Publisher Health

A new model to analyse infectious disease outbreak data has been developed by mathematicians that could be used to improve disease tracking and control.
Researchers from the University of Nottingham developed a new data-driven framework for modelling how infectious diseases spread through a population that could reduce errors in decisions made about disease control measures. Their findings have been published in PNAS.
The COVID-19 pandemic has highlighted that the ability to unravel the dynamics of the spread of infectious diseases is profoundly important for designing effective control strategies and assessing existing ones. Mathematical models of how infectious diseases spread continue to play a vital role in understanding, mitigating, and preventing outbreaks.
Dr Rowland Seymour led the study and explains: “Most of the infectious disease models contain specific assumptions about how transmission occurs within a population. These assumptions can be arbitrary, particularly when it comes to describing how transmission varies between individuals of different types or in different locations and can be lacking in appropriate biological or epidemiological justification. this can lead to erroneous scientific conclusions and misleading predictions.”
The researchers developed a data-driven framework for modelling how infectious diseases spread through a population by avoiding strict modelling assumptions which are often difficult to justify. The researchers used the method to enhance understanding of the 2001 UK Foot and Mouth outbreak in which over 6 million animals were culled with a cost to the public and private purse of over £8 billion.
The proposed methodology is very general making it applicable to a wide class of models, including those which take into account the population’s structure (e.g. households, workplaces) and individual’s characteristics (e.g. location and age).
Dr Rowland Seymour continues: “Infectious diseases both within human and animal populations continue to pose serious health and socioeconomic risks. We have developed a suite of contemporary statistical methods that dispenses with the need for the underlying transmission assumptions of existing models. Our approach enables instead the analysis to be driven by evidence in the data and hence allowing policy makers to make data-driven decisions about controlling the spread of a disease. Our work is another tool in the fight against the spread of infectious diseases and we are excited to develop this framework further.”
This work has opened several avenues for further research in this area, including improving its computationally efficiency and being applicable in real-time, i.e. when the outbreak is still ongoing. The latter is of material importance for policy makers and government authorities, so they can be responsive to the data that is emerging from the outbreak.
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Materials provided by University of Nottingham. Note: Content may be edited for style and length.

Ordinary potted house plants can potentially make a significant contribution to reducing air pollution in homes and offices, according to new research led by the University of Birmingham and in partnership with the Royal Horticultural Society (RHS).
During a series of experiments monitoring common houseplants exposed to nitrogen dioxide (NO2) — a common pollutant — researchers calculated that in some conditions, the plants could be able to reduce NO2 by as much as 20 per cent.
The researchers tested three houseplants commonly found in UK homes, easy to maintain and not overly expensive to buy. They included Peace lily (Spathiphyllum wallisii), Corn plant (Dracaena fragrans) and fern arum (Zamioculcas zamiifolia).
Each plant was put, by itself, into a test chamber containing levels of NO2 comparable to an office situated next to a busy road.
Over a period of one hour, the team calculated that all the plants, regardless of species, were able to remove around half the NO2 in the chamber. The performance of the plants was not dependent on the plants’ environment, for example whether it was in light or dark conditions, and whether the soil was wet or dry.
Lead researcher Dr Christian Pfrang said: “The plants we chose were all very different from each other, yet they all showed strikingly similar abilities to remove NO2 from the atmosphere. This is very different from the way indoor plants take up CO2 in our earlier work, which is strongly dependent on environmental factors such as night time or daytime, or soil water content.”
The team also calculated what these results might mean for a small office (15 m3) and a medium-sized office (100 m3) with different levels of ventilation. In a poorly ventilated small office with high levels of air pollution, they calculated that five houseplants would reduce NO2levels by around 20 per cent. In the larger space, the effect would be smaller — 3.5 per cent, though this effect would be increased by adding more plants.
