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Human health and development depend on dynamic networks of physical, and functional, interactions between proteins. However, the details of these networks – how they are formed and how they function – are largely unknown.

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CReM Researchers Awarded $14 Million to Understand and Treat Genetic Lung Diseases

A team of researchers led by Darrell N. Kotton, MD, the David C. Seldin Professor of Medicine, has been awarded a five-year, $14 million grant from the NIH’s National Heart, Lung, and Blood Institute (NHLBI) for their research, “Developing Pluripotent Stem Cells to Model and Treat Lung Disease.” The new award will fund an integrated, multi-investigator program project grant where four interacting labs headed by four physician-scientists, all located in the Center for Regenerative Medicine (CReM) of Boston University and Boston Medical Center, will develop next generation stem cell-based therapies for currently incurable genetic lung diseases affecting children and adults, including childhood and adult interstitial lung diseases, an inherited form of emphysema, cystic fibrosis and primary ciliary dyskinesia.

Click here to see the article

• Publications

The Kotton Lab publishes new paper on iPSC modeling of childhood interstitial lung disease caused by ABCA3 mutations

Mutations in ATP-binding cassette A3 (ABCA3), a phospholipid transporter critical for surfactant homeostasis in pulmonary alveolar type II epithelial cells (AEC2s), are the most common genetic causes of childhood interstitial lung disease (chILD). Treatments for patients with pathological variants of ABCA3 mutations are limited, in part due to a lack of understanding of disease pathogenesis resulting from an inability to access primary AEC2s from affected children. Here, we report the generation of AEC2s from affected patient induced pluripotent stem cells (iPSCs) carrying homozygous versions of multiple ABCA3 mutations. We generated syngeneic CRISPR/Cas9 gene-corrected and uncorrected iPSCs and ABCA3-mutant knockin ABCA3:GFP fusion reporter lines for in vitro disease modeling. We observed an expected decreased capacity for surfactant secretion in ABCA3-mutant iPSC-derived AEC2s (iAEC2s), but we also found an unexpected epithelial-intrinsic aberrant phenotype in mutant iAEC2s, presenting as diminished progenitor potential, increased NFκB signaling, and the production of pro-inflammatory cytokines. The ABCA3:GFP fusion reporter permitted mutant-specific, quantifiable characterization of lamellar body size and ABCA3 protein trafficking, functional features that are perturbed depending on ABCA3 mutation type. Our disease model provides a platform for understanding ABCA3 mutation–mediated mechanisms of alveolar epithelial cell dysfunction that may trigger chILD pathogenesis.

Click here to read the article

Latest publication from the Murphy Lab featured on the cover of Blood Advances: De Novo Hematopoiesis from the Fetal Lung!

Hemogenic endothelial cells (HECs) are specialized cells that undergo endothelial-to-hematopoietic transition (EHT) to give rise to the earliest precursors of hematopoietic progenitors that will eventually sustain hematopoiesis throughout the lifetime of an organism. Although HECs are thought to be primarily limited to the aorta-gonad-mesonephros (AGM) during early development, EHT has been described in various other hematopoietic organs and embryonic vessels. Though not defined as a hematopoietic organ, the lung houses many resident hematopoietic cells, aids in platelet biogenesis, and is a reservoir for hematopoietic stem and progenitor cells (HSPCs). However, lung HECs have never been described. Here, we demonstrate that the fetal lung is a potential source of HECs that have the functional capacity to undergo EHT to produce de novo HSPCs and their resultant progeny. Explant cultures of murine and human fetal lungs display adherent endothelial cells transitioning into floating hematopoietic cells, accompanied by the gradual loss of an endothelial signature. Flow cytometric and functional assessment of fetal-lung explants showed the production of multipotent HSPCs that expressed the EHT and pre-HSPC markers EPCR, CD41, CD43, and CD44. scRNA-seq and small molecule modulation demonstrated that fetal lung HECs rely on canonical signaling pathways to undergo EHT, including TGFβ/BMP, Notch, and YAP. Collectively, these data support the possibility that post-AGM development, functional HECs are present in the fetal lung, establishing this location as a potential extramedullary site of de novo hematopoiesis.

New publication from the Murphy Lab in Science Advances! They led a Team demonstrating that immune cells drive NET tumor progression and susceptibility to therapies

Neuroendocrine tumors (NETs) are rare cancers that most often arise in the gastrointestinal tract and pancreas. The fundamental mechanisms driving gastroenteropancreatic (GEP)–NET growth remain incompletely elucidated; however, the heterogeneous clinical behavior of GEP-NETs suggests that both cellular lineage dynamics and tumor microenvironment influence tumor pathophysiology. Here, we investigated the single-cell transcriptomes of tumor and immune cells from patients with gastroenteropancreatic NETs. Malignant GEP-NET cells expressed genes and regulons associated with normal, gastrointestinal endocrine cell differentiation, and fate determination stages. Tumor and lymphoid compartments sparsely expressed immunosuppressive targets commonly investigated in clinical trials, such as the programmed cell death protein–1/programmed death ligand–1 axis. However, infiltrating myeloid cell types within both primary and metastatic GEP-NETs were enriched for genes encoding other immune checkpoints, including VSIR (VISTA), HAVCR2 (TIM3), LGALS9 (Gal-9), and SIGLEC10. Our findings highlight the transcriptomic heterogeneity that distinguishes the cellular landscapes of GEP-NET anatomic subtypes and reveal potential avenues for future precision medicine therapeutics.

