Does socioeconomic status explain why Black people with MS have more disability?

Does socioeconomic status explain why Black people with MS have more disability?
Does socioeconomic status explain why Black people with MS have more disability?


A new study suggests that even when differences in socioeconomic status are taken into consideration, Black people with multiple sclerosis (MS) may be more negatively impacted by the disease than white people with MS. The research is published in the June 30, 2021, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study found that Black people with MS had lower scores on certain measures of neurological health, like dexterity and walking tests and showed more evidence of disease progression on brain scans.

“While lower socioeconomic status appears to be linked to doing worse on tests of neurologic performance in white people with MS, we do not see that for Black people with MS, at least at the single time point we examined,” said study author Lana Zhovtis Ryerson, MD, of NYU Langone Health in New York City, and a member of the American Academy of Neurology.

The study looked at 1,214 people who identified as Black and 7,530 people who identified as white. Researchers also took a more detailed look at socioeconomic status based on neighborhood for 288 of the Black people in the study and 1,046 of the white people.

Researchers also looked at common neurological tests for people with MS. In a 50-question cognitive processing test, the Black people with MS, on average, scored five points lower than white people with MS. For physical tests like the 25-foot walking test, Black people with MS were an average of 0.66 seconds slower. In a manual dexterity test, Black people with MS were an average of 2.11 seconds slower.

When looking at brain lesions, which can indicate disease progression, researchers found that Black people had, on average, larger lesion volumes on their brain scans compared to white people.

Researchers then looked at the smaller group of people, using a more detailed measure of socioeconomic status. For white people with MS, lower household income was associated with slower cognitive processing and walking speeds, while a worse score on the socioeconomic test was associated with slower cognitive processing and manual dexterity speeds. For Black people in the study, lower income was only associated with less manual dexterity. Having worse socioeconomic scores was not associated with differences in cognitive processing, walking or manual dexterity speeds.

“Future studies should consider the role of unmeasured factors like systemic racism to see if they may play a role in greater disability among Black people with MS,” Zhovtis Ryerson said. “These results also reinforce the need for more diverse clinical trials and research focusing on treatment strategies specifically for Black people to identify whether certain therapies or more aggressive early treatment could help slow down disability over time.”

A limitation of the study is that it was based on one point in time and may not reflect associations over time.

Breaking MS News -study finds unleashing Treg cells may lead to treatments for multiple sclerosis

Genetic deletion of Piezo1 in T cells leads to protection in autoimmunity
Multiple Sclerosis
Multiple Sclerosis

Genetic deletion of Piezo1 in T cells leads to protection in autoimmunity: In the absence of Piezo1, Tregs expand more and, due to their increased numbers, are more effective in containing the damage inflicted by the effector T cells during an autoimmune neuroinflammation. Effector T cell function is not affected in the absence of Piezo1. CREDIT UCI School of Medicine

 In a new University of California, Irvine-led study, researchers found that a certain protein prevented regulatory T cells (Tregs) from effectively doing their job in controlling the damaging effects of inflammation in a model of multiple sclerosis (MS), a devastating autoimmune disease of the nervous system.

Published this month in Science Advances, the new study illuminates the important role of Piezo1, a specialized protein called an ion channel, in immunity and T cell function related to autoimmune neuroinflammatory disorders.

“We found that Piezo1 selectively restrains Treg cells, limiting their potential to mitigate autoimmune neuroinflammation,” said Michael D. Cahalan, PhD, distinguished professor and chair in the Department of Physiology & Biophysics at the UCI School of Medicine. “Genetically deleting Piezo1 in transgenic mice, resulted in an expanded pool of Treg cells, which were more capable of effectively reducing neuroinflammation and with it the severity of the disease.”

T cells rely on specialized proteins, like Piezo1, to detect and respond to various diseases and conditions including bacterial infections, wound healing, and even cancer. Uncontrolled T cell activity, however, can give rise to autoimmune disorders in which the immune system attacks normal cells in the body. Tregs constantly curate immune responses and play a critical role in preventing autoimmunity.