While the effects of the plants in reducing NO2 are clear, the precise mechanism by which they do this remain a mystery. Dr Pfrang added: “We don’t think the plants are using the same process as they do for CO2 uptake, in which the gas is absorbed through stomata — tiny holes — in the leaves. There was no indication, even during longer experiments, that our plants released the NO2 back into the atmosphere, so there is likely a biological process taking place also involving the soil the plant grows in — but we don’t yet know what that is.”
Dr Tijana Blanusa, principal horticultural scientist at the RHS and one of the researchers involved in the study said: “This complements RHS efforts to understand scientific detail behind what we know to be a popular passion. Understanding the limits of what we can expect from plants helps us plan and advise on planting combinations that not only look good but also provide an important environmental service.”
In the next phase of the research, the team will be designing sophisticated tools for modelling air quality indoors encompassing a much wider range of variables. The new project, funded by the Met Office, will use mobile air quality measuring instruments to identify pollutants and test their effects in both residential and office spaces, producing a wealth of data to inform the tool’s development.
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Materials provided by University of Birmingham. Note: Content may be edited for style and length.

In order to better treat patients diagnosed with acute myeloid leukemia (AML), researchers need to understand the pathological processes and distinguish between different subgroups of the disease. With the help of proteome and genetic analysis, researchers at the Max Planck Institute of Biochemistry in Martinsried, together with cooperation partners from the Frankfurt University Hospital, German Cancer Research Center (DKFZ) as well as German Cancer Consortium (DKTK) have discovered a new subtype. This subtype shows increased amounts of mitochondrial proteins as well as an altered mitochondrial metabolism. In laboratory tests, these so-called Mito-AML cells can be combated more effectively with inhibitors against mitochondrial respiration than with conventional chemotherapeutic agents.
Acute myeloid leukemia (AML) is an aggressive cancer originating from blood cells. When immature blood cells in the bone marrow acquire certain aberrations in their genome they can become malignant and overgrow the bone marrow, the place where normally blood cells are produced. As a consequence, normal blood cells are suppressed by leukemia cells which leads to infections, bleeding and ultimatively death of patients. Most patients diagnosed with AML undergo chemotherapy.
In a multidisciplinary project, a team of researchers led by Matthias Mann from the Max Planck Institute of Biochemistry as well as Thomas Oellerich and Hubert Serve from the University Hospital Frankfurt, DKTK & DKFZ studied the proteome — i.e. the totality of all proteins — of AML cells. By combining the proteome and genome data, the researchers have identified several AML subgroups with specific biological features. One of the subgroups — the so-called Mito-AML — was only recognisable at the proteome level and had therefore not been discovered before. The new subgroup is characterised by a high number of mitochondrial proteins and an altered mitochondrial metabolism and shows clinical resistance to chemotherapy.
Possible approach for new therapies
Since mitochondria are the power plants of cells, the research team further investigated whether the disease-specific metabolic changes in Mito-AML can be therapeutically exploited. In a series of experiments, they found that drugs that interfere with mitochondrial respiration are highly effective in Mito-AML cell cultures and thus might be a more effective therapy compared to traditional chemotherapeutics. These agents include, for example, the drug venetoclax.
In the last decades genomic studies already identified molecular subtypes within the disease thereby opening up a perspective for personalized therapeutic approaches. This has certainly revolutionised the molecular understanding of the disease and laid the groundwork for personalised therapies. Despite these developments, the prognosis for AML remains poor. This highlights the urgent need to better understand the pathologically altered processes during AML and to search for more efficient therapies.
To study the protein expression profiles in AML cells, the team used mass spectrometry. This technology allows proteins to be identified and quantified by determining their specific weight. The protein expression profiles provide researchers with an overview of which proteins are present in the pathologically altered cells and in what quantities. In parallel, the team examined the human genome of AML cells using DNA and RNA sequencing technologies.
“The discovery of the Mito-AML subset demonstrates the great potential of proteomics technology for identifying clinically relevant biomarkers and drug targets. Our study clearly shows that genomic and proteomic data complement each other, allowing us to elucidate previously undescribed aspects of disease biology and to name innovative treatment approaches,” says Matthias Mann. “Our approach led to the discovery of new molecular AML subgroups with clinical relevance. It thus provides a proteomic systematics as a basis for a better molecular understanding and clinical classification of AML,” says Thomas Oellerich.
