Align rolls out AI app for home-directed treatment

 The makers of the Invisalign system of plastic orthodontic braces are launching an artificial-intelligence-powered program to allow people at home to track their treatment progress and advance to the next stage when they’re ready.

Align Technology’s Virtual Care AI will be built into the company’s smartphone app. The program will walk users through taking pictures of their teeth and then automatically assess the alignment and spacing of each tooth and compare them to the personalized settings established beforehand by the user’s doctor.

The app will then deliver an automated message instructing the wearer to proceed to the next set of aligners if their treatment is tracking well or to stay on their current aligner if they need more time.

“Aligner fit and seating are important clinical indicators of Invisalign treatment progress tracking and compliance,” Mitra Derakhshan, the company’s senior global clinical vice president, said in a release. In addition, the app can connect users and their doctors if their treatment is going off track, Derakhshan noted.

Align Technology first launched its Virtual Care platform in March 2020, during the earliest stages of the COVID-19 pandemic, to help physicians remotely monitor treatment progress. 

Now, the company said its AI tools are being rolled out worldwide—starting in the Americas, the Asia-Pacific region, Europe, the Middle East and Africa—with the automated notifications being registered as a medical device in some countries. 

https://www.fiercebiotech.com/medtech/invisalign-maker-rolls-out-ai-app-home-directed-treatment

Dietary supplementation may improve antibiotic-induced GVHD following stem cell transplants

 Researchers at The University of Texas MD Anderson Cancer Center have identified a specific gut bacterium involved in the progression of graft-versus-host disease (GVHD) after antibiotic treatment of allogeneic hematopoietic stem cell transplantation (allo-HSCT) and discovered that nutritional supplementation can prevent antibiotic-induced GVHD in preclinical models, according to a study published today in Cell.

Researchers led by Eiko Hayase, M.D., Ph.D., postdoctoral fellow, and corresponding author Robert Jenq, M.D., associate professor of Genomic Medicine, discovered that certain antibiotics alter the sugar composition of the gut, forcing a normally beneficial species of bacteria to consume mucin in the intestinal lining, which can lead to complications such as GVHD.

"Knowing that this family of bacteria prefers certain types of sugars, we hypothesized that adding a sugar would, in a way, distract it from attacking the mucin in the gut and reduce these effects, which was the case,” Hayase said. “Through nutritional changes in these models, we learned we can change the microbiome function and help avoid adverse events.”

Allogeneic hematopoietic stem cell transplantation is a specialized treatment for blood cancers, such as leukemia and lymphomas, in which patients receive healthy hematopoietic stem cells from a donor to replace their own, which may be malignant or damaged by other treatments. Broad-spectrum antibiotics often given during allo-HSCT have been linked to an increase in developing GVHD — a condition in which donor immune cells attack the recipient tissues — but the underlying reasons for this have remained unclear.

One option to prevent complications after antibiotic treatment in allo-HSCT patients is fecal microbiota transplantation (FMT), a clinical procedure that transfers healthy bacteria from a screened donor to the GI tract of the recipient. However, this method has not yet been studied in randomized clinical trials, highlighting an unmet need for alternative therapeutic strategies that can help prevent complications.

In this study, treating allo-HSCT laboratory models with meropenem — a commonly used broad-spectrum antibiotic — resulted in a thinned colonic mucus layer and intestinal GVHD. Interestingly, their microbiome changed significantly through antibiotic removal of beneficial bacteria and expansion of a specific species, Bacteroides thetaiotaomicron (BT), in the intestinal lining.

Further investigation showed a significant decrease in the amount of the sugar xylose in the gut after meropenem treatment. Noting this, the researchers administered oral xylose as a nutritional supplement and found the gut mucus layer once again thickened, as the BT was able to preferentially consume the sugar instead of the mucin lining.

While previous work has investigated the gut microbiome and its relationship to inflammation and GVHD, this study was able to specifically identify the bacteria responsible for contributing to thinned mucus lining. Moreover, there had not previously been a clear understanding of how the sugar composition in the gut is altered by antibiotics, or how it affects GVHD following allo-HSCT.

