya University have found that CpG DNA may be a therapeutic candidate for treatment of Alzheimer disease. They report their data in the November 2009 issue of The American Journal of Pathology.


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Alzheimer disease is the most common form of dementia, affecting approximately 1.6% of the population in the United States (nearly 19% in the 75-84 age group). It is an incurable, degenerate, and terminal disease thought to be caused by accumulation of oligomeric amyloid β (oAβ).

Microglia are the resident immune cells in the central nervous system; they remove damaged neurons, plaques, and infectious agents from the brain and spinal cord. Microglia cluster around senile Aβplaques in Alzheimer disease patients; however, the role of microglia in oAβtoxicity remains unclear. Doi et al discovered that microglial activation with unmethylated CpG DNA, which binds to an immune receptor on microglia, prevented oAβtoxicity and enhanced oAβ peptide clearance in culture. Furthermore, injection of CpG DNA directly into the brain mitigated both cognitive impairment and learning defects in a mouse model of Alzheimer disease. CpG DNA may therefore be a therapeutic candidate for treatment of Alzheimer disease.

Dr. Doi and colleagues conclude that "CpG, especially class B and C, may also be effective therapeutic agents against oAβ1-42 neurotoxicity in [Alzheimer disease]."

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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Doi Y, Mizuno T, Maki Y, Jin S, Mizoguchi H, Ikeyama M, Doi M, Michikawa M, Takeuchi H, Suzumura A. Microglia Activated with the Toll-Like Receptor 9 Ligand CpG Attenuate Oligomeric Amyloid β Neurotoxicity in in Vitro and in Vivo Models of Alzheimer's Disease. American Journal Of Pathology, 2009; DOI: 10.2353/ajpath.2009.090418
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