Navigating Through Alzheimer's Disease

            Dr. Fernandez explored the navigational impairments of Alzheimer's Disease (AD). Being one of the most prevalent disease for the elderly, it requires attention in order to find ways to cure the problem. Dr. Fernandez looked at the visual processing of optic flow to understand whether there is a higher threshold which leads to navigational impairments. Event related potentials were measured when the participants were subject to driving and navigation. It was clear that patients with early AD has diminishing response amplitudes.

McLachlan and his colleagues looked at AD in terms of memory and a potential threshold effect which may be present. In their experiment, they had three groups: young health individuals, older healthy individuals, and individuals who were diagnosed with AD. Each group was read sentences at one point and then presented more sentences either 1-2 hours and 4-14 days later. They were asked whether the sentences they were being presented were the same as the sentences they had read initially. The results suggested that both the young and older healthy individuals were mainly able to recognize the sentences if they were similar, though the patients with AD were not able to even for short delays. They tested this by looking at the speed of reading the sentence. It has been previously shown how if something is retained, one is able to read it faster.

This experiment was similar to that of Dr. Fernandez’s experiment in that it was measuring the delay patients with AD had when presented a stimulus. To improve the study, McLachlan and his colleagues could have considered looking at ERPs when the participants were given the sentences. This way, they could see what part of the brain was being stimulated initially when the sentences were in working memory and what parts of the brain showed activity when they were actively trying to recall. Perhaps there exist a threshold effect in that the memory of the sentences exists in the AD patients, but the connection is not strong enough for it to be verbalized consciously.

To really get to the cause of the disease, it is important to consider its effects. Patients with AD often have their cortex shrivel, the hippocampus shrinks, and the ventricles become enlarged. Ultimately, the problem boils down to the formation of plaques between the nerve cells. If we can understand the proteins involved in the formation of these plaques, we might be able to use CRISPR to knockout the gene which is resulting in the plaques.

Research in this field is essential as we strive to advance humanity. Because it is a growing problem, it is important to look at the different possible mechanisms of AD in hopes that we find a way to cure it. Currently we cannot cure this neurodegenerative disorder, but we can only down its progression. It is fascinating how one small protein can potentially be the difference between having AD and not having it. Surely, one day we will be able to conquer this disease as well!

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