Kotton Lab featured in Boston University Article on Lung Disease Research

For more than 20 years, a team of Boston University scientists have been on a quest to not just figure out how to treat incurable lung diseases, but also how to regenerate damaged lungs so they’re as good as new.

That is the goal of pulmonologist Darrell Kotton and his lab at the Center for Regenerative Medicine (CReM), a joint effort between the University and Boston Medical Center, BU’s primary teaching hospital. By refining their work using sophisticated stem cell technology, Kotton and his team are closer to realizing that vision than ever before.

In two new studies published in Cell Stem Cell, BU researchers detail how they engineered lung stem cells and successfully transplanted them into injured lungs of mice. Two lines of cells targeted two different parts of the lung: the airways, including the trachea and bronchial tubes, and the alveoli, the delicate air sacs that deliver oxygen to the bloodstream. Their findings could eventually lead to new ways for treating lung diseases, including severe cases of COVID-19, emphysema, pulmonary fibrosis, and cystic fibrosis, a disease caused by a genetic mutation.

The Mostoslavsky Lab Publishes New Platform to Make T Cells from iPSCs

A robust method of producing mature T cells from iPSCs is needed to realize their therapeutic potential. NOTCH1 is known to be required for the production of hematopoietic progenitor cells with T cell potential in vivo. Here we identify a critical window during mesodermal differentiation when Notch activation robustly improves access to definitive hematopoietic progenitors with T/NK cell lineage potential. Low-density progenitors on either OP9-hDLL4 feeder cells or hDLL4-coated plates favored T cell maturation into TCRab+CD3+CD8+ cells that express expected T cell markers, upregulate activation markers, and proliferate in response to T cell stimulus. Single-cell RNAseq shows Notch activation yields a 6-fold increase in multi-potent hematopoietic progenitors that follow a developmental trajectory toward T cells with clear similarity to post-natal human thymocytes. We conclude that early mesodermal Notch activation during hematopoietic differentiation is a missing stimulus with broad implications for producing hematopoietic progenitors with definitive characteristics.

Click here to access the full article

New Publication for the Murphy Lab, A ‘Blueprint’ for Longevity feature in USA Today, the New York Post and 75 other Media Outlets

Age-related changes in immune cell composition and functionality are associated with multimorbidity and mortality. However, many centenarians delay the onset of aging-related disease suggesting the presence of elite immunity that remains highly functional at extreme old age.

To identify immune-specific patterns of aging and extreme human longevity, we analyzed novel single cell profiles from the peripheral blood mononuclear cells (PBMCs) of a random sample of 7 centenarians (mean age 106) and publicly available single cell RNA-sequencing (scRNA-seq) datasets that included an additional 7 centenarians as well as 52 people at younger ages (20–89 years).

The analysis confirmed known shifts in the ratio of lymphocytes to myeloid cells, and noncytotoxic to cytotoxic cell distributions with aging, but also identified significant shifts from CD4+ T cell to B cell populations in centenarians suggesting a history of exposure to natural and environmental immunogens. We validated several of these findings using flow cytometry analysis of the same samples. Our transcriptional analysis identified cell type signatures specific to exceptional longevity that included genes with age-related changes (e.g., increased expression of STK17A, a gene known to be involved in DNA damage response) as well as genes expressed uniquely in centenarians’ PBMCs (e.g., S100A4, part of the S100 protein family studied in age-related disease and connected to longevity and metabolic regulation).

Collectively, these data suggest that centenarians harbor unique, highly functional immune systems that have successfully adapted to a history of insults allowing for the achievement of exceptional longevity.

Click here to see the article Click here to see the USA Today Article

The latest publication from the Kotton lab detailing the transcriptomic programs of iPSC-derived alveolar cells

Dysfunction of alveolar epithelial type 2 cells (AEC2s), the facultative progenitors of lung alveoli, is implicated in pulmonary disease pathogenesis, highlighting the importance of human in vitro models. However, AEC2-like cells in culture have yet to be directly compared to their in vivo counterparts at single-cell resolution. Here, we performed head-to-head comparisons among the transcriptomes of primary (1°) adult human AEC2s, their cultured progeny, and human induced pluripotent stem cell–derived AEC2s (iAEC2s). We found each population occupied a distinct transcriptomic space with cultured AEC2s (1° and iAEC2s) exhibiting similarities to and differences from freshly purified 1° cells. Across each cell type, we found an inverse relationship between proliferative and maturation states, with preculture 1° AEC2s being most quiescent/mature and iAEC2s being most proliferative/least mature. Cultures of either type of human AEC2s did not generate detectable alveolar type 1 cells in these defined conditions; however, a subset of iAEC2s cocultured with fibroblasts acquired a transitional cell state described in mice and humans to arise during fibrosis or following injury. Hence, we provide direct comparisons of the transcriptomic programs of 1° and engineered AEC2s, 2 in vitro models that can be harnessed to study human lung health and disease.

Human iPSC-hepatocyte modeling of Alpha-1-antitrypsin from the Wilson lab is out!

