Scientists Find A New Cause Of Memory Loss In Alzheimer’s Disease

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A study by Johns Hopkins Medicine researchers, published in the Journal of Alzheimer’s Disease, reveals a potential connection between serotonin levels and memory issues in people with mild cognitive impairment (MCI), which could be a precursor to Alzheimer’s disease (AD).

Involving over 90 adults, both with and without MCI, the study used PET scans to investigate the levels of serotonin, often referred to as the “happiness” chemical, in the brain.

The findings suggest that lower serotonin levels in certain brain areas might be involved in memory problems, including those seen in Alzheimer’s disease.

This adds to the growing evidence that changes in the brain can be detected long before an Alzheimer’s diagnosis, presenting new avenues for treatment strategies aimed at slowing or preventing disease progression.

Gwenn Smith, Ph.D., a professor at the Johns Hopkins University School of Medicine, explains, “We observed that people with MCI have a reduction in the serotonin transporter.

This is significant because it correlates with memory challenges, independent of MRI measures of neurodegeneration and PET measures of amyloid protein, which are also linked to Alzheimer’s.”

MCI is a critical diagnostic stage between normal aging and Alzheimer’s, marked by symptoms like frequent forgetfulness, trouble with word-finding, and loss of smell.

Understanding the progression from MCI to more severe cognitive deficits is crucial, as it might offer a window for early intervention.

However, the researchers note that their study establishes a correlation rather than causation between lower serotonin transporter levels and memory problems in MCI. Further longitudinal studies are necessary to clarify the role of serotonin in the progression from MCI to Alzheimer’s.

For this study, 49 volunteers with MCI and 45 healthy older adults underwent MRIs and two PET scans at Johns Hopkins between 2009 and 2022.

The PET scans focused on the serotonin transporter and the distribution of amyloid-beta (Aβ) protein in the brain, a key player in AD pathology.

Previous studies in mice at Johns Hopkins have shown serotonin degeneration precedes significant beta-amyloid deposits in the brain, with serotonin loss often linked to depression and anxiety.

The researchers found that MCI patients had both lower serotonin transporter levels (up to 25% lower in certain brain regions) and higher Aβ levels than healthy controls. The affected brain areas are responsible for functions like executive processing, emotion, and memory.

Smith highlights the significance of this correlation, suggesting that targeting serotonin could improve cognitive deficits and potentially depressive symptoms.

“If we can establish a direct link between serotonin loss and the progression from MCI to AD, new antidepressant medications might be a promising approach to enhance memory and mood, thereby slowing down the progression of the disease.”

Future studies will focus on longitudinal observations of MCI individuals, comparing serotonin degeneration with increases in Aβ and Tau protein levels, both associated with AD.

The researchers also plan to explore multi-modal antidepressant drugs to treat both depression and memory deficits, hoping to mitigate and halt AD symptoms.

This research offers a new perspective on tackling memory issues and Alzheimer’s disease, emphasizing the significance of early detection and intervention.

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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