A research study by Johns Hopkins Medicine exposes a link in between lower serotonin levels in the brain and memory problems in individuals with mild cognitive disability. This finding, published in the Journal of Alzheimers Disease, suggests that targeting serotonin might use a brand-new approach to treating memory issues and perhaps slowing Alzheimers disease progression.
Family pet scans of people with mild cognitive impairment discovered lower levels of serotonin, the brain chemical related to favorable mood, compared to those without it.
Comparing PET scans of more than 90 adults with and without moderate cognitive problems (MCI), Johns Hopkins Medicine researchers say relatively lower levels of the so-called “happiness” chemical, serotonin, in parts of the brain of those with MCI may play a role in memory problems consisting of Alzheimers disease.
The findings, just recently released in the Journal of Alzheimers Disease, provide assistance to growing evidence that measurable modifications in the brain happen in individuals with mild memory problems long before an Alzheimers medical diagnosis, and might use novel targets for treatments to slow or stop illness development.
Evidence of Brain Changes Preceding Alzheimers.
” The study reveals that individuals with moderate cognitive disability already show loss of the serotonin transporter. This measure that shows serotonin degeneration is related to issues with memory, even when we consider in our analytical design MRI steps of neurodegeneration and PET steps of the amyloid protein that are connected with Alzheimers Disease,” says Gwenn Smith, Ph.D., professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine.
Comprehending Mild Cognitive Impairment.
MCI describes the diagnostic phase between normal brain function in aging and Alzheimers Disease (AD). Signs of MCI consist of regular forgetfulness of current events, word finding difficulty, and loss of the sense of odor. Those with MCI may remain in this phase forever, or development to more severe types of cognitive deficits, giving seriousness to the search for predictive markers, and possible early prevention interventions, private investigators say.
The private investigators cautioned that their research study revealed a correlation in between lower serotonin transporter levels and memory issues in MCI, and was not developed to show causation or the role of serotonin in the development from MCI to AD. To answer these questions, additional research is needed to study gradually healthy controls and people with MCI to demonstrate the function of serotonin in illness development.
Study Design and Findings.
The research study team used PET scans to look specifically at the serotonin transporter– a neurotransmitter, or brain chemical long associated with positive mood, hunger and sleep– and to look at the amyloid-beta protein (Aβ) distribution in the brain. Studies in mice done at Johns Hopkins have revealed that serotonin degeneration occurs before the advancement of widespread beta-amyloid deposits in the brain.
Researchers found that MCI patients had lower levels of the serotonin transporter, and higher levels of Aβ than healthy controls. The MCI patients had up to 25% lower serotonin transporter levels in cortical and limbic regions than healthy controls. In particular, they report, lower serotonin transporter levels were found in cortical, limbic, and subcortical regions of the brains in those with MCI, locations specifically responsible for executive feeling, memory, and function.
” The connection we observed in between lower serotonin transporters and memory issues in MCI is essential due to the fact that we might have identified a brain chemical that we can securely target that might enhance cognitive deficits and, possibly, depressive symptoms,” says Smith. “If we can reveal that serotonin loss with time is straight involved in the transition from MCI to advertisement, just recently established antidepressant medications may be an efficient method to enhance memory deficits and depressive symptoms and hence, might be an effective method forward to slow disease development.”.
Future Research.
Researchers state future research studies include longitudinal follow-up of individuals with MCI to compare serotonin degeneration to the increase in and Aβ levels, in addition to the increase in levels of the Tau protein that is likewise related to advertisement compared to healthy grownups. They are also studying multi-modal antidepressant drugs to treat anxiety and memory deficits in hopes of alleviating and halting signs.
Referral: “Serotonin Degeneration and Amyloid-β Deposition in Mild Cognitive Impairment: Relationship to Cognitive Deficits” by Gwenn S Smith, Hiroto Kuwabara, Haijuan Yan, Najlla Nassery, Mark Yoon, Vidya Kamath, Michael Kraut, Neda F Gould, Alena Savonenko, Jennifer M Coughlin, Martin Lodge, Martin G Pomper, Ayon Nandi, Daniel Holt, Robert F Dannals and Jeannie M Leoutsakos, 24 October 2023, Journal of Alzheimers Disease.DOI: 10.3233/ jad-230570.
Other scientists at the Johns Hopkins University School of Medicine and Johns Hopkins Bloomberg School of Public Health who added to this research are Jennifer Coughlin, Robert Dannals, Neda Gould, Daniel Holt, Vidya Kamath, Michael Kraut, Hiroto Kuwabara, Jeannie Leoutsakos, Martin Lodge, Ayon Nandi, Najlla Nassery, Martin Pomper, Alena Savonenko, Haijuan Yan and Mark Yoon.
This research was partially supported by the National Institutes of Health.
The research study team utilized PET scans to look specifically at the serotonin transporter– a neurotransmitter, or brain chemical long associated with positive state of mind, hunger and sleep– and to look at the amyloid-beta protein (Aβ) circulation in the brain. Research studies in mice done at Johns Hopkins have actually shown that serotonin degeneration takes place before the advancement of widespread beta-amyloid deposits in the brain. Scientists discovered that MCI patients had lower levels of the serotonin transporter, and higher levels of Aβ than healthy controls. The MCI clients had up to 25% lower serotonin transporter levels in limbic and cortical areas than healthy controls. In specific, they report, lower serotonin transporter levels were discovered in cortical, limbic, and subcortical regions of the brains in those with MCI, areas particularly responsible for executive function, memory, and feeling.
