With lifespans constantly increasing and the age of medical technology at its peak, a counter-effect is being displayed through a hard-hitting, debilitating disease: Alzheimer’s Disease (AD). While there is still not a fundamental cure, some research has provided more information. One of the common findings that is associated with AD is the degeneration of the serotonin systems. Whether the lower levels amount to the cause or the effect of the disease is explored in a study done by the Johns Hopkins University School of Medicine.
To test the hypotheses that suggest the lower levels of serotonin, and, accordingly, auditory-verbal and visual-spatial memory deficits, would be observed in patients with Alzheimer’s, the author first and corresponding author, Gwenn Smith, Ph.D., and her team completed a trial including 56 participants. Of those 56, 28 were diagnosed with Mild Cognitive Impairment (MCI), a form of early AD, and 28 were healthy controls that were assessed as counterparts to the aforementioned participants. Because the experiment involved patients experiencing early cognitive decline, it was able to analyze the process in which serotonin functions as a driving factor of AD.
In order to measure the levels of serotonin present, Smith and her colleagues conducted positron emission tomography (PET) scans and implemented radioactive carbon for tracing. Specifically, they monitored the serotonin transporter (SERT), the protein that enables the release of the neurotransmitter. The results showed that the MCI patients had 38% lower SERT compared to the control counterparts. Additionally, not a single MCI patient had a higher SERT than their counterparts. Therefore, the correlation between a lower SERT and MCI or AD is shown.
The effect of such lower serotonin levels is also shown through the results of a standardized testing process each participant underwent. Through the analysis of the verbal memory scores, the 28 CMI patients experienced a 37% lower test score range compared to the control group. Not only are CMI patients found to have lower levels of SERT activity, but also the deficiency affects their cognitive abilities.
The discussion of the findings leads to the potential question of whether a serotonin additive in early-onset AD may be able to act as a treatment. Since this study provides greater evidence of the effects of serotonin in cognitive decline, it suggests that targeting the serotonin system will have more promise.
One potential treatment method that could be used for implementation is the same target therapy in treating patients with depression—selective serotonin reuptake inhibitors (SSRIs). SSRIs function by blocking the serotonin reabsorption, thereby increasing the amount of serotonin. Because the issue with CMI and AD patients are the subsequent lack of serotonin transporters, the medication may not work the same way. However, the targeting of serotonin receptors may, in fact, provide a better solution.
1. “Molecular Imaging of Serotonin Degeneration in Mild Cognitive Impairment.” Journal of Medical Human Genetics, Elsevier, 13 May 2017, www.sciencedirect.com/science/article/pii/S0969996117301109?via=ihub.
2. “Selective Serotonin Reuptake Inhibitors (SSRIs).” Mayo Clinic, Mayo Foundation for Medical Education and Research, 17 May 2018, www.mayoclinic.org/diseases-conditions/depression/in-depth/ssris/art-20044825.