Individuals homozygous for the ‘‘Z’’ mutation in alpha-1 antitrypsin deficiency are known to be at increased risk for liver disease. It has also become clear that some degree of risk is similarly conferred by the heterozygous state. A lack ofmodel systems that recapitulate heterozygosity in human hepatocytes has limited the ability to study the impact of a single Z alpha-1 antitrypsin (ZAAT) allele on hepatocyte biology. Here, we describe the derivation of syngeneic induced pluripotent stem cells (iPSCs) engineered to determine the effects of ZAAT heterozygosity in iPSC-hepatocytes (iHeps). We find that heterozygous MZ iHeps exhibit an intermediate disease phenotype and share with ZZ iHeps alterations in AAT protein processing and downstream perturbations including altered endoplasmic reticulum (ER) and mitochondrial morphology, reduced mitochondrial respiration, and branch-specific activation of the unfolded protein response in cell subpopulations. Our model of MZ heterozygosity thus provides evidence that a single Z allele is sufficient to disrupt hepatocyte homeostatic function.

New Publication from the Mostoslavsky Lab Describing a New Role for Notch Signaling in T-cell specification

A robust method of producing mature T cells from iPSCs is needed to realize their therapeutic potential. NOTCH1 is known to be required for the production of hematopoietic progenitor cells with T cell potential in vivo. Here we identify a critical window during mesodermal differentiation when Notch activation robustly improves access to definitive hematopoietic progenitors with T/NK cell lineage potential. Low-density progenitors on either OP9-hDLL4 feeder cells or hDLL4-coated plates favored Tcell maturation into TCRab+CD3+CD8+ cells that express expected T cell markers, upregulate activation markers, and proliferate in response to T cell stimulus. Single-cell RNAseq shows Notch activation yields a 6-fold increase in multi-potent hematopoietic progenitors that follow a developmental trajectory toward Tcells with clear similarity to post-natal human thymocytes.We conclude that early mesodermal Notch activation during hematopoietic differentiation is a missing stimulus with broad implications for producing hematopoietic progenitors with definitive characteristics.

Access the paper here

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The Wilson lab is focused on two major aspects of regenerative medicine:

1) Developing gene therapy approaches for the study and treatment of lung diseases: The ability to manipulate gene expression in specified lung cell populations has both experimental and therapeutic potential for lung disease. By developing viral vectors that transduce specific lung cell types in vivo, we hope to minimize potential off-target effects while maximizing our ability to target diseased cell populations. We work with lentiviral and AAV vectors to overexpress or knockdown expression of genes important to disease pathogenesis in the lung.

2) Utilizing induced pluripotent stem cells (iPSC) to study human lung and liver diseases: The Wilson lab is interested in the application of patient-derived iPS cells for the study of lung and liver diseases, such as alpha-1 antitrypsin deficiency (AATD).

The Hawkins Lab is interested in how the human lung develops and responds to injury to better understand human lung disease. Induced pluripotent stem cells (iPSCs) offer a unique opportunity to model human lung disease and bridge the gap between research in animal models and humans.

Using this iPSC platform, we are focused on understanding the molecular mechanisms that control human lung development. We hope to apply this knowledge to advance our understanding of and develop precision medicine approaches for lung disease.

The Murphy laboratory is composed of dynamic and passionate researchers who utilize multiple stem cell-based platforms to answer basic biological questions and combat disease. Central directions of the laboratory include: developmental hematopoiesis, the modeling of blood-borne disease, and discovery and therapeutic intervention in sickle cell disease, amyloidosis, and aging.

The Murphy Lab has pioneered: The world’s largest sickle cell disease-specific iPSC library and platforms and protocols that can used to recapitulate hematopoietic ontogeny and to develop and validate novel therapeutic strategies for the disease; The successful modeling of a protein folding disorder called familial amyloidosis demonstrating the ability to model a long-term, complex, multisystem disease in a relatively short time, using lineage-specified cells (hepatic, cardiac and neuronal) derived from patient-specific stem cells; The first iPSC library created from subjects with exceptional longevity (centenarians) that serves as an unlimited resource of biomaterials to fuel the study of aging and the development of novel therapeutics for aging-related disease.

www.murphylaboratory.com

@DRGJMurphy

The Serrano Lab studies neurodevelopment and cardiovascular development in the context of rare multi-systemic disorders originated by pathogenic variants in epigenetic modifiers like KMT2D.   

We aim to identify shared molecular and cellular mechanisms driving cardiovascular and brain development with particular interest in cell differentiation, migration, and cell cycle progression.   

Our lab combines rare disease modeling in zebrafish together with cardiovascular and neurobiology techniques and human iPSC-derived brain organoids and endothelial cells.   

We believe that a patient-forward focus to our projects will help us to get better understanding of disease mechanisms through basic science research. To this end, we are active in the collaborative community among field experts and rare disease patient-advocacy groups who drive our research program to identify therapeutic targets in patient-specific iPS cells.  

The Mostoslavsky Lab is a basic science laboratory in the Section of Gastroenterology in the Department of Medicine at Boston University.

Our goal is to advance our understanding of stem cell biology with a focus on their genetic manipulation via gene transfer and their potential use for stem cell-based therapy.

The Mostoslavsky’s Lab designed and constructed the STEMCCA vector for the generation of iPS cells, a tool that has become the industry standard for nuclear reprogramming. Project areas in the lab focuses on the use of different stem cell populations, including embryonic stem cells, induced Pluripotent Stem (iPS) cells, hematopoietic stem cells and intestinal stem cells and their genetic manipulation by lentiviral vectors.

Our laboratory have already established a large library of disease-specific iPS cells with a particular interest in utilizing iPS cells to model diseases of the liver, the gastrointestinal tract, prion-mediated neurodegenerative diseases and immune-based inflammatory conditions, using iPSC-derived microglia, macrophages and T/NK cells.

