Posted on Multiple Sclerosis

Insomnia and sleep apnea contribute to reports of cognitive decline in women with multiple sclerosis.


People with MS who have sleep disorders notice more changes in their thinking


For women with multiple sclerosis who report cognitive dysfunction — one of the most common and disabling symptoms of the disease — sleep disorders such as insomnia and sleep apnea may contribute to the perceived decline, a Michigan Medicine study suggests.

Researchers analyzed data from over 60,000 women using the 2013 and 2017 waves of the Nurses’ Health Study, a long-term study focusing on risk factors for chronic diseases in women. Using composite scores of self-reported diagnoses and symptoms, they found that women with multiple sclerosis were likelier than those without MS to report sleep disorders, including obstructive sleep apnea, insomnia and sleepiness.

Results published in Multiple Sclerosis Journal also reveal that sleep disorders identified in 2013 contributed to cognitive problems reported by women with MS in 2017, including ability to follow instructions and conversations and memory. Insomnia mediated more than 10% of these outcomes, and sleep apnea accounted for 34% of the total effect between MS and the ability to follow instructions.

“Sleep disorders have gained substantial recognition for their role in cognitive decline, which affects up to 70% of people with multiple sclerosis,” said lead author Tiffany Braley, M.D., director of the Multiple Sclerosis/Neuroimmunology Division and multidisciplinary MS Fatigue and Sleep Clinic at University of Michigan Health.

“Our results highlighted important pathways between sleep and perceptions of cognitive function in women with MS. We have previously identified important associations between objective cognitive performance and sleep in people with MS, but little is known about how sleep and MS interact together to impact long-term cognitive outcomes, particularly among women who are less likely to be diagnosed with sleep disorders,” Braley said.

Past studies have found that people with MS have a high burden of sleep disorders that have been shown to affect quality of life. As people with MS are at risk for sleep and cognitive problems, researchers sought to examine cognitive outcomes among nurses with MS and sleep disorders.    

“With this longitudinal study design, we are able to better estimate the burden of sleep disorders among nurses, compared to health care claims data of similar size, which include diagnosed people with sleep disorders,” said senior author Galit Levi Dunietz, Ph.D., an epidemiologist and associate professor in the Department of Neurology’s Division of Sleep Medicine. “However, as sleep disorders are frequently under-diagnosed, health care claims data miss many people with sleep disorders who were not evaluated for these conditions.”

Braley says interventions to delay cognitive decline in MS may be most effective in pre-symptomatic or early symptomatic stages.

“Perceived cognitive decline, even in the absence of objective changes, could be an important window of opportunity to identify treatable exacerbating factors, such as sleep disorders,” she said.

Posted on Diabetes

A new study shows medication adherence tool is the world’s first to predict hospital admissions and readmissions of Type 2 Diabetes patients.

Medication adherence


The SPUR tool, developed by Kingston University and healthcare technology company Observia, can help patients with Type 2 Diabetes take their medications correctly. CREDIT Kingston University

A pioneering behavioural diagnostic tool developed by Kingston University, London and healthcare technology company Observia to help patients take their medication as prescribed is the first holistic model in the world to accurately predict hospital admissions and readmissions in people with Type 2 Diabetes, according to a new study.

The SPUR tool was developed to help better understand the reasons for medication non-adherence, defined as the extent to which patients don’t take their medication as prescribed. Non-adherence was identified as a global issue by the World Health Organisation in 2003 and costs almost $300 billion per year in the United States and €1.25 billion across parts of Europe, according to a report by the International Longevity Centre UK.

This highlights that in addition to the impact on the health of patients, who may not experience all the intended benefits from their treatment, non-adherence has significant economic implications for healthcare systems across the world. These costs come from higher hospital admission rates, readmissions and increased lengths of stay.

The SPUR model, created in 2017, has now been found to be the first holistic model in the world to accurately predict hospital admissions and early readmissions by a new observational study published in the Patient Preference and Adherence Journal.

Testing 200 patients living with Type 2 Diabetes recruited by Kingston Hospital, study lead Kingston University PhD candidate Josh Wells, chief investigator and Head of Kingston’s Pharmacy Department Professor Reem Kayyali and healthcare statistician Dr Chao Wang found SPUR could predict patients’ non-adherence risk and also provide contextual information on patients’ behaviour to explain the reasons for that risk.

Those tested were of varying ages, ethnicities and genders, took a differing number of medicines and had a range of incomes and medical conditions, including Covid-19 diagnoses. Patients registering higher SPUR scores (increased adherence) saw a significantly lower number of admissions to hospital. They were far less likely to experience early readmission, defined as admissions occurring within 30 days of a previous discharge.

