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.
The research found that MS individuals had 50 % less amyloid plaque concentration, a key sign of Alzheimer’s, compared to non-MS people. This association between MS and a decreased risk of Alzheimer’s disease highlights possible immune-related mechanisms that can be used for therapeutic purposes.
Important Information:
- MS patients are 50 % less likely to develop amyloid plaques, a hallmark of Alzheimer’s.
- The brain’s immune response may help to lessen amyloid accumulation.
- This breakthrough opens up new strategies for Alzheimer’s study and possible solutions.
Origin: WUSTL
According to new research from Washington University School of Medicine in St. Louis, people with multiple sclerosis ( MS ) are far less likely than those without the condition to have the molecular hallmarks of Alzheimer’s disease.
The discovery suggests a new avenue of exploration through which to get Alzheimer’s treatments, said , Matthew Brier, MD PhD, an assistant professor of neuroscience and of radiography and the study’s initial artist.
” Our findings imply that some part of the science of multiple sclerosis, or the biology of MS people, is safe against Alzheimer’s disease”, Brier said. What protective feature of the disease might be identified and used in a controlled manner, it might help guide Alzheimer’s disease healing approaches.
The review, an example of scientific studies directly impacting study, was published in the , Annals of Neurology.
A partnership between WashU Medicine authorities in Alzheimer’s and MS, the research was prompted by a fear Brier’s coach and partner,  , Anne Cross, MD, had developed over years of treating patients with MS, an immune-mediated disorder that attacks the central nervous system.
Although her people did n’t develop the condition, they were still living longer enough to be at risk of Alzheimer’s or had a family record of the degenerative disease.
” I noticed that I could n’t find a single MS patient of mine who had typical Alzheimer’s disease”, said Cross, the Manny and Rosalyn Rosenthal and Dr. John Trotter MS Center Chair in Neuroimmunology.
” If they had mental problems, I would take them to the storage and aging specialists below at WashU Medicine for an Alzheimer’s judgment, and those doctors had always come back and tell me,’ No, this is not expected to Alzheimer’s disease.'”
Cognitive impairment caused by MS can be confused with symptoms of Alzheimer’s disease, Alzheimer’s can be confirmed with blood and other biological tests.
To confirm Cross ‘ observation, the research team used a new, FDA-approved blood test that was developed by WashU Medicine researchers. Known as PrecivityAD2, the blood test is , highly effective , at predicting the presence of amyloid plaques in the brain. These plaques, which were previously only able to be verified by brain scans or spinal taps, serve as an indicator of Alzheimer’s disease.
Brier, Cross and their colleagues recruited 100 patients with MS to take the blood test, 11 of whom also underwent PET scans at WashU Medicine ‘s , Mallinckrodt Institute of Radiology. Their findings were contrasted with those of a control group of 300 people who did not have MS but who had MS in terms of age, genetic risk for Alzheimer’s, and cognitive decline.
According to this blood test,” we discovered that 50 % fewer MS patients had amyloid pathology than their matched peers,” according to Brier.
This finding supported Cross ‘ claim that Alzheimer’s appeared to be less likely to develop in those who had MS. Although it is unclear how amyloid accumulation is connected to the cognitive decline that characterizes Alzheimer’s, plaque accumulation is generally accepted to be the first step in the biological cascade that causes cognitive decline.
The researchers also discovered that the more typical the patient’s MS history was in terms of age, severity, and overall disease progression, the less likely it was to have amyloid plaque accumulate in their brains compared to those who had atypical MS presentations. This suggests that Brier and Cross are planning to look into something about the nature of MS itself that is protective against Alzheimer’s disease.
MS patients typically experience multiple flare-ups of the illness over the course of their lifetimes. During these flare-ups, the immune system attacks the central nervous system, including within the brain. According to the researchers, it’s possible that this immune response reduces amyloid plaques as well.
” Perhaps when the Alzheimer’s disease amyloid pathology was developing, the patients with MS had some degree of inflammation in their brains that was spurred by their immune responses”, Brier said. Referring to work by co-author , David M. Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology, Brier noted that activated microglia, which are part of the brain’s immune response in MS, have been shown to clear amyloid from the brain in animal models.
Brier and Cross have begun the next phase of this study, both to investigate the potential human genetics involved and to examine the development of amyloid plaques in MS-positive animal models.
Several of Brier’s and Cross ‘ coauthors on this study are affiliated with C2N Diagnostics, a WashU Medicine startup that provided support for the investigation. The PrecivityAD2 test is based on technology licensed to C2N by the university.
About this research on dementia and multiple sclerosis
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
People with multiple sclerosis ( MS ) have a longer life expectancy, but we have not yet discovered a typical Alzheimer disease dementia syndrome. We made the hypothesis that Alzheimer disease pathology is not common in MS patients.
In 100 MS patients, the rate of amyloid-β plasma biomarker positivity was approximately half the rate in 300 non-MS controls matched on age, sex, apolipoprotein E proteotype, and cognitive status. Interestingly, most MS patients who did have amyloid-β pathology had features atypical for MS at diagnosis.
These findings provide new evidence for the link between MS and a reduced risk of Alzheimer’s disease, and they also offer new avenues for research.
