The new research from Washington University School of Medicine in St. Louis has found that people with Multiple Sclerosis (MS) are less likely to develop Alzheimer’s disease than people without MS.
Matthew Brier, MD PhD, an assistant professor of neurology and of radiology and the study’s first author commented that, “The discovery suggests a new avenue of research through which to seek Alzheimer’s treatments.”
The study, conducted in collaboration between WashU Medicine experts in Alzheimer’s and MS, highlighted that the patients with MS, a disease that attacks the central nervous system, live long enough to be at risk of Alzheimer’s or had a family history of the neurodegenerative disease, weren’t developing the disease.
Anne Cross The Manny and Rosalyn Rosenthal – Dr. John Trotter MS Center Chair in Neuroimmunology.
“I noticed that I couldn’t find a single MS patient of mine who had typical Alzheimer’s disease. If they had cognitive problems, I would send them to the memory and aging specialists here at WashU Medicine for an Alzheimer’s assessment, and those doctors would always come back and tell me, ‘No, this is not due to Alzheimer’s disease.'”
MS symptoms can be confused with the symptoms of Alzheimer’s disease, but Alzheimer’s can be confirmed with blood test known as PredictivityAD2 that shows the presence of amyloid plaques, the indicator of Alzheimer’s disease. To confirm this, the research team recruited 100 patients with MS to test their blood, and the results were later compared with people with genetic risk of Alzheimer’s.
“We found that 50% fewer MS patients had amyloid pathology compared to their matched peers, based on this blood test,” added Brier. The study also found that the patient’s with more typical MS history were less likely to develop amyloid plaques in their brain than those with atypical symptoms of MS.
The majority of MS patients experience multiple flare-ups of the illness during their lifetime. During these flare-ups, the immune system attacks the central nervous system. It’s possible that this immune activity also reduces amyloid plaques, according to the researcher.
“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 added.
Brier also stated 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, by referring to a work by co-author David M. Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology,
Brier and Cross are also exploring the possible human genetics and amyloid plaque development in animal models representing MS.