The Gouon-Evans lab investigates cellular and molecular mechanisms driving liver development, regeneration and cancer. We specifically interrogate the role of progenitor/stem cells and how they share similar molecular signature and functions during these 3 processes.

Our innovative tools include: 1) directed differentiation of human pluripotent stem cells (PSC) to generate in vitro liver progenitors and their derivative hepatocytes, the main functional cell type of the liver, 2) mouse models with lineage tracing strategy to track in vivo the fate of progenitor cells, 3) PSC derivative cell transplantation into mouse models with damaged livers as cell therapy for liver diseases, 3) dissection of liver cancer specimens from patients to identify and define the impact of specific cancer stem cells in liver oncogenesis.

Projects in the Gouon-Evans lab will lead to a better understanding of the liver development, to the establishment of multi-modular approaches for improving liver regeneration with PSC derivatives, and will reveal the impact of specific cancer stem cells as a target for diagnosis and therapy in liver oncogenesis.

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Genealogy Studies Program

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Nationally recognized online Genealogy Studies courses

Enroll by March 31 to lock in a 2-month, interest-free payment plan for the May session.

Use proven methodology to become more accurate and efficient.

Genealogy Studies

Genealogical principles course.

Length of course: 7 weeks Next session begins: May 7, 2024

Ideal for enthusiasts seeking to hone their research skills, this course is also an excellent first step toward our certificate program.

• Define terms and understand best practices
• Use public records and optimize searches
• Follow the Genealogical Proof Standard
• 10-16 hours per week

Genealogy Practicum Course — NEW!

Length of course: 7 weeks Next session begins: July 2, 2024

Learn essential skills and gain hands-on research experience creating important genealogical work products, such as research plans, logs, compiled genealogies, proof discussions, and research reports.

• Learn how to develop key genealogical work products by working on real-world cases
• Hone skills in planning and executing research, organizing familial relationships, documenting kinship, proving conclusions, and compiling research results
• 12-14 hours per week

Certificate in Genealogical Research

Length of course: 15 weeks Next session begins: May 7, 2024

Whether you are a highly-experienced hobbyist, budding professional, or an advanced researcher this rigorous program will challenge you to advance your skill set. The Certificate in Genealogical Research course is Boston University’s flagship course, which has been running since 2009 and is frequently updated to respond to new trends, sources, and methods within the genealogy field. Newly updated in 2023, the latest version of the course incorporates additional coursework on using DNA as a genealogical source, incorporates the field’s most up to date genealogy standards, and adds new additional forensic genealogy course content. The course is excellent preparation for those pursuing certification with the Board for Certification of Genealogists (BCG) or accreditation with the International Commission for the Accreditation of Professional Genealogists (ICAPGen).

• Become more effective in research planning, analysis and correlation
• Understand how to use DNA as a genealogical source in family history research and forensic genealogy
• Understand documentation and citation practices in the genealogy field
• Deliver accurate and professional written genealogical work
• 20-30 hours per week

Combine the convenience of online learning with expert instruction to help you gain skills to set you apart in this growing field. Work with noted Boston University instructors , including Certified Genealogists and practicing professionals in the genealogy field.

Our online courses offer:

• Flexible online format that lets you learn from any location at a time that is convenient for you
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• Opportunities to interact with peers and expand your professional network
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View the recorded webinar  with Program Director and professional genealogist, Melissa Johnson, CG as she answers questions from the live audience pertaining to BU’s online courses and shares tips on practicing genealogy research at home.

To learn more, contact an Enrollment Advisor at 617-502-8822 or complete the form below.

Past meets present in BU’s Genealogy Studies program

Members of NEHGS, NGS, APG, SCGS, NYG&B, AAHGS, CGS, IGSI, FSGS, ACGS & MSOG receive a 10% discount.

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• Boston University Libraries

CGS HU103: Team E - Literature & Art from the Ancient World through the Enlightenment (Ohri) Spring 2024

• Find Resources on 19th Cent. Boston
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Finding Books on 19th Century Boston, Art, & the Brahmins

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Suggested Searches:

• Boston -- 19th Century (subject search, limited to books)
• Boston -- 19th Century and Art (search limited to books)
• Boston Brahmin* (keyword search, limited to books & book chapters)

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• Boston & Its Neighborhoods - History (a resource guide)

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All positions have now been filled. Thank you for applying!

Thank you everyone for making our program such a success our three-year grant for the ’20-’21, ’21-’22, and ’22-’23 years has now run its course. we will be applying for a renewal but, due to the schedule of grant reviewing, do not anticipate being able to offer our program during the summer of 2024. we hope we will be back for the summer of 2025. please check in with us in late fall of 2024. in the meantime, do check out all the other amazing reu programs supported by the national science foundation: https://www.nsf.gov/crssprgm/reu/reu_search.jsp.

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What is the impact of rising groundwater levels in Massachusetts? Researchers looking for your help

By Jacob Wycoff

Updated on: March 21, 2024 / 8:51 AM EDT / CBS Boston

AMHERST - A professor at UMass Amherst is asking for people's help as his team researches the impact groundwater levels are having in Massachusetts.

Massachusetts is coming off one of the wettest years on record and one of the wettest winters on record, and we are now in one of the wettest Marches to date. It's no secret that our seas are rising and as of late, so are our rivers. One UMass Amherst professor is sounding a new alarm – a rising water table. 