While a limited number of medication adherence models have been linked to hospital admission, SPUR is the world’s first holistic behavioural model that can predict admission and early readmission in hospital patients, something Mr Wells was excited to be a part of.

“This will benefit the patient in not only terms of their care and experience with medicines but also a health economic benefit associated with harm reduction for NHS Trusts and other care services that may adopt the SPUR model within routine care,” he said.

Posted on Autism, Eye health

Autistic far less likely to have vision screening despite the high risk of severe eye disorders

Disparities exist within this population, with Black children having lowest screening rate
Disparities exist within this population, with Black children having lowest screening rate


Young children with autism are much less likely to receive vision screening than their peers, despite high risk for serious eye disorders, according to a study by Nemours Children’s Health published in Pediatrics.

“I noticed that many of our patients with autism have never had vision screening, even though it’s recommended for all young children,” said the study’s senior author Brittany Perry, DO, a pediatrician at the Nemours Swank Autism Center. “So, I wanted to study whether this might be a broader disparity – whether kids with autism receive vision screening less often than other kids.”

The study found that only 36.5% of children with autism had completed vision screenings at well visits, substantially less than the 59.5% rate for children without autism . Moreover, among children with autism, the screening rate for Black children (27.6%) was considerably lower than that for White children (39.7%) and for children classified as multiracial (39.8%).

Early childhood is crucial for vision development, and early detection and treatment of eye problems can prevent long-term vision loss. The research team examined data from 63,829 well visits of children ages 3 to 5 from 2016 to 2019, across a primary care network encompassing Delaware, Pennsylvania and Florida.

Researchers said that the Florida facilities had much higher rates of vision screening for kids with autism (45.7%) than those in the Delaware and Pennsylvania (28.1%). They noted that 80% of Florida medical practices used the vision-testing method of photoscreening, compared to only 13% in the Delaware and Pennsylvania.

Photoscreening, which uses a specialized camera or video system to capture detailed images of a child’s eyes, is particularly helpful for children with autism because they cannot always understand and verbally respond to instructions or questions in conventional visual acuity tests. The American Academy of Pediatrics (AAP) recommends annual instrument-based vision screening particularly for children with developmental delays. The researchers said that reimbursement is necessary for greater photoscreening use in primary care – a concern that AAP has also noted.

“Increased use of photoscreening may prove to be a great tool for reducing disparities and increasing vision screening in more vulnerable populations with autism,” Perry said.

“The key takeaway from this study for providers is to be aware that these disparities exist for all children with autism, so we can work to provide better care,” she added. “And for parents, it may help them to better advocate for their children with autism and to request a vision screening at a well visit, or a referral to an eye specialist, if their child is overdue.”

Posted on Autism

International Society for Autism Research (INSAR) 22nd Annual Meeting to be held in Stockholm, Sweden May 3- 6, 2023

Leading autism researchers, clinicians, and advocates from around the world will gather to share latest findings and discoveries
Leading autism researchers, clinicians, and advocates from around the world will gather to share latest findings and discoveries


The International Society for Autism Research (INSAR) will hold its 2023 Annual Meeting – the organization’s 22nd – from Wednesday, May 3 through Saturday, May 6, 2023, bringing together a global, multidisciplinary group of hundreds of autism researchers, clinicians, advocates, self-advocates, and students to exchange the latest scientific learnings and discoveries that are advancing the expanding understanding of autism and its complexities. This year’s meeting will be held in-person in Stockholm, Sweden at Stockholmsmässan, the largest exhibition facility in the Nordic region.

The INSAR Annual Meeting is the world’s largest gathering of scientists and specialists who continue to catalyze innovative research into all aspects of autism spectrum disorder, including its nature, causes, and treatments. The 22nd INSAR Annual Meeting will include in-person presentations of oral papers and posters, and panel sessions and demonstrations of new and emerging technologies. Select sessions will be recorded during the live event and repurposed as separate educational offerings starting in June 2023.

This year’s INSAR Lifetime Achievement Award will honor Dr. Jan Buitelaar, Radboud University. The INSAR Research Advocate Award will be presented to Harald Neerland, president of Autism-Europe. Other awards presented at this year’s meeting will include the 2023 INSAR Cultural Diversity Research Award, which will honor the SPARK Research Team, as well as the INSAR Early Career Investigator Awards, Dissertation Awards and Slifka/ Ritvo Innovation in Autism Research Award.

