A recent study, published in the Journal of Alzheimer’s Disease, has uncovered a significant connection between lower levels of serotonin, often dubbed the “happiness chemical,” in the brain, and mild cognitive impairment (MCI), a condition that often precedes Alzheimer’s disease.
This research could pave the way for new treatments targeting early stages of memory decline.
The study, involving more than 90 adults, both with and without MCI, utilized PET scans to explore changes in the brain.
Gwenn Smith, a professor at the Johns Hopkins University School of Medicine, explains that people with MCI already show a loss of the serotonin transporter.
This reduction is linked to memory problems and is evident even when considering other factors like neurodegeneration and amyloid protein levels, which are associated with Alzheimer’s disease.
MCI is an intermediate stage between the expected cognitive decline of normal aging and the more serious decline of dementia. It includes symptoms like frequent forgetfulness, trouble finding words, and loss of the sense of smell.
Not everyone with MCI progresses to Alzheimer’s, but some do, making the search for predictive markers and early interventions crucial.
The study established a correlation between lower serotonin transporter levels and memory issues in MCI but did not prove causation or define serotonin’s role in progressing from MCI to Alzheimer’s.
Further long-term research comparing healthy individuals and those with MCI is needed to clarify serotonin’s role in disease progression.
The research included 49 volunteers with MCI and 45 healthy older adults. They underwent MRI and PET scans between 2009 and 2022 to measure brain structure changes, serotonin transporter levels, and amyloid-beta protein distribution in the brain.
Amyloid-beta is believed to play a central role in Alzheimer’s pathology. Previous studies have shown serotonin degeneration occurs before the development of widespread beta-amyloid deposits in the brain, and its loss is often associated with depression and psychological disorders.
Findings indicated that MCI patients had up to 25% lower serotonin transporter levels in areas of the brain responsible for executive function, emotion, and memory, and also higher levels of amyloid-beta compared to healthy controls.
Smith highlights the importance of this correlation, as it identifies a brain chemical that could be targeted to potentially improve cognitive deficits and depressive symptoms.
If future studies confirm serotonin’s direct involvement in the transition from MCI to Alzheimer’s, antidepressants might be an effective approach to slow disease progression.
Future research plans include longitudinal studies to track serotonin degeneration, amyloid-beta, and tau protein levels in MCI patients compared to healthy adults.
There is also a focus on studying antidepressant drugs to treat depression and memory deficits in hopes of mitigating symptoms and halting disease progression.
The study, involving additional coauthors from Johns Hopkins University School of Medicine and the Bloomberg School of Public Health, reports no conflicts of interest.
This pioneering research opens new avenues in understanding and potentially treating early stages of Alzheimer’s and related memory disorders.
If you care about Alzheimer’s, please read studies about the likely cause of Alzheimer’s disease , and new non-drug treatment that could help prevent Alzheimer’s.
For more information about brain health, please see recent studies about diet that may help prevent Alzheimer’s, and results showing some dementia cases could be prevented by changing these 12 things.
The research findings can be found in the Journal of Alzheimer’s Disease.
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