Connection between Cancer and Alzheimer's Disease

An intriguing finding by researchers at Brigham and Women's Hospital, Harvard Medical School, seems to link neuronal death in Alzheimer's with proteins expressed by some cancers.

Neurons in the brain generally do not divide. It is therefore perplexing that in Alzheimer's disease, and other dementias associated with a protein called tau, dying neurons actually re-express proteins normally seen during cell division or in cancer. It has previously been unclear whether such cell-division proteins cause neuronal death, protect neurons from death, or are irrelevant.

In the present work, the scientists used a fruit-fly model of Alzheimer's disease to examine the relationship of cell-division proteins to neurodegeneration. The power of this model, which recapitulates key features of the human disease, lies in the ability to use genetic tools to establish a causal correlation between a molecular pathway and neuronal death. Khurana and his colleagues found that, as in human disease, abnormal expression of cell-cycle proteins accompanied neuronal death in their fly model. Most importantly, loss of neurons could be prevented when the cell cycle was genetically blocked or when flies were fed anticancer drugs. Cell-cycle activation depended upon a hyperactive cell growth molecule, TOR (target of rapamycin), also known to be abnormally activated in Alzheimer's disease. By establishing these causal connections, this study suggests that anticancer drugs are potential therapies for Alzheimer's disease and related disorders. More broadly, the results point to an intriguing correlation between cancer and dementia, two of the most important diseases in the elderly.

Hat tip to medicineworld.org and sciencedaily.com.

This is a preliminary finding from fruit flies, but a provocative finding nonetheless. Often important discoveries occur in microbes and lower animals before finding their way to human research, and then into mainstream medicine.