“We are not aware of anyone previously trying a sugar supplementation strategy for suppressing gut inflammation from GVHD, so this offers a compelling, low-risk approach in helping allo-HSCT patients who need to be on broad-spectrum antibiotics in order to treat infections,” Jenq said. “This is a novel approach, and we are excited to work on translating this into human trials. If nutritional supplementation with specific sugars works the same way in humans, it could simplify the way we approach therapeutic strategies for similar complications.”

The authors stress that broad-spectrum antibiotics remain beneficial for allo-HSCT patients, and further investigation is needed to understand how this approach can be evaluated in clinical trials. Currently, researchers are collecting human Bacteroides specimens in patients undergoing bone marrow transplants to investigate whether they also preferentially break down mucin.

This research was supported by the National Institutes of Health (2R01HL123112-06, R01 DK118024, 5P30CA016672-42), the Cancer Prevention and Research Institute of Texas (RR160089), and the American Society for Transplantation and Cellular Therapy New Investigator Award (FP00012028). A full list of collaborating authors and their disclosures can be found with the full paper here.

https://www.eurekalert.org/news-releases/966332

Hormone oxytocin may have heart healing properties

 The neurohormone oxytocin is well-known for promoting social bonds and generating pleasurable feelings, for example from art, exercise, or sex. But the hormone has many other functions, such as the regulation of lactation and uterine contractions in females, and the regulation of ejaculation, sperm transport, and testosterone production in males.

Now, researchers from Michigan State University show that in zebrafish and human cell cultures, oxytocin has yet another, unsuspected, function: it stimulates stem cells derived from the heart’s outer layer (epicardium) to migrate into its middle layer (myocardium) and there develop into cardiomyocytes, muscle cells that generate heart contractions. This discovery could one day be used to promote the regeneration of the human heart after a heart attack. The results are published in Frontiers in Cell and Developmental Biology.

“Here we show that oxytocin, a neuropeptide also known as the love hormone, is capable of activating heart repair mechanisms in injured hearts in zebrafish and human cell cultures, opening the door to potential new therapies for heart regeneration in humans,” said Dr Aitor Aguirre, an assistant professor at the Department of Biomedical Engineering of Michigan State University, and the study’s senior author.

Stem-like cells can replenish cardiomyocytes

Cardiomyocetes typically die off in great numbers after a heart attack. Because they are highly specialized cells, they can’t replenish themselves. But previous studies have shown that a subset of cells in the epicardium can undergo reprogramming to become stem-like cells, called Epicardium-derived Progenitor Cells (EpiPCs), which can regenerate not only cardiomyocytes, but also other types of heart cells.

“Think of the EpiPCs as the stonemasons that repaired cathedrals in Europe in the Middle Ages,” explained Aguirre.

Unfortunately for us, the production of EpiPCs is inefficient for heart regeneration in humans under natural conditions.

Zebrafish could teach us how to regenerate hearts more efficiently

Enter the zebrafish: famous for their extraordinary capacity for regenerating organs, including the brain, retina, internal organs, bone, and skin. They don’t suffer heart attacks, but its many predators are happy to take a bite out of any organ, including the heart – so zebrafish can regrow their heart when as much as a quarter of it has been lost. This is done partly by proliferation of cardiomyocytes, but also by EpiPCs. But how do the EpiPCs of zebrafish repair the heart so efficiently? And can we find a ‘magic bullet’ in zebrafish that could artificially boost the production of EpiPCs in humans?

Yes, and this ‘magic bullet’ appears to be oxytocin, argue the authors.

To reach this conclusion, the authors found that in zebrafish, within three days after cryoinjury – injury due to freezing – to the heart, the expression of the messenger RNA for oxytocin increases up to 20-fold in the brain. They further showed that this oxytocin then travels to the zebrafish epicardium and binds to the oxytocin receptor, triggering a molecular cascade that stimulates local cells to expand and develop into EpiPCs. These new EpiPCs then migrate to the zebrafish myocardium to develop into cardiomyocytes, blood vessels, and other important heart cells, to replace those which had been lost.