Groundwater levels are rising

David Boutt is a professor of hydrology at UMass Amherst. He's part of a team that's investigating our rising groundwater levels, which he says has been rising for the last 40 to 50 years. They have been digging into what that means with respect to climate change and hydrological change in the northeast. 

In 2023, it seemed like every other week there was a flooding concern. Flash flooding caused massive damage in Leominster and Attleboro, and state-wide, plenty of homes were impacted. 

"I often field calls from homeowners that are saying I've never had water in my basement. I've got these flooding issues, I'm trying to understand what's going on. I never had water in my basement but now I do," Boutt said, recalling conversations from his field work. 

As is the case with a lot of meteorological variables in New England, there is a tremendous amount of hydrological data dating back to the 1940s but much of that data isn't where people live. 

That's where YOU come in. 

How you can help the groundwater research

Boutt and his team created a Google Form for a survey where you can enter your own data. 

"It probably takes a few minutes out of your time to respond to. We asked a few questions just about, like, have you experienced wet conditions on your property or in your basement, which months of the year," said Boutt. The data his team collects will go into predictive models they're building. 

Extreme years like 2023 may be the new normal in the future, so your neighborhood may help answer important questions, like "how do we best invest in infrastructure projects that take into account [this flooding]," added Boutt. 

Boutt also told WBZ TV he's very interested in seeing how rising sea levels contributes to rising water tables – something called "salt water intrusion." A dual threat for coastal communities. 

• Climate Change
• Eye on Earth
• UMass Amherst

Jacob Wycoff is a meteorologist at WBZ-TV and will contribute to weekend morning newscasts. Jacob is a member of the National Weather Association and the American Meteorological Society.

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How Does Science Misinformation Affect Americans from Underrepresented Communities?

New bu-led research suggests false information festers due to structural dynamics, including historic discrimination.

Photo via iStock/MicrovOne

Rich Barlow

Anyone who spends time on social media knows that we’re awash in misinformation—particularly around science and health. But new Boston University–led research has found historically excluded and marginalized Americans may be more vulnerable to inaccurate notions about science due to “structural and institutional power dynamics.”

In a paper published in Science Communication , the researchers—five from the BU College of Communication and one from Baylor University—conducted two focus groups in 2021 with 19 Black and Latino social media users in Greater Boston. The participants weren’t selected on income, but rather as members of groups that have faced historical discrimination, says Michelle Amazeen , COM’s associate dean of research and the study’s lead investigator.

“They had to qualify as what we call ‘misinformation-receptive’ or ‘misinformation-vulnerable’ on the topic of climate change,” she says, using terms coined by coresearcher Arunima Krishna , a COM associate professor of mass communication, advertising, and public relations. The former term refers to people susceptible to misinformation either because they’ve accepted it before or hold extreme attitudes or high motivation about climate change. The latter refers to people displaying either extreme attitudes toward climate change or “high knowledge deficiency” about it, putting them at moderate risk of misinformation susceptibility.

In their paper, the researchers said their discussion with focus group participants revealed “relative disengagement from science-related news and information” and that power dynamics impeded “access to accurate information and indicate how missing voices must be included in the efforts at media and information literacy initiatives.” The other COM researchers were Yi Grace Ji , an assistant professor of mass communication, advertising, and public relations; Chris Chao Su , an assistant professor of emerging media studies; and James J. Cummings , an assistant professor of emerging media studies. The study received funding from the Rita Allen Foundation.

The Brink spoke with Amazeen, a COM associate professor of mass communication, about the study’s findings and if it revealed any new approaches to tackling misinformation.

With Michelle Amazeen

The brink: what is new about your study.

Amazeen: A handful of [previous] researchers talked with underrepresented communities. What’s novel about our study is that we were able to identify and talk with people who were susceptible to misinformation. We prescreened them just [about] climate, but we have reason to believe that people’s vulnerability to one type of science-related misinformation spreads to other topics.

The Brink: In the focus groups, what were the questions you asked?

Amazeen: We talked about media usage and, in one group in particular, nobody mentioned engaging with news; it wasn’t top of mind for them. When I asked them about it, a few of them said, “If I need to—if I’m taking a trip and I need to know the weather, or when the coronavirus happened.” They would tune into news about that. But it wasn’t part of their daily routine to engage with news. Some of it was because the groups really didn’t see themselves reflected in the news—people who looked liked them in the news, the journalists. More often, the people who looked like them were being accused of being violent or predators or that sort of thing.  I specifically had to ask about science-related topics; that didn’t come up organically, either. Climate came up, COVID-19 came up—this was in the summer of 2021, so the vaccines were out. Also, health and wellness— that was the topic that really engaged a lot of them. I didn’t bring it up; they brought it up.

The Brink: Define the issues that they brought up.

Amazeen: What’s in our foods; being able to eat healthy and take care of ourselves; dealing with things like diabetes. They don’t know what to believe; there’s a lot of conflicting information. One brought up—and others chimed in—food additives, such as [preservative] BHT and [whitener] titanium dioxide. In Europe, these chemicals are banned, but the CDC and other agencies have said, in the quantities that they’re in, they don’t pose any harm. But there are other links that people are seeing on the internet, saying, “this is bad for you.”   One of the participants, while we were conducting the focus group, said, “I just Googled it. Is BHT bad for you? The first thing that pops up is, ‘There’s no evidence that BHT is harmful in the amounts used in packaged food.’ First thing. I didn’t click anything. I just did a basic Google search. But then the funny thing is, right after that, it says, ‘General Mills to remove antioxidant BHT from its cereals.’ So, if it’s harmless…”  I think there’s a lot of distrust about what they’re being told. There’s a history of marginalized groups being taken advantage of by our government.

