At Georgetown University Medical Center, tiny, almost meniscal dosage amounts of a Leukemia-inhibiting drug known as nilotinib, were being administered to lab mice in a clinical trial to see the effects of the drug on inhibiting the formation of certain proteins in the brain, which if allowed to proceed unchecked, would build up and cause any number of diseases, from Parkinson’s disease and even Alzheimer’s disease, to a lesser known disease known as Lewry body disease.
Neurologist and senior investigator for this study, Charbel E-H Moussa, MB and PhD, head of the dementia laboratory at Georgetown University stated that when this utilized drug, nilotinib, is used to treat CML, or chronic myelogenous leukemia. When used in high enough and safe doses, it causes the cancer cells to go into a state of autophagy, pushing them to cannibalize their own organelles, which leads to the death of tumor cells.
In the study that was performed, for the first time, cancer drugs were being utilized for a different cause. Mice in the lab that over-expressed a specific protein, known as alpha-Symuclein, were given one Milligram of nilotinib every two days. Previous testing of the drug concluded that it would get rid of the toxic protein found in the brain, the cells would go into a state of autophagy and within a matter of treatments, the lab mice treated with the drug had drastically better movement and functionality than the untreated mice.
At the end of the experiment, Moussa hypothesized that in order for therapy of these neurological diseases to be effective, it must happen as soon as possible. Later usage may result in retardation of further extracellular formation, as well as the accumulation of intracellular proteins such as Lewy bodies, which was the whole point of using the Leukemia drug in the first place.
Michaeline L. Hebron, Irina Lonskaya, and Charbel E.-H. Moussa. Nilotinib reverses loss of dopamine neurons and improves motor behavior via autophagic degradation of α-synuclein in Parkinson's disease models. Hum. Mol. Genet., May 10, 2013 DOI: 10.1093/hmg/ddt192
Georgetown University Medical Center (2013, May 10). Cancer drug prevents build-up of toxic brain protein. ScienceDaily.
Recent studies in at this month’s Alzheimer’s Association International Conference in Vancouver, Canada has shown that the way a person walks is linked to cognitive function. That is, the speed and style by which a person walks correlates with cognitive changes that may eventually lead to the development of Alzheimer’s disease (AD). Signs of cognitive failure include walking at a slower pace, and fluctuated or uncontrolled walking. Usual studies of AD involve patients who do not move, but the thinking capabilities of the human brain have a strong relationship with its movement skills. While research for the link between walking and mental function has been going on for the past decade, it has been recently taken into new heights because these studies have revealed more specifics about the relationship. For example, the variation and pace in walking is linked with a person’s ability to plan and organize, while rhythm is associated with the speed by which information is processed. The decline in cognitive functions has a parallel relationship with a decrease in walking speed. Newer studies have been incorporated more detailed and advanced approaches than previous research in terms of measuring changes in gait, such as making the participants multitask or having them use electronic walkways. These studies may lead to a new method in which symptoms of AD can be detected earlier on, as to prevent the development of the disease. It also reinforces the idea that dementia can be delayed with an activity that should be common to humankind, exercise.
For further details on these studies and on Alzheimer’s disease, please visit:
Keywords: Alzheimer’s disease; walking; exercise; cognitive functions
July 24, 2012