Similar effect on human tissue cultures

Crucially, the authors showed that oxytocin has a similar effect on human tissue in vitro. Oxytocin – but none of 14 other neurohormones tested here – stimulates cultures of human Induced Pluripotent Stem Cells (hIPSCs) to become EpiPCs, at up to twice the basal rate: a much stronger effect than other molecules previously shown to stimulate EpiPC production in mice. Conversely, genetic knock-down of the oxytocin receptor prevented the the regenerative activation of human EpiPCs in culture. The authors also showed that the link between oxytocin and the stimulation of EpiPCs is the important ‘TGF-β signaling pathway’, known to regulate the growth, differentiation, and migration of cells.

Aguirre said: “These results show that it is likely that the stimulation by oxytocin of EpiPC production is evolutionary conserved in humans to a significant extent. Oxytocin is widely used in the clinic for other reasons, so repurposing for patients after heart damage is not a long stretch of the imagination. Even if heart regeneration is only partial, the benefits for patients could be enormous.”

Aguirre concluded: “Next, we need to look at oxytocin in humans after cardiac injury. Oxytocin itself is short-lived in the circulation, so its effects in humans might be hindered by that. Drugs specifically designed with a longer half-life or more potency might be useful in this setting. Overall, pre-clinical trials in animals and clinical trials in humans are necessary to move forward.”

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JOURNAL

Frontiers in Cell and Developmental Biology

DOI

10.3389/fcell.2022.985298 

METHOD OF RESEARCH

Experimental study

SUBJECT OF RESEARCH

Human tissue samples

ARTICLE TITLE

Oxytocin promotes epicardial cell activation and heart regeneration after cardiac injury

ARTICLE PUBLICATION DATE

30-Sep-2022

COI STATEMENT

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest

https://www.eurekalert.org/news-releases/966281

SuperAger brains contain ‘super neurons’

 ·  SuperAger neurons are even larger than those in individuals 20 to 30 years younger

·  These neurons do not have tau tangles that are a hallmark of Alzheimer’s
·  Larger neurons in the brain’s memory region are a biological signature of SuperAging trajectory

 Neurons in an area of the brain responsible for memory (known as the entorhinal cortex) were significantly larger in SuperAgers compared to cognitively average peers, individuals with early-stage Alzheimer’s disease and even individuals 20 to 30 years younger than SuperAgers — who are aged 80 years and older, reports a new Northwestern Medicine study.

These neurons did not harbor tau tangles, a signature hallmark of Alzheimer’s disease.

“The remarkable observation that SuperAgers showed larger neurons than their younger peers may imply that large cells were present from birth and are maintained structurally throughout their lives,” said lead author Tamar Gefen, an assistant professor of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine. “We conclude that larger neurons are a biological signature of the SuperAging trajectory.”  

The study of SuperAgers with exceptional memory was the first to show that these individuals carry a unique biological signature that comprises larger and healthier neurons in the entorhinal cortex that are relatively void of tau tangles (pathology).

The study will be published Sept. 30 in The Journal of Neuroscience.

The Northwestern SuperAging Research Program studies unique individuals known as SuperAgers, 80+ year-olds who show exceptional memory at least as good as individuals 20 to 30 years their junior. 

“To understand how and why people may be resistant to developing Alzheimer’s disease, it is important to closely investigate the postmortem brains of SuperAgers,” Gefen said. “What makes SuperAgers’ brains unique? How can we harness their biologic traits to help elderly stave off Alzheimer’s disease?”  

Scientists studied the entorhinal cortex of the brain because it controls memory and is one of the first locations targeted by Alzheimer’s disease. The entorhinal cortex comprises six layers of neurons packed on top of one another.Layer II, in particular, receives information from other memory centers and is a very specific and crucial hub along the brain’s memory circuit.  

