Sometimes, one has no choice but to believe in divine inspiration. How else to explain a group of pre-Christian Greek philosophers who came up with atomic theory, or St. Augustine writing about the Big Bang and evolution in the fourth century? How else to explain a group of neuroscientists at Case Western Reserve University School of Medicine deciding to look at a cancer drug as a possible cure for Alzheimer’s?
On of the worst misrepresentations about stem cell therapy is the idea that it could be used for treatment of Alzheimer’s. Stem cells replace lost tissue. Alzheimer’s is caused by the brain not removing amyloid beta which occurs naturally and is usually flushed by a cholesterol carrier called Apolipoprotein E (ApoE). The amyloid beta packs together to cause plaque, which cuts off the pathways for electrical impulses moving across synapses. It was Gary Landreth, PhD. at Case Western who discovered the connection between ApoE and the clearance of amyloid beta. Landreth and his research team decided, for whatever reason, to test the cancer drug bexarotene as a possible booster for ApoE. The results have been spectacular.
The drug stimulates retinoid X receptors, which in turn impact how much ApoE is produced in the brain. They tested it on mice. Within six hours of administering the drug to the mice, the level of amyloid beta had fallen. The effect lasted for up to three days. But more importantly, the reduction in amyloid beta resulted in significant improvements in the range of impairments associated with Alzheimer’s. Alzheimer’s infected mice forget how to build nests. They don’t recognize nesting materials as such. They also lose their sense of smell. Two days after receiving the bexarotene, the mice had not only remembered what nesting material was, but were building nests. They were also able to differentiate smells again. After the administration of the drug, 75% of the plaque in the brain had cleared, flushed away in the same manner it does in normal brains. The bexarotene had caused the brain’s immune cells to eat the amyloid beta deposits.
There is a genetic factor to Alzheimer’s. Humans have ApoE2, ApoE3 and ApoE4. Having the ApoE4 gene increases the potential for developing Alzheimer’s. It is the speed at which bexarotene works that has amazed the researchers. As Paige Cramer, PhD. candidate at Case Western and first author of the report in Science magazine, said, “Previously, the best existing treatment for Alzheimer’s disease in mice required several months to reduce plaque in the brain.” Professor Landreth added, “This is a particularly exciting and rewarding study because of the new science we have discovered and the potential promise of a therapy for Alzheimer’s disease. We need to be clear; the drug works quite well in mouse models of the disease. Our next objective is to ascertain if it acts similarly in humans. We are at an early stage in translating this basic science discovery into a treatment.”
Because bexarotene is already used in cancer treatment, it has met some of the basic requirements for FDA approval for human trials. It has a good safety and side-effect record. The researchers hope this will hasten approval for testing on humans.
Support for the research, which Landreth calls a “far-fetched idea” came from the Blanchette Hooker Rockefeller Foundation, the Thome Foundation and the National Institutes of Health, one fo those pesky little socialist programs in the Federal budget that Republicans want to kill.
There are over 5 million Alzheimer’s victims in America right now with millions more expected as my generation reaches the highest risk age for development.