This new insight was made possible through close collaboration between clinicians at Frankfurt University and the Study Alliance Leukemia (SAL), a nationwide network to improve the treatment of AML, and basic scientists. “It helps us understand why some patients respond better to different forms of therapy than others,” says Hubert Serve. Next, medical researchers want to test the laboratory results in clinical trials on patients.
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Materials provided by Max-Planck-Gesellschaft. Note: Content may be edited for style and length.

A research team led by scientists at Albert Einstein College of Medicine has devised a novel and highly promising strategy for overcoming a key cause of cancer deaths: the ability of cancer cells to thrive in the face of chemotherapy drugs designed to destroy them.
As described in the March 7 issue of Nature Communications, investigators used a two-drug combination to achieve chemotherapy’s goal: to make cancer cells self-destruct via the biological process known as apoptosis, often referred to as programmed cell death. The treatment worked againsthumancancer cell lines that resisted apoptosis despite exposure to different types of chemotherapy, and also against apoptosis-resistant human tumors implanted in mice (i.e., xenograft mouse models).
“Targeted therapies that home in on specific genetic vulnerabilities of cancers have vastly improved treatment in recent years, but not everyone has benefited,” said Evripidis Gavathiotis, Ph.D., professor of biochemistry and of medicine at Einstein, co-leader of the Cancer Therapeutics Program at the NCI-designated Albert Einstein Cancer Center, and corresponding author on the paper. “We need new, broadly active therapies that can attack a range of cancers while causing fewer side effects than current treatments, and we hope our new therapeutic strategy will prove to be a viable option.”
Eliminating Unwanted Cells
The body relies on apoptosis for getting rid of unwanted cells — excess cells pruned during embryological development, for example, and damaged cells that need to be removed so they don’t survive to develop into cancer cells. Both chemotherapy and radiation rely on damaging cancer cells severely enough that they’ll undergo apoptosis — which, unfortunately, does not always happen.
Every cell in the body contains the seeds of its own destruction: some two dozen apoptotic proteins that engage in a life-or-death balancing act. Some proteins stimulate apoptosis (pro-apoptotic proteins), while others block the process (anti-apoptotic proteins). DNA damage, for example, tips the balance in favor of cell death — causing the cell to express and activate pro-apoptotic proteins that ultimately kill the cell by poking holes in its mitochondria. The new drug combination discovered by Dr. Gavathiotis and colleagues kills apoptosis-resistant cancer cells by boosting the active form of one pro-apoptotic protein in particular: BAX, dubbed the “executioner protein.”
Enhancing the “Executioner Protein”

A newly discovered protein helps bacteria recognize stress hormones in the human body and direct their motion in the host.
In humans and animals, catecholamines such as epinephrine, norepinephrine, and dopamine are common stress hormones. Stress can increase the body’s susceptibility to bacterial infections. In the laboratory, stress hormones stimulate the growth of various pathogens. This had already been observed in Salmonella (Salmonella enterica serovar Typhimurium), and other intestinal bacteria, Escherichia coli and the causative agent of cholera, Vibrio cholerae. Furthermore, epinephrine and norepinephrine make it easier for bacteria to infect the body’s cells. And these hormones also influence the biosynthesis of virulence factors, which enable pathogens to adhere to, penetrate, and destroy cells.
“We therefore suspected that some bacteria use such hormones as signals to recognize the eukaryotic host environment,” says LMU microbiologist Professor Kirsten Jung. “But the molecular basis was not known.” Together with Professor Stephan A. Sieber from the Technical University of Munich (TUM) and other researchers, Jung has now identified the binding site of epinephrine and the epinephrine derivative phenylephrine in the bacterium Vibrio campbellii. As the team reports in PNAS, the target of both molecules is the protein CheW. “The biological significance of the mechanism is that bacteria recognize, for example, that they are no longer in sea water, but in the intestine of a host,” explains Jung.