The Brink: Are you talking about things like the Tuskegee study [which in 1932 began studying syphilis in Black men without their informed consent]?

Amazeen: Exactly, and they brought that up.

The Brink: How many actually fell for scientific misinformation?

Amazeen: Some of them did. There were a few who were not vaccinated [against COVID]. One of them said [the vaccine] didn’t go through clinical trials; it did. Somebody said that it causes autism; that’s been debunked, as well. Other people brought up how the government has come after physicians who don’t prescribe certain things or raise questions about procedures or vaccines—and even implied that the government has killed people who have brought up those questions. They brought up COVID being developed as a bioweapon, referring to the Yan reports [a disinformation campaign promoted by, among others, former President Trump adviser Steve Bannon].

The Brink: In this social media era, lots of people are susceptible to misinformation. What makes that problem more acute, or different, among marginalized folks?

Amazeen: We were in no way trying to imply that these communities are more susceptible [than anyone else]. I think the point is that misinformation and disinformation have been weaponized and targeted to these populations , to sow divides, especially as it relates to the election. That’s not science-related. But there is evidence that Russia tried to create confusion about the safety of [COVID] vaccines, and that very well could have been targeted to communities that tend to already be more distrustful of the medical community. They’re less likely to have primary care physicians, a network in the medical community that they can turn to.

We were in no way trying to imply that these communities are more susceptible [than anyone else]. I think the point is that misinformation and disinformation have been weaponized and targeted to these populations. Michelle Amazeen

The Brink: What can be done about this?

This came up toward the end of our discussion. They wanted to hear from local leaders—whether it’s congresspeople, clergy members, school board members—to talk about science-related issues. But I think misinformation is going to continue to be rampant. Interventions are no match, they’re not a panacea for us being inundated by so much misinformation. And it’s not just on social media. There’s plenty of it on the internet, on cable or radio. One ray of hope we talked about was the public education system making media literacy part of the curriculum. Hand in hand, public education, the public library system, and local communities can work synergistically to educate people about what’s happening. It’s hard to keep up with how quickly technology is evolving, though. ChatGPT wasn’t a thing when I did these focus groups. Deep-fake videos used to require expensive equipment and a good deal of time. Today, you can get something downloaded almost instantaneously and make something that looks realistic. We need to be using any and all the tools that we have, and media literacy education seems to be one of the sharpest, most effective tools we have. I’m hopeful that a new, comparative study I’m involved in will bear this out.

This interview has been edited for brevity and clarity.

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Rich Barlow is a senior writer at BU Today and  Bostonia  magazine. Perhaps the only native of Trenton, N.J., who will volunteer his birthplace without police interrogation, he graduated from Dartmouth College, spent 20 years as a small-town newspaper reporter, and is a former  Boston Globe  religion columnist, book reviewer, and occasional op-ed contributor. Profile

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Welcome to the largest and most comprehensive study of centenarians and their families in the world!

To discover the secrets of a long and healthy life.

Para Español, presiona AQUÍ

Check out our most recent webinar!

Webinar – new england centenarian study – february 29, 2024.

The New England Centenarian Study (NECS) has been enrolling and studying centenarians and their family members since 1995. The NECS has been based at Boston University’s Chobanian and Avedisian School of Medicine since 2002 and it is codirected by Robert D. Evans Distinguished Professor Tom Perls MD, MPH  and Stacy Andersen, PhD .

Paola Sebastiani, PhD and her biostatistics group based at the Center for Quantitative Methods and Data Science (Tufts Medical Center) leads our data analyses efforts and Professor Sebastiani is the co-lead principal investigator the Integrative Longevity Omics Study and the Centenarian Project of the Longevity Consortium.

Some of Our Key Findings:

• Exceptional longevity runs strongly in families.
• Among centenarians, disability is compressed towards at least their early- to mid-nineties.
• At older ages of survival, e.g., age 105+ years, morbidity (age-related diseases) is also compressed towards the end of these exceptionally long lives.
• The genetic influence upon survival increases with older and older ages of survival beyond the nonagenarian years.
• This genetic influence probably involves many genetic variants with individually modest effects, but as a group, they have a strong effect.
• But for some rare exceptions, centenarians have just as many disease-associated genetic variants as the average population. Thus, their genetic advantage is likely due to variants that slow aging and decrease risk for aging-related diseases such as heart disease, stroke, cancer, diabetes and Alzheimer’s Disease.

View our March 2022 Webinar here: Centenarians and Their Families

Our currently funded studies.

The New England Centenarian Study oversees four studies of exceptional longevity that are funded by the National Institute on Aging (NIA), an institute of the National Institutes of Health (NIH).

Visit the Studies page to learn more about each study.

Discoveries & Publications (of >180 peer reviewed papers)

Visit the publications page for more from our investigators., genetic signatures of exceptional longevity in humans.

Genes play a critical and complex role in facilitating exceptional longevity. The genetic influence becomes greater and greater with older and older ages, especially beyond 100 years of age.