“Given the demonstrated ability of Piezo1 to restrain Treg cells, we believe that inhibiting Piezo1 could lead to new treatments for neuroinflammatory disorders, like MS,” explained Amit Jairaman, PhD, and Shivashankar Othy, PhD, lead authors of the study, both project scientists in the Department of Physiology & Biophysics.

Piezo1 conducts ions when cells are subjected to mechanical forces. Research over the last decade has shed light on the role of Piezo1 in regulating vital physiological functions including red blood cell (RBC) volume, blood pressure, vascular development, bone formation, and differentiation of neural stem cells. However, its role in modulating immune response has not been appreciated before. And, while it was known that calcium conducting ion channels, like Piezo1, direct various aspects of T cell function, researchers were surprised to find that Piezo1 was not essential for a whole host of T cell functions that rely on calcium, such as lymph node homing, interstitial motility, activation, proliferation, or differentiation into effector T cells.

“We found the role of Piezo1 appears to be quite specific to Tregs. Therefore, targeting Piezo1 might be a new and ideal strategy to cure MS while preserving the immune system’s ability to fight new infections,” added Othy, whose research over last 12 years has focused on finding ways to harness the therapeutic potential of Treg cells.

Further investigation of the function of Piezo1 is needed to understand therapeutic potential, and to more fully understand the processes through which cells sense and respond to mechanical stimuli during immune responses.

Distinctive gut microbiome unrelated to diet may characterize children with autism

Significantly fewer gut bugs linked to neurotransmitter activity

Gut health
Gut health
Children with autism seem to have a distinctive and underdeveloped range and volume of gut bacteria (microbiome) that isn’t related to their diet, suggests a small study published online in the journal Gut. They have significantly fewer bacteria linked to neurotransmitter activity and 5 species of bacteria that aren’t typically found in the guts of children without the condition, suggesting that there may be a characteristic microbial profile for autism, which may pave the way for treatment early on, say the researchers. Apart from genetic factors, it has been suggested that the gut microbiome may have a part to play in autism spectrum disorders. And the evidence suggests that the pathway between gut bacteria and the central nervous system, referred to as the gut-brain axis, has a profound effect on social behaviours. Diagnosing autism spectrum disorder can be difficult, because there is no definitive medical test and diagnosis is based on physician assessment. The researchers therefore wanted to see if 3-6 year olds with autism might harbour a microbiome that differs significantly from that of typically developing children, which might be used to facilitate early treatment. They compared the range, volume, and associated functions of bacteria in the stool samples of 128 Chinese children, 64 of whom had autism spectrum disorder and 64 of whom didn’t. The factors most strongly and independently associated with microbiome composition in the stool samples were age, autism, and weight (BMI). Diet wasn’t an influential factor. The stool samples of children with autism displayed a greater variety of microbes than those matched for age and weight who didn’t have the condition. Clostridium, Dialister and Coprobacillus were enriched in children with autism while Faecalibacterium was significantly decreased. Several Clostridium species enriched in children with autism closely interacted with each other and formed a connected group. Clostridia species have been linked with autism via the production of clostridial toxins which can damage the central nervous system, point out the researchers. And the gut microbiome composition in children with autism differed substantially from that of children without the condition, with five bacterial species largely accounting for the difference: Alistipes indistinctus; candidate division_TM7_ isolate_TM7c (single cell organism); Streptococcus cristatus; Eubacterium limosum; and Streptococcus oligofermentans. These differences were further confirmed in a separate group of 18 children, 8 with autism and 10 without. Importantly, bacteria associated with neurotransmitter activities were substantially reduced in children with autism. Some 26 age-related bacterial species were identified as proxies of typical development of the gut microbiome by age. But these associations were absent in children with autism, suggesting abnormal development of the gut microbiome during the early life of these children, say the researchers. This is a small study and the gut microbiome can vary according to geographical region. Nevertheless, the researchers write: “Our study shows for the first time that the gut microbiota of children with [autism] is abnormally developed and lags that of age-matched peers. “As development of microbial communities within the [gastrointestinal] tract during childhood represents a critical window of human growth and health, shifts in the gut microbiota during early life development may have important functional roles in the pathogenesis of [autism spectrum disorder] and thus warrants extensive investigation.” And they conclude: “Our study supports the potential role of non-invasive prediction of [autism spectrum disorder] based on faecal bacteria markers and age-related bacteria development profile. “Future therapeutics targeting reconstitution of gut microbiota in early life and increasing abundance of neurotransmitter-synthesised bacteria such as Faecalibacterium should be explored for [autism spectrum disorder].”

