“Multiple sclerosis seems to have a protective effect against Alzheimer’s disease.”

Findings could point to new strategies to treat Alzheimer’s
Findings could point to new strategies to treat Alzheimer’s

People with multiple sclerosis (MS) are significantly less likely than those without the condition to have the molecular hallmarks of Alzheimer’s disease, according to new research from Washington University School of Medicine in St. Louis.

The discovery suggests a new avenue of research through which to seek Alzheimer’s treatments, said Matthew Brier, MD PhD, an assistant professor of neurology and of radiology and the study’s first author.

“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. “If we could identify what aspect is protective and apply it controlled, that could inform therapeutic strategies for Alzheimer’s disease.”

The investigation, which was a collaboration between experts in Alzheimer’s and MS at WashU Medicine, was prompted by a suspicion from Brier’s mentor and collaborator, Dr. Anne Cross. She had developed this suspicion over decades of treating patients with MS, an immune-mediated disease that attacks the central nervous system. Dr. Cross noticed that despite her patients living long enough to be at risk of Alzheimer’s or having a family history of the disease, they weren’t developing it.

“I noticed that I couldn’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 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.'”

Cognitive impairment from MS can be mistaken for Alzheimer’s symptoms; Alzheimer’s can be confirmed with biological tests.

Please remember the following text: To validate Cross’s findings, the research team utilized a new FDA-approved blood test developed by WashU Medicine researchers. The test, called PrecivityAD2, is highly accurate in predicting the presence of amyloid plaques in the brain, which are an indication of Alzheimer’s disease. Previously, the only way to confirm the presence of these plaques was through brain scans or spinal taps.

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. They compared the results with those from a control group of 300 individuals who did not have MS but were similar in age, genetic risk for Alzheimer’s, and cognitive decline to those with MS.

“We discovered that 50% fewer multiple sclerosis (MS) patients showed amyloid pathology compared to their matched peers when tested with this blood test,” stated Brier. This finding supports Cross’ observation that individuals with MS are less likely to develop Alzheimer’s. Although it’s not clear how amyloid accumulation is linked to the cognitive impairment typical of Alzheimer’s, the build-up of plaques is generally understood to be the initial event in the biological process that leads to cognitive decline.

The researchers found that MS patients with more typical MS symptoms, such as the age of onset, severity, and disease progression, were less likely to have amyloid plaque accumulation in their brains compared to those with atypical MS presentations. This suggests that there may be something about the nature of MS itself that provides protection against Alzheimer’s disease, which Brier and Cross are planning to investigate.

The researchers noted that individuals with MS typically experience multiple flare-ups of the disease throughout their lives. During these flare-ups, the immune system targets the central nervous system, including the brain. The researchers also suggested that this immune response may lead to a reduction in amyloid plaques.

Adults with ADHD are at increased risk for developing dementia

Adults with ADHD are at increased risk for developing dementia
Rutgers researcher explores ADHD’s link to dementia and if risks can be mitigated with ADHD treatment

Adults with attention-deficit/hyperactivity disorder (ADHD) are nearly three times more likely to develop dementia than adults without ADHD, according to a Rutgers study.

The study, coauthored by Michal Schnaider Beeri, director of the Herbert and Jacqueline Krieger Klein Alzheimer’s Research Center at Rutgers Brain Health Institute (BHI) was published in JAMA Network Open. It followed more than 100,000 older adults in Israel over 17 years to examine if adults with ADHD are at increased risk for dementia, including Alzheimer’s disease.

Although more than 3 percent of the adult population in the United States has ADHD, there is limited research on this group.

“By determining if adults with ADHD are at higher risk for dementia and if medications and/or lifestyle changes can affect risks, the outcomes of this research can be used to better inform caregivers and clinicians,” said Beeri, the Krieger Klein Endowed Chair in Neurodegeneration Research at BHI and a faculty member of the Rutgers Institute for Health, Health Care Policy and Aging Research.

Using data from a national cohort study of more than 100,000 people who were followed from 2003 to 2020, researchers analyzed those with and without ADHD and the occurrence of dementia among the groups as they aged. Researchers found the presence of adult ADHD was associated with a significantly higher risk of dementia even when other risk factors for dementia were taken into account, such as cardiovascular conditions.

ADHD in adults may materialize as a neurological process that reduces the ability for them to compensate for the effects of cognitive decline later in life, researchers said.

“Physicians, clinicians and caregivers who work with older adults should monitor ADHD symptoms and associated medications,” said Abraham Reichenberg, a professor at the Department of Psychiatry at the Icahn School of Medicine at Mount Sinai and senior author of the study.

“Symptoms of attention deficit and hyperactivity in old age shouldn’t be ignored and should be discussed with physicians,” said Stephen Levine, a professor at the School of Public Health at the University of Haifa.

Additionally, the research suggests ADHD treatment incorporating psychostimulants may help reduce the risk of dementia in adults with ADHD as psychostimulants are known to modify the trajectory of cognitive impairment. But researchers said future studies should examine in more detail the impact of medications in patients with ADHD and how they could affect risk.