In the study, scientists show that SuperAgers harbor large, healthier neurons in layer II of the entorhinal cortex compared to their same-aged peers, individuals with early stages of Alzheimer’s disease and even individuals 20 to 30 years younger. They also showed that these large layer II neurons were spared from the formation of tau tangles.  

Taken together, the findings suggest that a neuron spared from tangle formation can maintain its structural integrity (i.e., remain healthy and large). The inverse also seems to be true: Tau tangles can lead to neuronal shrinkage. 

Participants in the SuperAger study donate their brains for research. 

For the study, scientists examined the brains of six SuperAgers, seven cognitively average elderly individuals, six young individuals and five individuals with early stages of Alzheimer’s. Then they measured the size of neurons in layer II of the entorhinal cortex (compared to layers III and V). They also measured the presence of tau tangles in these cases. 

For reasons that remain unknown, cell populations in the entorhinal cortex are selectively vulnerable to tau tangle formation during normal aging and in early stages of Alzheimer’s. 

“In this study, we show that in Alzheimer’s, neuronal shrinkage (atrophy) in the entorhinal cortex appears to be a characteristic marker of the disease,” Gefen said. 

“We suspect this process is a function of tau tangle formation in the affected cells leading to poor memory abilities in older age,” Gefen said. “Identifying this contributing factor (and every contributing factor) is crucial to the early identification of Alzheimer’s, monitoring its course and guiding treatment.” 

Future studies are needed to understand how and why neuronal integrity is preserved in SuperAgers. Gefen wants to focus on probing the cellular environment. 

“What are the chemical, metabolic or genetic features of these cells that render them resilient?” she asked. She also plans to investigate other hubs along the memory circuit of the brain to better understand the spread of or resistance to disease. 

“We expect this research to be amplified and more impactful through a $20 million expansion of the SuperAging Initiative now enrolling five sites in the U.S. and Canada,” said Emily Rogalski, associate director of the Mesulam Center for Cognitive Neurology and Alzheimer’s Disease at Northwestern University Feinberg School of Medicine.

This study was supported by the National Institute on Aging of the National Institutes of Health (grant numbers P30AG013854, R01AG062566, R01AG067781, R01AG045571, R56AG045571 and U19AG073153). 

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JOURNAL

JNeurosci

METHOD OF RESEARCH

Observational study

ARTICLE TITLE

Neuronal Integrity in SuperAging

ARTICLE PUBLICATION DATE

30-Sep-2022

https://www.eurekalert.org/news-releases/966316

Emergency department-based ICU seen improving survival without raising costs

 Across the country, many intensive care units are strained for capacity. This prolongs the boarding process in the emergency department, when critically ill patients -- for whom every minute and hour is crucial -- wait for open ICU beds.

To provide more rapid access to critical care, University of Michigan Health opened its Emergency Critical Care Center in 2015, one of the first ICUs in the country to be housed within an emergency department.

A previous study found that the deployment of this model improved quality of care and patient outcomes by decreasing both mortality rates and ICU admission rates for emergency department patients. And according to a new study published in JAMA Network Open, the ED-based ICU model does so without raising costs.

In a follow-up study, researchers at Michigan Medicine analyzed over 230,000 adult emergency department visits between September 2012 and late April 2017, comparing costs from before and after the Emergency Critical Care Center opened in mid-2015. Results reveal that direct total cost per visit, when adjusting for inflation, held flat after implementation of the ED-ICU model.

"For all patients visiting the emergency department, from those with ankle sprains to those with critical illness, we are seeing similar costs per visit with better clinical outcomes -- which equates to higher value by utilizing the ED-ICU model," said Benjamin Bassin, M.D., first author of the paper and director of the Emergency Critical Care Center, or EC3, at U-M Health.

When examining solely critically ill ED patients, researchers found total direct cost per encounter decreased by 22.1% with implementation of the ED-ICU. The reduced costs, researchers say, are likely due to early, coordinated critical care delivered in the ED-ICU, rather than when an ICU bed became available.