Studies with the model organism V. campbellii
“We wanted to know how bacteria recognize catecholamines as signaling molecules,” says the LMU scientist. “Which receptors control this process?” Her experiments consisted of several individual steps.
For the study, Sieber developed a method for chemically modifying epinephrine and phenylephrine, so that the researchers could directly isolate complexes from the catecholamines and the bound bacterial proteins. A prerequisite of the experiments was that the new compounds would not have any biological characteristics that the unmodified molecules did not have. Jung’s group did laboratory experiments to demonstrate this was so. Epinephrine binds iron, whereas the epinephrine derivative phenylephrine does not. With their choice of compounds, the researchers wanted to rule out effects that arise when the bacteria have a better supply of iron.
Jung and Sieber worked with Vibrio campbellii as a model organism. The marine bacterium infects fish, shrimp, squid, and many other marine invertebrates. They added Vibrio campbellii to the chemically modified catecholamines and lysed the cells. Next, they extracted from the lysate all proteins to which a molecule had bound and characterized them by using proteome analysis. This resulted in a particular enrichment of the soluble chemotaxis protein CheW.
Subsequently, Jung’s group isolated the CheW protein directly from bacteria, purified it, and measured its binding affinity to catecholamines. In the process, the researchers discovered something surprising: the hormones do not bind to the chemoreceptors themselves, as originally expected, but to the coupling protein CheW, which is located between receptors and a signal transduction cascade. This entire stimulus perception system controls the motion of the bacterium in a chemical gradient.
“Our study provides new insights into the communication of bacteria with their host,” summarizes Jung. “We were able to show that the swimming behavior of bacteria is modified by host hormones, which is controlled by CheW.” Motility, and in particular directed motility, is decisively important for host colonization, as bacteria deliberately seek to colonize an organism and conquer all niches. In the next step, Jung now wants to find out whether the same mechanism can be detected in other bacteria.

Researchers from Columbia Engineering, Fiocruz’s Center for Technological Development in Health and the Oswaldo Cruz Institute in Brazil, Memorial Sloan Kettering Cancer Center, and Rockefeller University recently reported that, by combining inhibitors of polymerases and exonucleases — enzymes that allow SARS-CoV-2 to reproduce — they were able to reduce SARS-CoV-2 replication 10 times more than when using just the polymerase inhibitors. They also identified a polymerase inhibitor with a unique modification that largely resists its removal from the RNA by the exonuclease. Their findings from both the molecular and cellular levels reveal the great potential of novel antiviral drug combinations to stop the spread of COVID-19 and other coronavirus diseases. The study was published February 22 by Communications Biology, an open access journal from Nature Portfolio.
“COVID has created an unprecedented public health crisis, with severe effects on the global economy and infrastructure; however, we can use the power of science to stop this pandemic,” said the Columbia team leader Jingyue Ju, Samuel Ruben-Peter G. Viele Professor of Engineering; professor of chemical engineering and pharmacology; and director, Center for Genome Technology & Biomolecular Engineering. “We expect drug combinations like the ones we found will powerfully inhibit RNA viruses such as SARS-CoV-2 and other coronaviruses that could lead to future pandemics. Because polymerase and exonuclease are highly conserved enzymes in coronaviruses with very rare mutations appearing in variants, we anticipate that therapeutics developed to target these enzymes should be widely applicable to all coronaviruses with the potential to cause serious disease.”
SARS-CoV-2, the coronavirus causing the global COVID-19 pandemic, uses a protein called polymerase to replicate its RNA genome inside infected human cells. In theory, terminating the polymerase reaction should stop the propagation of the coronavirus, leading to its eradication by the human host’s immune system. However, SARS-CoV-2 has two key enzymes that allow it to replicate: the polymerase which reproduces its RNA and a proofreading exonuclease that corrects errors in the replication process.