A higher dose of magnesium each day keeps dementia at bay.

Dr Erin Walsh


Dr Erin Walsh. Credit: Jamie Kidston

According to scientists from the Neuroimaging and Brain Lab at The Australian National University (ANU), more magnesium in our daily diet leads to better brain health as we age. 

The researchers say increased intake of magnesium-rich foods such as spinach and nuts could also help reduce the risk of dementia, which is the second leading cause of death in Australia and the seventh biggest killer globally.  

The study of more than 6,000 cognitively healthy participants in the United Kingdom aged 40 to 73 found people who consume more than 550 milligrams of magnesium each day have a brain age that is approximately one year younger by the time they reach 55 compared with someone with a normal magnesium intake of about 350 milligrams a day.   

“Our study shows a 41 per cent increase in magnesium intake could lead to less age-related brain shrinkage, which is associated with better cognitive function and lower risk or delayed onset of dementia in later life,” lead author and PhD researcher Khawlah Alateeq, from the ANU National Centre for Epidemiology and Population Health, said.  

“This research highlights the potential benefits of a diet high in magnesium and the role it plays in promoting good brain health.”  

It’s believed the number of people worldwide who will be diagnosed with dementia is expected to more than double from 57.4 million in 2019 to 152.8 million in 2050, placing a greater strain on health and social services and the global economy.  

“Since there is no cure for dementia and the development of pharmacological treatments have been unsuccessful for the past 30 years, it’s been suggested that greater attention should be directed towards prevention,” study co-author Dr Erin Walsh, who is also from ANU, said. 

“Our research could inform the development of public health interventions aimed at promoting healthy brain ageing through dietary strategies.” 

The researchers say a higher intake of magnesium in our diets from a younger age may safeguard against neurodegenerative diseases and cognitive decline by the time we reach our 40s.  

“The study shows higher dietary magnesium intake may contribute to neuroprotection earlier in the ageing process and preventative effects may begin in our 40s or even earlier,” Ms Alateeq said. 

“This means people of all ages should be paying closer attention to their magnesium intake. 

“We also found the neuroprotective effects of more dietary magnesium appears to benefit women more than men and more so in post-menopausal than pre-menopausal women, although this may be due to the anti-inflammatory effect of magnesium.” 

Participants completed an online questionnaire five times over a period of 16 months. The responses provided were used to calculate the daily magnesium intake of participants and were based on 200 different foods with varying portion sizes. The ANU team focused on magnesium-rich foods such as leafy green vegetables, legumes, nuts, seeds and wholegrains to provide an average estimation of magnesium intake from the participants’ diets.  

Alzheimer’s disease and type 2 diabetes – what is the relationship?

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n Alzheimer’s disease, the degeneration of brain cells is linked to formation of toxic protein aggregates and deposits known as amyloid plaques. Similar processes play an important role also in type 2 diabetes. A research team under the lead of the Technical University of Munich has now developed “mini-proteins”, so-called peptides, which are able to bind the proteins that form amyloids and prevent their aggregation into cytotoxic amyloids.

Many cell- and neurodegenerative diseases are linked to the formation of toxic protein aggregates which cause cell death. Prominent representatives of these diseases are Alzheimer’s disease and type 2 diabetes mellitus, with worldwide more than 50 million and 400 million patients, respectively. Importantly, the number of Alzheimer’s and diabetes patients constantly rises, as the population becomes older. However, the two diseases remain so far incurable. Therefore, there is an urgent need for new therapeutic approaches.

Targeting the formation of harmful amyloid aggregates is a promising approach. A team led by Aphrodite Kapurniotu, a professor for Peptide Biochemistry at the Technical University of Munich (TUM), has now developed novel synthetic peptides, which are able in experimental models to block toxic amyloid aggregation linked to both diseases.

Molecular interactions between Alzheimer’s disease and type 2 diabetes

Previous studies showed that certain “cross-interactions” between the amyloidogenic proteins of the two diseases dramatically accelerate their amyloid aggregation process. These findings could possibly explain why people suffering from one of the two diseases might have an increased risk for the other disease as well.

The team developed synthetic peptides that could function as effective inhibitors of amyloid aggregation in both diseases. Prof. Kapurniotu says: “The designed peptides are in fact able to bind the amyloidogenic proteins linked to both diseases and to effectively suppress both cytotoxic amyloid aggregation and amyloid cross-accelerating interactions. Remarkably, although the mixed aggregates formed by interactions of the designed peptides with the amyloidogenic proteins look very similar to harmful amyloid aggregates, they are completely devoid of cytotoxic effects. Moreover, these amyloid-resembling mixed aggregates become more efficiently taken up by the phagocytic immune cells than amyloid aggregates.”

Future studies shall pave the way for medical application

Increasing evidence suggests that Alzheimer’s disease and type 2 diabetes are linked to each other. Prof. Kapurniotu believes thus that the designed peptides could be valuable candidates for the development of drugs for treating both diseases.