• Because many genes are involved, one needs to include many different genes at once (rather than one at a time) in what is called a genetic profile to accurately categorize who is a centenarian and who is not, based on genetic data alone.
• We found 281 genetic markers that are 61% accurate in predicting who is 100 years old, 73% accurate in predicting who is 102 years old or older and 85% accurate in predicting who is 105 years old or older. In other words, the prediction gets better with older and older ages beyond 100 which goes along with our hypothesis that the genetic component of exceptional longevity gets greater and greater with older and older age.
• These 281 markers point to at least 130 genes, many of which have been shown to play roles in Alzheimer’s, diabetes, heart disease, cancers, high blood pressure, and basic biological mechanisms of aging.
• Centenarians have just as many genetic variants (but for a few rare exceptions) associated with increased risk for age-related diseases (like Alzheimer’s, heart disease, stroke, diabetes and cancer) as people in the general population. Therefore, their tremendous survival advantage may in great part be due to the existence of longevity associated genetic variants that are protective and counter the negative effects of such disease gene variants.
• Participants in our study have genetic profiles that can be constructed from these 281 genetic markers (each of which has 3 variations) and these in turn are associated with specific probabilities of achieving very old age. Very interestingly, sub-groups of subjects have genetic profiles in common (what we call genetic signatures). Ninety percent of the 801 centenarians in the New England Centenarian Study can be characterized  by one of  27 genetic signatures.
• These genetic signatures are also associated with different predispositions to subgroups of centenarians such as those that completely escape heart disease, or those that delay Alzheimer’s disease until the last 5% of their very long lives. This method of generating signatures will be very useful for better understanding the underlying genetics of protection from age-related diseases, modulators of rates of aging and for the field of predictive and precision medicine.

Citation: Genetic Signatures of Exceptional Longevity in Humans . Paola Sebastiani, Nadia Solovieff, Andrew T. DeWan, Kyle M. Walsh, Annibale Puca, Stephen W. Hartley, Efthymia Melista, Stacy Andersen, Daniel A. Dworkis, Jemma B. Wilk, Richard H. Myers, Martin H. Steinberg, Monty Montano, Clinton T. Baldwin, Josephine Hoh, Thomas T. Perls.  PloS ONE 2012. DOI: 10.1371/journal.pone.0029848.

Related Citations: Meta-analysis of genetic variants associated with human exceptional longevity . Paola Sebastiani, Harold Bae1, Fangui X. Sun, Stacy L. Andersen, E. Warwick Daw, Alberto Malovini, Toshio Kojima, Nobuyoshi Hirose, Nicole Schupf, Annibale Puca, Thomas T Perls. Aging (Albany NY) 2013 September; 5(9): 653–661.  Published online 2013 August 24. PMCID: PMC3808698

Increasing sibling relative risk of survival to older and older ages and the importance of precise definitions of “aging”, “life span” and “longevity” . Sebastiani P, Sun F, Andersen S, Black M, Perls T.  J Gerontology Biol Sci. 2015;71 :340-346.

Stevenson M, Bae H, Schupf N, Andersen S, Zhang Q, Perls T, Sebastiani P. Burden of disease variants in participants of the long life family study. Aging (Albany NY). 2015 Feb 5. http://www.impactaging.com/papers/v7/n2/pdf/100724.pdf

Limitations and risks of meta-analyses of longevity studies. Sebastiani P, Bae H, Gurinovich A, Soerensen M, Puca A, Perls TT.  Mech Ageing Develop. 2017 http://www.sciencedirect.com/science/article/pii/S0047637416301774

Four Genome-Wide Association Studies Identify New Extreme Longevity Variants. Sebastiani P, Gurinovich A, Bae H, Andersen S, Malovini A, Atzmon G, Villa F, Kraja AT, Ben-Avraham D, Barzilai N, Puca A, Perls TT.  J Gerontol A Biol Sci Med Sci. 2017 Mar 15. doi: 10.1093/gerona/glx027.

The Older You Get, The Healthier You’ve Been

Early on in The New England Centenarian Study, we thought that centenarians had to markedly delay or even escape age-related diseases like heart attacks, stroke, diabetes and Alzheimer’s, or else they would never be able to get to their very old ages. In fact, in 1980, a Stanford researcher named James Fries proposed the “Compression of Morbidity” hypothesis which states that as one approaches the limit of human life span, they must compress the time that they develop diseases towards the very end of their life and he proposed that people around the age of 100 do this.

However, in 2003 we found that many of our centenarian subjects had age related diseases even before the age of 80 (about 43%, and whom we called “survivors” ), after the age of 80 (about 42% and whom we called “delayers” ) and lastly, those who had no mortality-associated diseases at age 100 (about 15% and whom we called “escapers” ). The key though was that 90% of all of the centenarians were still independently functioning at the average age of 93 years. Somehow, despite the presence of diseases, people who become centenarians don’t die from those diseases, but rather they are able to deal with them much better than other people and remain independently functioning more than 30 years beyond the age of 60.

Therefore it seemed to us that for these study participants, it was not so much the compression of morbidity that was important to their survival, but rather a compression of disability.

Citation: Evert J, Lawler E, Bogan H, Perls T. Morbidity profiles of centenarians: survivors, delayers, and escapers. J Gerontol A Biol Sci Med Sci. 2003 Mar;58(3):232-7. doi: 10.1093/gerona/58.3.m232. PMID: 12634289.