Rare inherited variants in previously unsuspected genes may confer significant risk for autism


New Study in Nature Genetics uses SPARK database to investigate variants that are less damaging than de novo mutations, but contribute almost as much risk

DNA and autism
DNA and autism

Researchers have identified a rare class of genetic differences transmitted from parents without autism to their affected children with autism and determined that they are most prominent in “multiplex” families with more than one family member on the spectrum. These findings are reported in Recent ultra-rare inherited variants implicate new autism candidate risk genes, a new study published in Nature Genetics.

The hunt is on in earnest for the genes involved in autism, now that technology and vastly lower costs allow the aggregation of thousands of genomes of people with autism and their family members. Knowing precisely which genes are at play will enable greater understanding of the condition known as autism and may ultimately lead to treatments for those who desire them.

This new study is notable because the majority of autism genes discovered to date have been identified through studies of de novo mutations, genetic differences that first arise in the person with autism but are not present in either of their parents. The findings indicate that researchers should not assume that the set of autism genes altered by de novo mutations are the same genes as these newly identified inherited rare variants.

According to lead author Amy B. Wilfert, Ph.D., of the University of Washington, in an analysis of 10,905 people with autism, researchers identified and replicated a rare class of genetic variants that are passed (over-transmitted) from parents without autism to children with autism.

“While most autism studies focus on de novo mutations, this study focuses on rare inherited mutations, which are often understudied in autism,” says Dr. Wilfert. “We find that these variants are individually less damaging than de novo mutations but have the potential to contribute almost as much risk and impact the same molecular pathways, through a distinct set of genes. These variants, however, are only able to persist in the general population for a few generations before being selected out by evolution.”

“It is widely understood that de novo mutations cannot and do not explain all of the genetic causes of autism, a phenomenon sometimes referred to as ‘missing heritability,’ ” says Pamela Feliciano, Ph.D., Scientific Director, SPARK (Simons Powering Autism Research). The SPARK Consortium contributed more than 50 percent of the genetic data analyzed in this study, including exomes from 21,331 SPARK participants — 6,539 of them individuals with autism spectrum disorder (ASD). The number of genomes accessible to scientists at this time enables the search for certain categories of genetic changes — such as de novo changes and ultra-rare inherited variants — but not all of them. As more genomes come online, larger categories of variants will be accessible for analysis.

“Interestingly, the vast majority of those variants (95%) are not found in genes already known to be autism genes, indicating that there is much more to be learned about autism genetics,” says Dr. Feliciano, noting that this study is the first step in a much larger investigation. “While the current study is not large enough to confidently identify individual genes that have these rare inherited variants, we are learning more about these genes. Future research that focuses on multiplex families is increasingly important to yield novel insights.”

The researchers also said the study confirmed their expectations that this class of rare inherited variants is more prominent in families with multiple members with autism than in families with only one affected individual. Consistent with this finding, children with ASD in these families are more likely to carry two of these variants as compared with their unaffected siblings.

The study also highlighted the need for greater diversity when conducting research of this kind, because investigators were less able to detect rare variants in people who belong to ancestral groups that are underrepresented in genomic research, including people of African, East Asian and South Asian descent.

5 Diet Tips for Diabetes

5 Diet Tips for Diabetes - YouTube


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