The presence of the exonuclease for proofreading is unique to the coronaviruses and is needed to reduce the number of mutations and thereby maintain the integrity and function of the large RNA genomes of coronaviruses. Thus, the vaccine approach has been quite effective in containing the COVID-19 pandemic because the coronaviruses do not mutate as frequently as influenza virus and HIV, which have no proofreading function and therefore mutate more frequently.
Nucleotide-based viral polymerase inhibitors are very successful drugs for treating HIV and hepatitis viruses B and C infections. However, because of the presence of the proofreading exonuclease in SARS-CoV-2, which can remove these inhibitors from the RNA, the polymerase inhibitor Remdesivir, the sole FDA-approved drug for COVID-19, is not as effective as hoped for in preventing serious disease. If the exonuclease could be concurrently inhibited or its activity evaded, viral replication would be more efficiently blocked.
The research team, led by Ju and Dr. Thiago Souza, Full Researcher at the Oswaldo Cruz Institute’s Center for Technological Development in Health, decided to investigate whether the combination of polymerase and exonuclease inhibitors could work together to inhibit replication of SARS-CoV-2 more effectively, or if polymerase inhibitors with certain modifications could resist removal by the exonuclease. The Columbia Engineering team conceived the overall project and performed the molecular-level studies to identify interactions among the inhibitors and enzymes, using a novel mass-spectrometry-based approach. The Brazilian team designed and conducted the cellular studies to measure the inhibitory effects of drug combinations on virus reproduction. Dr. Thomas Tuschl’s group at Rockefeller University and Dr. Dinshaw Patel’s team at Memorial Sloan Kettering Cancer Center produced the polymerase and exonuclease complexes used in the molecular studies.
Souza’s group demonstrated that the polymerase and exonuclease inhibitors work together to block the virus’s ability to reproduce in infected lung cells. “While these results were obtained in a cell culture model, we purposely chose inhibitors already approved as drugs for treatment of other common virus infections, such as those caused by HIV and hepatitis viruses, with the aim of being able to quickly advance them to clinical trials,” Souza noted.
The team is now exploring whether the enhanced antiviral effects of the combination drugs can be demonstrated in a COVID-19 animal model, with acceptable pharmacological properties. If the results are positive, these drugs can be moved rapidly to clinical trials as they have been previously approved for treatment of other viral infections. They have also established an initiative with a consortium of pharmacologists, virologists, medicinal chemists, and structural biologists to develop new therapeutics with enhanced potency and safety profiles for COVID-19 based on the discoveries reported in this study.
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Materials provided by Columbia University School of Engineering and Applied Science. Original written by Holly Evarts. Note: Content may be edited for style and length.

By employing artificial intelligence (AI) and robotics to formulate therapeutic proteins, a team led by Rutgers researchers has successfully stabilized an enzyme able to degrade scar tissue resulting from spinal cord injuries and promote tissue regeneration.
The study, recently published in Advanced Healthcare Materials, details the team’s ground-breaking stabilization of the enzyme Chondroitinase ABC, (ChABC) offering new hope for patients coping with spinal cord injuries.
“This study represents one of the first times artificial intelligence and robotics have been used to formulate highly sensitive therapeutic proteins and extend their activity by such a large amount. It’s a major scientific achievement,” said Adam Gormley, the project’s principal investigator and an assistant professor of biomedical engineering at Rutgers School of Engineering (SOE) at Rutgers University-New Brunswick.
Gormley expressed that his research is also motivated, in part, by a personal connection to spinal cord injury.
“I’ll never forget being at the hospital and learning a close college friend would likely never walk again after being paralyzed from the waist down after a mountain biking accident,” Gormley recalled. “The therapy we are developing may someday help people such as my friend lessen the scar on their spinal cords and regain function. This is a great reason to wake up in the morning and fight to further the science and potential therapy.”
Shashank Kosuri, a biomedical engineering doctoral student at Rutgers SOE and a lead author of the study noted that spinal cord injuries, or SCIs, can negatively impact the physical, psychological, and socio-economic well-being of patients and their families. Soon after an SCI, a secondary cascade of inflammation produces a dense scar tissue that can inhibit or prevent nervous tissue regeneration.
