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Alzheimer's Disease: Some Cells More Prone to Death

Aug. 8, 2010 — A group led by Dr. Andreas Lösche of the University of Leipzip, Germany has discovered that hyperploid neurons, which have greater than the normal number of chromosomes, are more prone to cell death in Alzheimer's disease. They present these findings in the July 2010 issue of The American Journal of Pathology.


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Alzheimer's disease, the most common form of dementia, affects nearly 19% of people 75-84 years of age. Alzheimer's disease in incurable and degenerative, and results in death for the patient and considerable burden on the caregiver. Disease progression is associated with neuronal cell death.

Although a low-level of aneuploidy, an abnormal number of chromosomes, may contribute to neuronal diversity, high levels of aneuploidy may result in developmental abnormalities and disease. Ardendt et al explored the effects of hyperploidy, having greater than the normal number of chromosomes, in Alzheimer's disease pathogenesis. They identified increased numbers of hyperploid cells in preclinical stages of Alzheimer's disease and showed that hyperploid neuronal cells in Alzheimer's disease have selectively higher levels of cell death than normal neuronal cells. These results highlight hyperploidy, perhaps as a result of a failure of neuronal differentiation, as critical pathogenic event in neurodegeneration.

Dr. Lösche's group suggests that "hyperploidy … [is one] critical molecular event … shared between neurodegeneration and malignant cell transformation … [and that these data] direct our attention to a failure of neuronal differentiation as the critical pathogenetic event and potential therapeutic target in neurodegeneration."

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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. Arendt et al. Selective Cell Death of Hyperploid Neurons in Alzheimer's Disease. American Journal Of Pathology, 2010; DOI: 10.2353/ajpath.2010.090955
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