Dementia

Posted on ADHD, Alzheimer's, Dementia

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.

Posted on Dementia

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.  

Posted on Dementia, Diabetes

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

Things to Consider When Finding the Right Nursing Home for Your Loved One

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.

Posted on Dementia, Multiple Sclerosis, Parkinson's Disease

Discovery raises possibility of new medication for Alzheimer’s, Parkinson’s and MS

Medical Compliance
Medical Compliance

Researchers from Oregon Health & Science University have for the first time demonstrated it’s possible to use a synthetic thyroid hormone to regulate a gene implicated in neurodegenerative diseases like Alzheimer’s, Parkinson’s and multiple sclerosis.

The findings from tests in cells and mice, published today in the journal Cell Chemical Biology, raise the possibility of development of new medication to treat debilitating diseases.

“This is the first example reported that shows it’s possible to increase the expression of the TREM2 gene in a way that will lead to healing in certain diseases,” said senior author Tom Scanlan, Ph.D., professor of physiology and pharmacology in the OHSU School of Medicine. “This will generate a lot of excitement.”

The paper’s first author is Skylar J. Ferrara, Ph.D., a postdoctoral fellow in the OHSU School of Medicine’s chemical physiology and biochemistry department. 

The discovery builds on a 2013 publication linking genetic variants of TREM2 to risk of Alzheimer’s disease.

The new research from OHSU builds on that work by showing that it’s possible to turn on TREM2 expression and the TREM2 pathway using a compound originally developed more than two decades ago to lower cholesterol.

Researchers administered an analog of the compound that penetrates into the central nervous system of mice. They discovered they were able to increase the expression of TREM2 and reduce damage to myelin. Myelin is the insulation-like protective sheath covering nerve fibers that’s damaged in disorders like multiple sclerosis. 

The pathway activated by the TREM2 gene is also implicated in neurodegenerative diseases, including Alzheimer’s and Parkinson’s.

“TREM2 is a receptor,” Scanlan said. “It senses damaged cellular debris from disease and responds in a healing, productive way. The thought is, if you can simply turn up its expression, then that’s going to lead to a therapeutic effect in most neurodegenerative diseases.” 

Joseph Quinn, M.D., professor of neurology in the OHSU School of Medicine, who treats patients with Parkinson’s and Alzheimer’s, said the findings are promising. Quinn wasn’t involved in the research.

“TREM2 is a viable ‘target’ for treatment in Alzheimer’s disease, based on genetics and other studies,” Quinn said. “This new report has important implications for testing a new therapeutic approach for Alzheimer’s, including raising the potential for developing a new medication to regulate TREM2.”

The synthetic thyroid hormone compound, known as sobetirome and similar analogs, is already licensed by an OHSU spinoff company to conduct clinical trials for central nervous system diseases, including multiple sclerosis. In contrast to other basic science discoveries in mice, Scanlan said this latest discovery connects this class of compounds to Alzheimer’s, Parkinson’s and other neurodegenerative diseases, advancing the science that much closer to clinical trials in people with debilitating disease.  

“The possibility of doing clinical trials is not millions of miles away,” Scanlan said. “It would be an achievable thing.”