The enzyme successfully stabilized in the study, ChABC, is known to degrade scar tissue molecules and promote tissue regeneration, yet it is highly unstable at the human body temperature of 98.6° F. and loses all activity within a few hours. Kosuri noted that this necessitates multiple, expensive infusions at very high doses to maintain therapeutic efficacy.
Synthetic copolymers are able to wrap around enzymes such as ChABC and stabilize them in hostile microenvironments. In order to stabilize the enzyme, the researchers utilized an AI-driven approach with liquid handling robotics to synthesize and test the ability of numerous copolymers to stabilize ChABC and maintain its activity at 98.6° F.
While the researchers were able to identify several copolymers that performed well, Kosuri reported that one copolymer combination even continued to retain 30% of the enzyme for up to one week, a promising result for patients seeking care for spinal cord injuries.
The study received support from grants funded by the National Institutes of Health, the National Science Foundation, and The New Jersey Commission on Spinal Cord research. In addition to Gormley and Kosuri, the Rutgers research team also included SOE Professor Li Cai and Distinguished Professor Martin Yarmush, as well as several SOE-affiliated students. Faculty and students from Princeton University’s Department of Chemical and Biological Engineering also collaborated on the project.
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Materials provided by Rutgers University. Original written by Emily Everson Layden. Note: Content may be edited for style and length.

Pancreatic cancer is one of the most aggressive and deadly tumor types and notorious for its resistance to virtually all types of treatment, including newer immunotherapies.
A new study — in mice — from Washington University School of Medicine in St. Louis suggests that blocking a major inflammatory pathway that is activated in pancreatic cancer makes the tumors sensitive to chemotherapy and a type of immunotherapy that prompts the immune system’s T cells to attack the cancer cells. The therapy more than doubled survival in a mouse model of pancreatic cancer.
The study’s results, published March 7 in the journal Gastroenterology, lend additional support for the rationale behind a new national clinical trial that will evaluate the same treatment strategy in patients with pancreatic ductal adenocarcinoma — the most common malignant tumor of the pancreas. The researchers plan to enroll about 50 patients nationwide.
Washington University researchers at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine will lead the national trial that is part of the National Cancer Institute’s (NCI) Experimental Therapeutics Clinical Trials Network, a collaboration of industry, academic medical centers and researchers focused on early clinical investigations of innovative cancer therapies. The network includes more than 30 clinical sites in the U.S. and Canada.
“Washington University has a lot of strengths in bringing science from the lab to the clinic,” said senior author Kian-Huat Lim, MD, PhD, an associate professor of medicine and principal investigator for translational science on the national trial. “With this therapy, we are going after a pathway that we know is involved in driving the aggressiveness of pancreatic cancer. The results of this study are promising in that it showed a way to break through the defenses of this tumor type, making it susceptible to our therapeutics, including combinations of chemotherapy and newer immunotherapies that stimulate T cells to fight the cancer.”
The researchers, including first author Vikas Somani, PhD, a postdoctoral research associate in Lim’s lab in the Division of Oncology in the Department of Medicine, found that a protein called IRAK4 drives inflammation in pancreatic tumors and leads to T cell exhaustion, meaning the T cells can’t function as they should to attack harmful cells, including cancer. The researchers tested an IRAK4 inhibitor, called CA-4948, and found that the treatment reduced inflammatory signaling in the tumors in mice and improved the ability of T cells to infiltrate the tumors and kill pancreatic cancer cells. The therapy also sensitized the tumors to a type of immunotherapy called checkpoint immunotherapy, which “take the brakes off” T cells, improving their ability to attack tumor cells.

Investigators have discovered that a biodegradable nanoparticle used in medical sutures could combat a rare, sometimes-fatal autoimmune disease.