"Previous studies have shown the boarding process of waiting in the ED for an inpatient ICU bed to become available is associated with lower survival rates for critically ill patients across disease states," said Nathan Haas, M.D., co-author of the paper and assistant medical director of U-M Health's EC3.

"Providing high-quality critical care to patients earlier via an ED-ICU can likely slow progression of disease severity and prevent complications that would occur during the ED boarding process, resulting in both improved downstream outcomes and overall cost reductions."

Since the implementation of EC3 in 2015, leaders at U-M Health collaborated with over 15 health systems in the U.S. and seven internationally that have sought to establish similar ED-ICU models. Researchers believe the findings of cost neutrality will lead to many more hospitals embracing the concept.

"We have been contacted by many hospitals both nationally and internationally considering this model based on the improved patient outcomes reported in our previous study," said Robert Neumar, M.D., Ph.D., senior author of the paper and chair of the Department of Emergency Medicine at U-M Health. "Combining the evidence of improved quality with no increase in overall cost defines the positive health care value of the ED-ICU model. As a result, we anticipate health systems across the country will have increased interest in adopting the model."

The Emergency Critical Care Center at U-M Health was made possible by a gift from the Joyce and Don Massey Family Foundation

Additional authors include Nana Sefa, M.D., M.P.H., Richard Medlin, M.D., Timothy A. Peterson, M.D., M.B.A., Kyle Gunnerson, M.D., Steve Maxwell, M.B.A., James A. Cranford, Ph.D., Stephanie Laurinec, B.S., Christine Olis, M.B.A., Renee Havey, D.N.P., Robert Loof, M.H.A., all of Michigan Medicine

Bassin reported receiving salary support from the Joyce and Don Massey Family Foundation during the conduct of the study. No other disclosures were reported.

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Story Source:

Materials provided by Michigan Medicine - University of Michigan. Original written by Noah Fromson. Note: Content may be edited for style and length.

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Journal Reference:

1. Benjamin S. Bassin, Nathan L. Haas, Nana Sefa, Richard Medlin, Timothy A. Peterson, Kyle Gunnerson, Steve Maxwell, James A. Cranford, Stephanie Laurinec, Christine Olis, Renee Havey, Robert Loof, Patrick Dunn, Debra Burrum, Jennifer Gegenheimer-Holmes, Robert W. Neumar. Cost-effectiveness of an Emergency Department–Based Intensive Care Unit. JAMA Network Open, 2022; 5 (9): e2233649 DOI: 10.1001/jamanetworkopen.2022.33649

https://www.sciencedaily.com/releases/2022/09/220928112958.htm

Immune function remodeled by mitochondrial shape

 A new study focused on the immune system's Th17 cells suggests that the shape and function of their mitochondria (the powerhouse of cells) is important in autoimmune and inflammatory disorders, such as multiple sclerosis. T helper 17 (Th17) cells are a type of CD4+ T immune cell, which collectively help make antibodies, activate enemy-eating cells and recruit more soldiers to the battlefront.

The research, led by Erika Pearce, Ph.D., at the Bloomberg~Kimmel Institute for Cancer Immunotherapy at the Johns Hopkins Kimmel Cancer Center, suggests that learning how mitochondria impact Th17 cells is key to understanding how to control them.

The study, published Sept. 28 in the journal Nature, identifies several avenues for trying to influence the behavior of these important cells, with the goal of dampening their autoimmune activity.

When a T cell is first exposed to an enemy, it responds to signals from the enemy and the environment to become one of several types of specialized T cells, each armed with distinct functions in the immune response. While all T helper cell subtypes are crucial to the body's fight against foreigners, their imbalance can also cause disease, including type 1 diabetes, asthma, allergies and chronic inflammation.

"If we could control T cells, we could arguably control many, if not most, infections, autoimmunities and cancers," says Pearce, the study's senior author and a Johns Hopkins Bloomberg Distinguished Professor in the Department of Oncology and the Department of Biochemistry and Molecular Biology.