For the first time, recorded video interviews with selected scientists discussing their newsworthy research will be available to media beginning May 3. The researchers will also be available for one-on-one interviews prior to the INSAR 2023 Annual Meeting and during the conference. Please contact apockriss@rubenstein.com or skaplan@rubenstein.com to arrange.

To register to attend the INSAR Annual Meeting, visit the INSAR website. INSAR Membership is not required.

Media wishing to attend must register in advance here.

Research will be presented on topics including:

  • Understanding clinical heterogeneity
  • Precision health for neurodiverse communities
  • Inclusion in research on early identification and intervention
  • Models of care for underserved communities and low resource settings 
  • Understanding the diverse experiences of aging autistic adults
Posted on Diabetes

Losing a key type of pancreatic cell may contribute to diabetes.

A transplanted pseudoislet made from CD63hi beta cells.


A transplanted pseudoislet made from CD63hi beta cells. Weill Cornell Medicine

Multiple types of beta cells produce insulin in the pancreas, helping to balance blood sugar levels. Losing a particularly productive type of beta cell may contribute to the development of diabetes, according to a new study by Weill Cornell Medicine investigators.

In the study, published March 16 in Nature Cell Biology, Dr. James Lo, associate professor of medicine at Weill Cornell Medicine, and colleagues measured gene expression in individual beta cells collected from mice to determine how many different types of beta cells exist in the pancreas. The team discovered four distinct beta cell types, including one that stood out. The cluster 1 group of beta cells produced more insulin than other beta cells and appeared better able to metabolize sugar. The study also showed that this beta cell type loss might contribute to type 2 diabetes.


             

“Before this, people thought a beta cell was a beta cell, and they just counted total beta cells,” said Dr. Lo, who is also a member of the Weill Center for Metabolic Health and the Cardiovascular Research Institute at Weill Cornell Medicine and a cardiologist at NewYork-Presbyterian/Weill Cornell Medical Center. “But this study tells us it might be important to subtype the beta cells and that we need study the role of these special cluster 1 beta cells in diabetes.”

Drs. Doron Betel, Jingli Cao, Geoffrey Pitt and Shuibing Chen at Weill Cornell Medicine teamed up with Dr. Lo to carry out the study.

The investigators used a technique called single-cell transcriptomics to measure all the genes expressed in individual mouse beta cells and then used that information to group them into four types. The cluster 1 beta cells had a unique gene expression signature that included high expression of genes that help cellular powerhouses called mitochondria to break down sugar and power them to secrete more insulin. Additionally, they could distinguish the cluster 1 beta cells from the other beta cell types by its high expression of the CD63 gene, which enabled them to use the CD63 protein as a marker for this specific beta cell type.

“CD63 expression provided us a way to identify the cells without destroying them and allowed us to study the live cells,” he said.

When the team looked at both human and mouse beta cells, they found that cluster 1 beta cells with high CD63 gene expression produce more insulin in response to sugar than the three other types of beta cells with low CD63 expression.

“They are very high-functioning beta cells,” Dr. Lo said. “We think they may carry the bulk of the workload of producing insulin, so their loss might have profound impacts.”

In mice fed an obesity-inducing, high-fat diet and mice with type 2 diabetes, the numbers of these insulin-producing-powerhouse beta cells decreased.

“Because the numbers of cluster 1/high CD63 cells went down, you may have less insulin production, which may play a major role in diabetes development,” he said.

Transplanting beta cells with high CD63 production into mice with type 2 diabetes restored their blood sugar levels to normal. But removing the transplanted cells caused high blood sugar levels to return. Transplanting low CD63 production beta cells into the mice didn’t restore blood sugar to normal levels. The transplanted low CD63 beta cells instead appeared dysfunctional.

The discovery may have important implications for the use of beta cell transplants to treat diabetes, Dr. Lo said. For example, it may be better to transplant only high CD63- beta cells. He noted that it might also be possible to transplant fewer of these highly productive cells. Dr. Lo’s team also found that humans with type 2 diabetes had lower levels of high CD63 beta cells compared to those without diabetes.

Next, Dr. Lo and his colleagues would like to find out what happens to the high CD63-producing beta cells in mice with diabetes and how to keep them from disappearing.

“If we can figure out how to keep them around longer, surviving and functional, that could lead to better ways to treat or prevent type 2 diabetes,” he said.

They would also like to study how existing diabetes treatments affect all types of beta cells. GLP-1 agonists, which help increase the release of insulin in people with diabetes, interact with high and low CD63-producing beta cells.

“Our study also shows that GLP-1 agonists might also be a way to get the low CD63-producing beta cells to work better,” Dr. Lo said.