Summary: Research has revealed that individuals with multiple sclerosis (MS) are significantly less likely to exhibit the molecular signs of Alzheimer’s disease, suggesting a protective element in MS that could inspire new Alzheimer’s treatments.
“Our findings imply that some component of the biology of multiple sclerosis, or the genetics of MS patients, is protective against Alzheimer’s disease,” Brier said.
Such plaques are an indicator of Alzheimer’s disease and previously only could be verified with brain scans or spinal taps.
MS patients generally have multiple flare-ups of the illness over the course of their lifetimes.
About this multiple sclerosis and dementia research news Author: Mark Reynolds Source: WUSTL Contact: Mark Reynolds – WUSTL Image: The image is credited to Neuroscience News Original Research: Closed access.
“Unexpected low rate of amyloid-β pathology in multiple sclerosis patients” by Matthew Brier et al.
Annals of Neurology Abstract Unexpected low rate of amyloid-β pathology in multiple sclerosis patients The life expectancy of people with multiple sclerosis (MS) has increased, yet we have noted that development of a typical Alzheimer disease dementia syndrome is uncommon.
Interestingly, most MS patients who did have amyloid-β pathology had features atypical for MS at diagnosis.
A protective factor in multiple sclerosis (MS) may inspire new treatments for Alzheimer’s disease, as research has shown that people with MS are much less likely to display the molecular symptoms of the disease.
According to the study, compared to non-MS people, MS patients had 50% less amyloid plaque accumulation, a crucial sign of Alzheimer’s disease. This association between MS and a lower risk of Alzheimer’s disease underscores immune-related mechanisms that could be targeted for treatment approaches.
Important Information:.
Amyloid plaques, a defining feature of Alzheimer’s disease, are 50% less common in MS patients.
The reduction of amyloid accumulation in the brain in multiple sclerosis may be facilitated by the immune response.
This finding provides new opportunities for studying Alzheimer’s disease and developing possible therapies.
WUSTL was the source.
The molecular indicators of Alzheimer’s disease are far less common in people with multiple sclerosis (MS) than in people without the illness, according to recent research from Washington University School of Medicine in St. Louie.
Lead author of the study Matthew Brier, MD, PhD, an assistant professor of radiology and neurology, said the finding points to a new line of inquiry for Alzheimer’s treatment.
According to Brier, “Our results suggest that there may be a genetic component to multiple sclerosis patients’ immunity against Alzheimer’s disease, or that there may be aspects of the biology of MS.”. Therapeutic approaches for Alzheimer’s disease might be informed if we could pinpoint the protective factor and apply it in a controlled manner. “.
The work was published in the Annals of Neurology and is an illustration of how clinical observations influence research directly.
The investigation, which involved collaboration between WashU Medicine specialists in Alzheimer’s and MS, was spurred by a suspicion that Brier’s mentor and collaborator, Anne Cross, MD, had grown suspicious of over the course of treating patients with MS, an immune-mediated condition that targets the central nervous system, for many years.
Her patients weren’t getting Alzheimer’s, even though they were living long enough to be at risk for it or had a family history of the neurodegenerative condition.
Dr. John Trotter MS Center Chair in Neuroimmunology Manny and Rosalyn Rosenthal Cross said, “I noticed that I couldn’t find a single MS patient of mine who had typical Alzheimer’s disease.”.
“When they experienced cognitive issues, I referred them to the memory and aging experts at WashU Medicine for an evaluation for Alzheimer’s disease, and each time, those physicians would say, ‘No, this is not related to Alzheimer’s disease.'”. “”.
Alzheimer’s disease symptoms can be mistaken for MS-related cognitive impairment; however, blood and other biological tests can distinguish Alzheimer’s from MS-related cognitive impairment.
The study team employed a recently FDA-approved blood test that was created by WashU Medicine researchers in order to validate Cross’ findings. The blood test, called PrecivityAD2, is very good at foretelling if amyloid plaques are present in the brain. These plaques, which previously could only be confirmed by spinal taps or brain scans, are a sign of Alzheimer’s disease.
One hundred MS patients were gathered by Brier, Cross, and associates to participate in the blood test; eleven of these patients also had PET scans performed at WashU Medicine’s Mallinckrodt Institute of Radiology. Their outcomes were contrasted with those of a control group consisting of 300 people who did not have MS but whose ages, genetic susceptibilities to Alzheimer’s disease, and levels of cognitive decline were comparable to those of MS patients.
“This blood test showed that, in comparison to their matched peers, 50% fewer MS patients had amyloid pathology,” said Brier.
It is unclear how amyloid accumulation is related to the cognitive impairment characteristic of Alzheimer’s disease, but plaque accumulation is widely believed to be the initial step in the biological cascade that results in cognitive decline. This finding corroborated Cross’s observation that Alzheimer’s appeared to be less likely to develop among those with MSdot.
Additionally, compared to patients with atypical presentations of MS, the researchers found that patients with more typical MS histories—that is, those with similar age of onset, severity, and overall disease progression—were also less likely to have amyloid plaque accumulation in their brains. This finding raises the possibility that there is something about MS itself that protects against Alzheimer’s disease, a possibility that Brier and Cross plan to explore.
Throughout their lifetimes, MS patients typically experience several flare-ups of the illness. The central nervous system, including the brain, is attacked by the immune system during these flare-ups. The researchers speculated that this immune activity might also lessen amyloid plaques.
Brier speculated that the MS patients may have had some degree of immune-related brain inflammation during the development of the Alzheimer’s disease amyloid pathology. Brier mentioned that activated microglia—a component of the brain’s immune response in multiple sclerosis—have been demonstrated to remove amyloid from the brain in animal models, citing research by co-author David M. Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology.
The next phases of this research have been started by Brier and Cross, who aim to test the development of amyloid plaque in animal models that mimic multiple sclerosis and identify any potential human genetic components.
A number of the coauthors on this study, including Brier and Cross, are connected to C2N Diagnostics, a WashU Medicine startup that funded the research. The PrecivityAD2 exam is built on technology that the university has licensed to C2N.
About this news on dementia and multiple sclerosis research.
Written by Mark Reynolds.
WUSTL is the source.
WUSTL’s Mark Reynolds can be reached.
Photo credit: This image is courtesy of Neuroscience News.
First research: restricted access.
“An unexpectedly low incidence of amyloid-β pathology in patients with multiple sclerosis” Matthew Brier et al. Neurology Annals.
Inabst.
Unexpectedly low prevalence of amyloid-β pathology in MS patients.
Although the life expectancy of individuals with multiple sclerosis (MS) has increased, it is rare for them to develop the classic dementia syndrome of Alzheimer’s disease. According to our hypothesis, Alzheimer disease pathology is unusual in people with multiple sclerosis.
After controlling for age, sex, apolipoprotein E proteotype, and cognitive status, the rate of amyloid-β plasma biomarker positivity in 100 MS patients was about half that of 300 non-MS controls. Remarkably, at the time of diagnosis, the majority of MS patients with amyloid-β pathology had characteristics not typical of MS.
The findings indicate new directions for future research and corroborate the notion that MS is linked to a lower risk of Alzheimer’s disease.