The study began when researchers in Pearce's laboratory, which was then at the Max Planck Institute in Freiburg, Germany, noticed a trait peculiar to Th17 cells. Among three main T effector cell types, only Th17 cells had elongated mitochondria; that is, their inner powerplants were fused together into larger structures. "That was strange because elongated mitochondria are usually seen in resting cells and not in activated cells," says first author Francesc Baixauli, Ph.D., a former postdoctoral fellow at the Max Planck Institute.

The researchers knew that the OPA1 gene regulates mitochondrial fusion, so they deleted it in Th17 cells and found that their mitochondria reverted to a more fragmented size and shape. However, the cells also stopped doing their main job -- producing the signaling molecule interleukin-17 (IL-17).

To confirm this result in an organism, the researchers deleted the OPA1 gene in mice and promoted a disease in these animals that models human multiple sclerosis, which is driven by their Th17 cells. With OPA1 deleted, not only did their cells stop making IL-17, but their disease symptoms abated.

Wondering how OPA1 deletion stopped the production of IL-17, the team first thought that the cells' mitochondria simply weren't producing enough energy. However, they found that OPA1 deletion did not affect energy production, and that OPA1 was crucial to the production of IL-17 regardless of whether the cells' metabolic activity was high or low. Then, they found that a central biochemical process occurring in the mitochondria had been altered, causing the buildup of a metabolite known to influence DNA and the transcriptional program of the cell. "That molecule was dampening the ability of the cell to read its DNA, and consequently IL-17 was no longer produced," says Baixauli.

To identify the connection between these responses and OPA1 deletion, the researchers compared proteins produced by normal Th17 cells and those without OPA1. In cells missing OPA1, they found a large increase in the activated form of the protein LKB1, which is a metabolic sensor that regulates cellular metabolism, cell division and mitochondrial function. When they deleted both OPA1 and LKB1 from cells, IL-17 production was restored, and the mitochondrial processes returned to normal.

"We think that LKB1 senses mitochondrial stress and alters the mitochondria's biochemical reactions appropriately, which affects the production of IL-17," says Pearce. "We now have a short list of molecules known to influence this key aspect of Th17 function, which can be the tipping point between its helpful and harmful roles. Our future research will continue to explore these relationships so that we can hopefully one day therapeutically modify them."

Other researchers were Klara Piletic, Daniel J. Puleston, Matteo Villa, Cameron S. Field, Lea J. Flachsmann, Andrea Quintana, Nisha Rana, Joy Edwards-Hicks, Mai Matsushita, Michal A. Stanczak, Katarzyna M. Grzes, Agnieszka M. Kabat, Mario Fabri, George Caputa, Beth Kelly, Mauro Corrado, Yaarub Musa, Katarzyna J. Duda, Gerhard Mittler, David O'Sullivan, Thomas Jenuwein and Joerg M. Buescher at the Max Planck Institute, and Hiromi Sesaki, Edward J. Pearce and David E. Sanin at The Johns Hopkins University.

The research was supported by the Max Planck Society, the Leibniz Prize, the National Institutes of Health (R01AI156274 and R35GM144103), The Johns Hopkins University and a Bloomberg Distinguished Professorship, a Marie Sklodowska-Curie Actions individual fellowship, a Sir Henry Wellcome fellowship and an Alexander von Humboldt postdoctoral fellowship.

Erika Pearce is a member of the ImmunoMet Therapeutics Scientific Advisory Board, and Erika Pearce and Edward Pearce are founders and scientific advisers to Rheos Medicines.

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Story Source:

Materials provided by Johns Hopkins Medicine. Note: Content may be edited for style and length.