Researchers found that a unique macrophage, an immune cell that removes bacteria or dead cells, plays a key role in the chronic inflammation and scarring in the lungs and skin of people with scleroderma, or systemic sclerosis. This macrophage, called MARCO+, was found to be elevated in people with the orphan disease, which affects around 70,000 Americans and currently has no effective treatment.
The research team injected mice with biodegradable PLG nanoparticles, short for poly (lactic-co-glycolic) acid. The results, published in JCI Insight, reveal that PLG specifically targeted MARCO+ inflammatory cells and prevented skin and lung fibrosis. Even more striking, nanoparticle treatment could even reverse fibrosis in these mice, says John Varga, M.D., senior author of the paper and chief of the Michigan Medicine Division of Rheumatology.
“The findings reveal a stark difference: untreated mice had terrible scarring in the lungs, and those treated with this nanoparticle saw the disease decease in severity or completely disappear,” said John Varga, M.D., senior author of the paper and chief of the Michigan Medicine Division of Rheumatology. “This is a promising step towards targeted treatment for patients with early scleroderma that could potentially mitigate the worst effects of the disease.”
The research team believes the MARCO+ cells become activated in people with scleroderma and circulate in the blood stream, traveling to the tissues and causing scar formation. While the PLG nanoparticle reduced fibrosis in mouse models, Varga says future studies are needed to determine exactly how it prevents the MARCO+ activation.
PLG is already approved by the U.S. Food and Drug Administration for creating biodegradable sutures. In previous studies, Varga’s co-authors found that PLG decreased inflammation in mouse models of myocardial infarction. It is not currently available as a treatment for patients.
“We hope that this type of therapy will one day be evaluated in clinical trials for scleroderma,” Varga said. “People with scleroderma are at great risk for skin and lung thickening that impacts function, and we look for any way to stop that from happening.”
Disclosures: Stephen D. Miller is a co-founder of, member of the Scientific Advisory Board, grantee of, and holds stock options in COUR Pharmaceutical Development Company and onCOUR Pharma, Inc., which holds the patent for the PLG nanoparticle technology.
Additional authors include Swati Bhattacharyya, Swarna Bale, both of Michigan Medicine, and Dan Xu, Wenxia Wang, Igal Ifergan, Ming-Yi Alice Chiang Wong, Daniele Procissi, Anjana Yeldandi, Robert G Marangoni, Craig Horbinski, and Stephen D. Miller, all of Northwestern University Feinberg School of Medicine.
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Materials provided by Michigan Medicine – University of Michigan. Original written by Noah Fromson. Note: Content may be edited for style and length.

Researchers have discovered two types of brain cells that play a key role in dividing continuous human experience into distinct segments that can be recalled later. The discovery provides new promise as a path toward development of novel treatments for memory disorders such as dementia and Alzheimer’s disease.
In a study led by Cedars-Sinai, researchers have discovered two types of brain cells that play a key role in dividing continuous human experience into distinct segments that can be recalled later. The discovery provides new promise as a path toward development of novel treatments for memory disorders such as dementia and Alzheimer’s disease.
The study, part of a multi-institutional BRAIN Initiative consortium funded by the National Institutes of Health and led by Cedars-Sinai, was published in the peer-reviewed journal Nature Neuroscience. As part of ongoing research into how memory works, Ueli Rutishauser, PhD, professor of Neurosurgery, Neurology, and Biomedical Sciences at Cedars-Sinai, and co-investigators looked at how brain cells react as memories are formed.
“One of the reasons we can’t offer significant help for somebody who suffers from a memory disorder is that we don’t know enough about how the memory system works,” said Rutishauser, senior author of the study, adding that memory is foundational to us as human beings.
Human experience is continuous, but psychologists believe, based on observations of people’s behavior, that memories are divided by the brain into distinct events, a concept known as event segmentation. Working with 19 patients with drug-resistant epilepsy, Rutishauser and his team were able to study how neurons perform during this process.
Patients participating in the study had electrodes surgically inserted into their brains to help locate the focus of their epileptic seizures, allowing investigators to record the activity of individual neurons while the patients viewed film clips that included cognitive boundaries.