Alzheimer's: A New Hope

       Since its discovery in 1906 Alzheimer's disease has become a popular topic of study in the modern medical and research fields. While many discoveries have been made in recent years we still have yet to grasp a complete understanding of the destructive nature of this disease. While it is understood that the major damage in patients with Alzheimer's is caused by amyloid plaques and tau-tangles, located mainly in the hippocampus, an important area for memory formation, the process by which these formations effect memory has yet to be discovered.While the main focus of treatment has centered around stopping the formation of the plaques and tangles a group of scientists from the University in New South Wales in Australia have suggested a new molecular mechanism that could provide the information necessary for novel methods of treatments in the future.

      Their research centered around what molecular changes are occurring in a patient's brain when they have Alzheimer's but are not symptomatic enough for a clear diagnosis. They discovered that the beta-amyloids that make up the amyloid plaques act as neuro-toxins in the brain. Specifically, they disintegrate the neural cell adhesion molecule II (NCAMII) which helps structurally fortify synaptic membranes in the hippocampus. This destruction means that while patients might not exhibit the neuronal death that is characteristic of later stages of Alzheimer's they would have a decrease in the connectivity of their neural networks which would exhibit similar symptoms since the neurons can no longer effectively communicate causing a loss in function without an easily detectable physical change. Furthermore, it suggests that new treatments could target the replenishment of these NCAMIIs in order to delay or even possibly prevent symptoms of Alzheimer's from arising. However, it should be noted that this study was conducted on people with or without the disease after they had been diseased and the levels of NCAMIIs compared so the specific mechanism of how beta-amyloids destroy NCAMIIs has yet to be discovered and one could theoretically see different results in living specimens.


   

     However, the doubt (or the question left unanswered) from this initial investigation has seen some answers found in the practical application of their knowledge in animal studies. The injection of neural cell adhesion molecules, or their analogs, into rat models of Alzheimer's disease have seen the decrease in neuronal (pyramidal) cell death that is caused by amyloid plaques late in the disease as well as a reduction in the overall pathology of the disease. While these studies did not specifically look at the direct relationship of increasing the amount of NCAMII in animal studies, I believe that the success of similar compounds that have shown to have similar effects on the symptomology of Alzheimer's disease provides good evidence that this knowledge could possibly be used to formulate future treatments.

     There is so much more we have to learn about this very degenerative disease, but there is hope that the discoveries that we are so vehemently pursuing today will enable us to find alleviation for sufferers tomorrow.

References

Corbett, N. J., Gabbott, P. L., Klementiev, B., Davies, H. A., Colyer, F. M., Novikova, T., & Stewart, M. G. (2013). Amyloid-Beta Induced CA1 Pyramidal Cell Loss in Young Adult Rats Is Alleviated by Systemic Treatment with FGL, a Neural Cell Adhesion Molecule-Derived Mimetic Peptide. Plos ONE, 8(8), 1-11. doi:10.1371/journal.pone.0071479

Djogo, N., Jakovcevski, I., Müller, C., Lee, H. J., Xu, J., Jakovcevski, M., & ... Schachner, M. (2013). Adhesion molecule L1 binds to amyloid beta and reduces Alzheimer's disease pathology in mice. Neurobiology Of Disease, 56104-115. doi:10.1016/j.nbd.2013.04.014

http://www.medicalnewstoday.com/articles/303280.php?tw

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