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Journal Reference:

1. Francesc Baixauli, Klara Piletic, Daniel J. Puleston, Matteo Villa, Cameron S. Field, Lea J. Flachsmann, Andrea Quintana, Nisha Rana, Joy Edwards-Hicks, Mai Matsushita, Michal A. Stanczak, Katarzyna M. Grzes, Agnieszka M. Kabat, Mario Fabri, George Caputa, Beth Kelly, Mauro Corrado, Yaarub Musa, Katarzyna J. Duda, Gerhard Mittler, David O’Sullivan, Hiromi Sesaki, Thomas Jenuwein, Joerg M. Buescher, Edward J. Pearce, David E. Sanin, Erika L. Pearce. An LKB1–mitochondria axis controls TH17 effector function. Nature, 2022; DOI: 10.1038/s41586-022-05264-1

https://www.sciencedaily.com/releases/2022/09/220928112955.htm

Lipids in blood predict nerve damage risk among patients with type 2 diabetes

 Of the 37 million Americans with diabetes, up to 50% may end up with nerve damage, or diabetic neuropathy, that can be painful and disabling.

While some medications can reduce pain, scientists continue searching for factors that cause patients to develop diabetic neuropathy -- to identify ways to reduce the risk of harmful symptoms.

One study at Michigan Medicine finds multiple lipid biomarkers are linked to the development of neuropathy in patients with type 2 diabetes.

Researchers examined serum samples from nearly 70 members of the Gila River Indian community with type 2 diabetes who were tested for neuropathy 10 years later. They analyzed 435 different species of lipids, which are organic compounds composed of fats and oils.

Results published in the Annals of Clinical and Translational Neurology reveal that participants with high scores for diabetic neuropathy had changes in lipids reflecting impaired energy metabolism.

"We have the potential to test for these lipid biomarkers in patients with type 2 diabetes to identify those with the highest risk of developing peripheral neuropathy and facilitate more focused management of those patients," said senior author Eva L. Feldman, M.D., Ph.D., James W. Albers Distinguished Professor at U-M and the Russell N. DeJong Professor of Neurology and director of the NeuroNetwork for Emerging Therapies at Michigan Medicine.

While there were differences between basic lipid profiles of participants with and without neuropathy, researchers found a pattern in blood lipid profiles 10 years prior to a person developing neuropathy that showed signaling dysfunction in a critical pathway called b-oxidation. This pathway converts lipids into sources of nerve energy, and, when impaired, energy-starved nerves undergo damage, leading to neuropathy.

"As we learn more about the relationship between serum lipid species and neuropathy, it will open up the possibility of targeted therapeutic treatment, both with drugs and lifestyle interventions," Feldman said. "Our findings support the concept that unsaturated healthy fats are a better source of energy for nerves that highly saturated fats. We strongly recommend a Mediterranean-type diet to maintain a healthy nervous system."

Feldman also advocates exercise, which increases the efficiency of the b-oxidation pathway. "Engaging in a healthy diet and exercise program is the key to preventing neuropathy," she said.

Additional authors include Farsad Afshinnia M.D., Evan L. Reynolds Ph.D., Thekkelnaycke Rajendiran, Ph.D., Tanu Soni B.S., Jaeman Byun Ph.D., Masha G. Savelieff Ph.D., Brian C. Callaghan M.D., Subramaniam Pennathur M.D., all of University of Michigan, Helen C. Looker Ph.D., Robert G. Nelson M.D., both of the National Institute of Diabetes and Digestive and Kidney Diseases, George Michailidis Ph.D., University of Florida.

This study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases from grants R 24 DK082841 and K99 DK129785.

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Story Source:

Materials provided by Michigan Medicine - University of Michigan. Original written by Noah Fromson. Note: Content may be edited for style and length.

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Journal Reference:

1. Farsad Afshinnia, Evan L. Reynolds, Thekkelnaycke M. Rajendiran, Tanu Soni, Jaeman Byun, Masha G. Savelieff, Helen C. Looker, Robert G. Nelson, George Michailidis, Brian C. Callaghan, Subramaniam Pennathur, Eva L. Feldman. Serum lipidomic determinants of human diabetic neuropathy in type 2 diabetes. Annals of Clinical and Translational Neurology, 2022; 9 (9): 1392 DOI: 10.1002/acn3.51639

https://www.sciencedaily.com/releases/2022/09/220929132540.htm