Compression of Morbidity Generally Does Not Apply at Age 100, But Rather at Much Rarer Ages, approximately 106+ years

We found that when we were investigating Jim Fries’ compression of morbidity hypothesis, studying people around age 100 was not old enough. After all, the limit of human life span is not 100 years, but instead 122 years. Once we enrolled our hundredth super-centenarian (those age 110+ years old), by far the largest collection of supers in the world, we were able to investigate whether or not people who truly approach the limit of human lifespan actually compress their morbidity towards the end of their lives.

In our study of a reference group, nonagenarians (subjects in their nineties), centenarians (ages 100-104), semi-supercentenarians (ages 105-109) and supercentenarians(ages 110+), the subjects had progressively shorter periods of their lives spent with age-related diseases, from 17.9% of their lives in the referent group, to 9.4% in the nonagenarians and down to 5.2% in the supercentenarians. These findings support the compression of morbidity hypothesis and the idea that there truly is a limit to human life span. We also noted that the supercentenarians were much more alike in terms of the markedly delayed age of onset of age-related diseases compared to the study participants age 100-104 who were quite heterogeneous.

The phenotypic or clinical homogeneity among the supers indicates they must have some factors (presumably genetic) in common that allow them to be so similar. We believe that our oldest subjects give us the best chance and discovering these genes.

Citations: Health span approximates life span among many supercentenarians: Compression of morbidity at the approximate limit of life span  Andersen SL, Sebastiani P, Dworkis DA, Feldman L, Perls T. J Gerontol A Biol Sci Med Sci 2012;67A:395-405.

Families Enriched for Exceptional Longevity also have Increased Health-Span: Findings from the Long Life Family Study . Paola Sebastiani, Fangui X. Sun, Stacy L. Andersen, Joseph H. Lee, Mary K. Wojczynski, Jason L. Sanders, Anatoli Yashin, Anne B. Newman, Thomas T. Perls. Front Public Health. 2013; 1: 38.  PMCID: PMC3859985.

Whole Genome Sequences of 2 Supercentenarians

The New England Centenarian Study, along with collaborators at the Scripps Institute and the University of Florida, Gainesville, performed and published the first-ever whole genome sequence of a supercentenarian –and actually not one super, but two, both over the age of 114 years and one was a man and the other a woman. As with our paper on the genetic signatures of exceptional longevity, we found here as well that centenarians have just as many genetic variants associated with diseases as the general population. However, they likely also have longevity-associated variants that counteract such disease genes, thus allowing for slower aging and increased resistance to age-related diseases.

In this paper we also found several genes that occurred in our published genetic prediction model which had coding regions that led to differences in gene function. These findings support the validity of the genetic prediction model. The New England Centenarian Study has posted the whole genome sequences of these two subjects on a data repository (called dbGaP) based at the National Institutes of Health.

Citation: Whole genome sequences of  male and female supercentenairnas, Both ages >114 years.  Sebastiani P, Riva A, Montano M, Pham P, Torkamani A, Scherba E, Benson G, Milton JN, Baldwin CT, Andersen S, Schork NJ, Steinberg MH, Perls T.  Frontiers in Genetics of Aging 2012;2.

Middle Age Mothers Live Longer and the evolutionary pressure for genes that slow aging and decrease risk for aging related diseases that adversely impact reproduction

There is a growing body of evidence for a substantial genetic influence upon survival to the most extreme ages. An important question is what would be the selection pressure(s) for the evolution of longevity associated genetic variants.  The pressure to have a longer period of time during which women can bear children and therefore have more of them and therefore have greater success in passing one’s genes down to subsequent generations could be one such pressure.  This hypothesis is consistent with the disposable soma theory where the trade-off in energy allocation between reproductive fitness and repair/maintenance functions can be delayed when longevity associated variants facilitate slower aging and the delay or prevention of age-related diseases that also adversely affect fertility.

Several studies have noted an association between older maternal age and an increased odds of exceptional survival. The New England Centenarian Study assessed maternal age history in its sample of female centenarians and a birth-cohort-matched referent sample of women who survived to the cohort’s average life expectancy. Women who gave birth to a child after the age of 40 (fertility assistance was not technologically available to this cohort) had a four times greater odds of being a centenarian.

Numerous investigators are now searching for and investigating genes that influence reproductive fitness in terms of their ability to also influence rate of aging and susceptibility to age-related diseases.

Citations: Middle-aged mothers live longer.  Perls TT, Alpert L, Fretts RC. Nature. 1997 Sep 11;389(6647):133.PMID: 9296486

Extended maternal age at birth of last child and women’s longevity in the Long Life Family Study.  Sun F, Sebastiani P, Schupf N, Bae H, Andersen SL, McIntosh A, Abel H, Elo IT, Perls TT. Menopause. 2015 Jan;22(1):26-31.

Our Data Sharing Policy

The data that we generate are unique and very difficult to come by both because of the rarity of centenarians and also the expense involved in generating the huge amount of clinical and biological data described above. In accordance with NIH/NIA policy all the data that we generate (without sharing participant or family identities) will be posted on the following NIA supported web-portals for sharing with researchers from around the world. Doing so maximizes the research field’s opportunity to make impactful discoveries.

The New England Centenarian Study Investigators are most thankful to the following funders and donors for their financial support and guidance:

• The Paulette and Marty Samowitz Foundation
• The William M. Wood Foundation
• The American Federation of Aging Research
• The Chobanian and Avedisian School of Medicine’s Department of Medicine and Geriatrics Section and the Robert Dawson Evans Distinguished Professorship
• The National Institute on Aging, National Institutes of Health