More importantly, Bexarotene is already in use in human patients, making it easier to determine if the drug will have similar benefits for Alzheimer’s patients.

According to Alzheimer’s Foundation statistics, 5.4 million Americans suffer from this debilitating disease. Alzheimer’s devastates patient’s cognitive abilities, with the most notable symptom being profound and worsening memory loss. While some amount of memory loss is to be expected with old age, Alzheimer’s patients lose the ability to recognize family members, their surroundings, and ultimately require 24-hour care and hospitalization.

Alzheimer’s is thought to be the result of the building up of beta-amyloid proteins, which coalesce into plaques within the brain. In addition to effects on the mouse immune system which could help clear plaques, treatment with Bexarotene seems to modulate the production of ApoE (Apolipoprotein E), an important cholesterol transporter that can interact with and clear these beta-amyloid proteins.

If this treatment works as well in humans as in mice (where effects were noted within hours of treatment) we should know soon if there is a new hope for those affected by this devastating ailment.

Just recently, a group of researchers at the University of Maryland School of Medicine have identified a variant of a gene that is believed to play a major role in determining why people do not respond to a popular anti-clotting medication. This gene variant, carried by as many as a third of the general population can put patients at increased risk for subsequent heart attacks, strokes and other serious cardiovascular problems. The interesting thing is, that this increased risk is not due to patients genetic predisposition for these disorders, but because it renders their medication ineffective.

Medicines that we introduce into our bodies often require one or several important mechanisms to unfold their intended effects: they may have to be actively transported into our cells, biochemically altered and thereby activated, or they may require deactivation and/or removal in order to not do more harm then good. Any of these processes may involve proteins on one level or another and, therefore, depend on genes. Thus, as we have maps that indicate the loci associated with genetic disorders (visit Tour > genome spots in DNA Interactive), we will soon have maps that tell us where to look if we wish to know our predisposition to the medications we use to cure ailments: whether they will do us any good, are totally useless or, in a worst case scenario, can even harm us.