summary: Researchers have discovered a potential link between reduced levels of the 'happiness' chemical serotonin and mild cognitive impairment (MCI), which could improve understanding of Alzheimer's disease (AD). It is possible to proceed.
Their research shows that MCI patients have significantly reduced serotonin transporter levels, a factor that can contribute to memory impairment and potentially Alzheimer's disease. This finding offers a new avenue for treatment, as serotonin levels may be a target for early intervention to slow or stop disease progression.
However, this study emphasizes correlation rather than causation and calls for further research to investigate the role of serotonin in the transition from MCI to AD.
Important facts:
- MCI patients showed up to 25% lower levels of the serotonin transporter in certain brain regions compared to healthy controls.
- The study, which ran from 2009 to 2022, involved 49 volunteers with MCI and 45 healthy adults, and used MRI and PET scans to analyze brain changes and serotonin transporter levels.
- Researchers have found that targeting serotonin levels may not only improve memory problems but also reduce symptoms of depression, providing a potential strategy to slow the progression of Alzheimer's disease. suggests.
sauce: Johns Hopkins University
Researchers at the Johns Hopkins School of Medicine compared PET scans of more than 90 adults with and without mild cognitive impairment (MCI) and found that parts of the brains of MCI patients had low levels of serotonin, the so-called “happiness” chemical. He said it may be having an impact because the levels are relatively low. Role in memory disorders such as Alzheimer's disease.
The findings were first published online on September 13th. Alzheimer's Disease Journal, There is growing evidence that measurable changes in the brain occur in people with mild memory loss long before they are diagnosed with Alzheimer's disease, and new treatments are emerging to slow or stop the disease's progression. Potential targets.
“This study shows that people with mild cognitive impairment already show loss of the serotonin transporter. Even when you consider PET measurements of amyloid proteins associated with memory problems,” said Dr. Gwen Smith. , professor of psychiatry and behavioral sciences at Johns Hopkins University School of Medicine.
MCI represents a diagnostic stage between normal age-related brain function and Alzheimer's disease (AD). Symptoms of MCI include frequent forgetting of recent events, difficulty finding words, and loss of smell.
Because MCI patients may remain in this stage indefinitely or progress to more severe cognitive impairment, there is an urgent need to explore predictive markers and potentially early preventive interventions, the researchers said.
The researchers said that this study shows a correlation between decreased serotonin transporter levels and memory impairment in MCI and was not designed to demonstrate a causal relationship or role for serotonin in the progression from MCI to AD. I warned you that there is no. To answer these questions, further studies are needed to study healthy controls and MCI patients over time and demonstrate the role of serotonin in disease progression.
For the study, Hopkins scientists studied 49 MCI volunteers and conducted MRI scans and two positron electron beam tests to measure changes in brain structure at Johns Hopkins University between 2009 and 2022. We recruited 45 healthy adults aged 55 years and older who underwent a tomography tomography (PET) scan. .
The research team used PET scans to specifically examine the serotonin transporter (a neurotransmitter, or brain chemical that has long been associated with positive mood, appetite, and sleep) and the amyloid beta protein (Aβ) in the brain. ) distribution was investigated. Aβ is thought to play a central role in the pathology of AD.
Mouse studies conducted at Johns Hopkins University have shown that serotonin degeneration occurs before widespread beta-amyloid deposits develop in the brain. Loss of serotonin is often associated with depression, anxiety, and mental disorders.
Researchers found that MCI patients had lower levels of the serotonin transporter and higher levels of Aβ compared to healthy controls. MCI patients had up to 25% lower serotonin transporter levels in cortical and limbic regions compared to healthy controls.
In particular, they report that MCI patients showed decreased levels of serotonin transporters in cortical, limbic, and subcortical regions of the brain, areas specifically responsible for executive function, emotion, and memory.
“The correlation that we observed between reduced serotonin transporters and memory impairment in MCI is important because it suggests that there may be safe targets in the brain that could ameliorate cognitive impairment and potentially depressive symptoms. “We could have identified the chemical,” Smith said.
“If we can prove that the decrease in serotonin over time is directly involved in the transition from MCI to AD, then recently developed antidepressants could be an effective way to improve memory loss and depressive symptoms. “This could potentially be a powerful way to slow the progression of the disease.”
The researchers say that future studies will include long-term follow-up of MCI patients to compare serotonin degeneration and increased Aβ levels, as well as increased tau protein levels associated with AD, compared to healthy adults. It states that it will be possible. They are also researching multidisciplinary antidepressants to treat depression and memory problems in hopes of alleviating and stopping symptoms.
Other scientists from the Johns Hopkins University School of Medicine and Johns Hopkins Bloomberg School of Public Health who contributed to this study were Jennifer Coughlin, Robert Danals, Neda Gould, Daniel Holt, Vidya Kamath, Michael Kraut, Hiroto Kuwabara, Jeannie Leusakos, and Martin Lodge. , Ayon Nandi, Najla Nassery, Martin Pomper, Alena Savonenko, Haijuan Yang, Mark Yun.
All authors have no conflicts to disclose.
Funding: This research was supported in part by the National Institutes of Health.
About this Alzheimer's disease research news
author: kristen crocker
sauce: Johns Hopkins University
contact: Kristen Crocker – Johns Hopkins University
image: Image credited to Neuroscience News
Original research: Closed access.
“Serotonin degeneration and amyloid β deposition in mild cognitive impairment: relationship with cognitive impairmentWritten by Gwen Smith et al. alzheimer's disease journal
abstract
Serotonin degeneration and amyloid β deposition in mild cognitive impairment: relationship with cognitive impairment
background: Neuropathological and neuroimaging studies have demonstrated degeneration of the serotonergic system in Alzheimer's disease (AD). Neuroimaging studies have extended these observations to mild cognitive impairment (MCI), the preclinical stage of Alzheimer's disease. Serotonin degeneration has also been observed in transgenic amyloid mouse models, before amyloid-β (Aβ) is widely distributed in the cortex.
objective: In this study, we evaluated the regional distribution of serotonin transporter (5-HTT) and Aβ in MCI patients and healthy elderly controls, as well as the contribution of 5-HTT and Aβ to cognitive impairment.
Method: Forty-nine MCI participants and 45 healthy elderly controls underwent positron emission tomography (PET) imaging for 5-HTT and Aβ, structural magnetic resonance imaging, and neuropsychological evaluation.
result: We observed lower cortical, striatal, and limbic 5-HTT and higher cortical Aβ in MCI compared to healthy controls. Reduced 5-HTT, primarily in limbic regions, correlated with greater deficits in auditory verbal memory, visuospatial memory, and semantic, but not phonemic, fluency. Higher cortical Aβ was associated with greater deficits in auditory verbal and visuospatial memory, and in semantic, but not phonemic, fluency. When modeling the association between cognition, gray matter volume, and Aβ, the inclusion of 5-HTT in the limbic system and selected cortical regions improves the relationship between auditory verbal and visuospatial memory and semantic models. compatibility was significantly improved, but phonemic fluency was not.
Conclusion: These results support the role of serotonin degeneration in the memory and semantic fluency deficits observed in MCI.
