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When Derek Small watched his father’s early-onset dementia worsen nearly a decade ago, he observed symptoms of neuroinflammation and synaptic dysfunction. Although not a scientist by training, Small already had years of experience launching biotech companies focused on drug discovery development and clinical trials for various disorders and diseases.

Derek Small. Courtesy of Derek Small

Motivated by his father’s dementia journey, Small shifted the focus of his Indianapolis-based venture creation firm, Luson Bioventures, to solely invest in neuroscience biotech startups. Small and a team of Indiana University School of Medicine researchers have since co-founded a startup, Monument Biosciences, dedicated to developing the next generation of Alzheimer’s disease treatments.

“If you have dementia, it’s like you’re a completely different person. Not only do you not remember people’s names, but you also can’t even really function,” said Small, whose father, John Small, died in 2017 at the age of 74. “After all I had been working on in drug discovery, neuroinflammation and synaptic dysfunction were the two phenotypes coming through to me that I felt like we had drugs that could help, or we had ways to target with new drugs.”

After launching a different biotech startup focused on synaptic dysfunction in 2018, Small searched for collaborators to study neuroinflammation.

“I was talking with scientists and pharmaceutical companies all over the world about novel neuroinflammation approaches,” Small said. “I wasn’t just looking in the Midwest.”

That global search eventually led Small back to Indianapolis, where he met Alan Palkowitz, research professor of medicine at the IU School of Medicine and the president and CEO of the Indiana Biosciences Research Institute.

Alan Palkowitz. Photo by Liz Kaye, Indiana University Palkowitz, the former vice president of discovery chemistry research and technologies at Eli Lilly and Company, co-leads the school’s Alzheimer’s disease drug discovery center, called Target Enablement to Accelerate Therapy Development for Alzheimer’s Disease, or TREAT-AD.

“I was extremely excited to learn that a pharmaceutical industry veteran like Alan — someone who has led countless drug-discovery-to-clinical-translation programs in his 25-plus years at Eli Lilly — and the TREAT-AD team were not only working on neuroinflammation,” Small said, “but they were also thinking much bigger than the other research groups I had met with to date around the world and were focusing on a next-generation approach that perfectly aligned with our strategy at Luson Bioventures.”

Monument Biosciences, which is housed within the Indiana Biosciences Research Institute, started to incubate in 2023. Small partnered with Palkowitz and his TREAT-AD co-principal investigators Bruce T. Lamb and Timothy Richardson, along with several other researchers at the IU School of Medicine. The nonprofit research institute is also the home to Luson Bioventures, Syndeio Biosciences and the TREAT-AD laboratories.

“Even in our initial application for TREAT-AD, we envisioned a future scenario where the output of our work would have the potential to reach patients,” Palkowitz said, “We ultimately saw the best way to accomplish this is through a company that could recruit investment and build the right infrastructure to focus on clinical development.

“Derek wanted to start a company focusing on neuroinflammation, which had been the emphasis of our TREAT-AD center. It really was a natural convergence.”

Postdoctoral fellow Chandrama Ahmed and Alex Culver, director of discovery sciences at Monument Biosciences, view images of the brain’s immune cells. Photo by Liz Kaye, Indiana University

IU School of Medicine researchers leading the way

The IU School of Medicine has several programs dedicated to Alzheimer’s disease research, from basic and translational science to clinical research and innovation. The comprehensive program even drew the attention of Bill Gates, the co-founder of Microsoft.

Bruce Lamb. Photo courtesy of IU School of Medicine “When people finally come and see things at the IU School of Medicine, I think they’re shocked about all the activity around Alzheimer’s disease research and the sophistication that’s here relative to anything on either coast,” said Lamb, the executive director of the Stark Neurosciences Research Institute. “When we give people a tour, you can immediately see their perspective change once they see what’s happening.”

In addition to Palkowitz, Lamb and Richardson, Monument Biosciences co-founders from the IU School of Medicine include Stephanie Bissell, Adrian Oblak, Brent Clayton, Jeff Dage and Jared Brosch. Cristian Lasagna-Reeves, a former IU School of Medicine faculty member, is also a co-founder. The group includes investigators who study the biology of Alzheimer’s disease, medicinal chemistry, disease biomarkers and clinical research.

Before launching Monument Biosciences, Small had worked closely with Anantha Shekhar, the former executive associate dean for research at the IU School of Medicine. Small and Shekhar has previously co-founded startups Gate Neurosciences, Syndeio Biosciences and Anagin.

“It’s really extraordinary and actually underappreciated how much the IU School of Medicine has contributed to the neuroscience field,” Small said. “They have world-class quality science, great people and full-service patient care for dementia and Alzheimer’s disease. I consider it one of the top research consortiums in the world for Alzheimer’s disease and related dementias.”

Bridging the gap between basic science and clinical trials

Biotech startups have often bridged the gap — sometimes referred to as the “valley of death” — between basic research and drug development.

“If we’re really thinking about accelerating innovation to patients, placing assets into a company and raising money through investors who are motivated in this space is a great formula,” Palkowitz said. “But at the same time, we’re able to continue to advance science and build on the work we’ve done within TREAT-AD.”

Through Luson Bioventures, Small has launched and led several neuroscience and infectious disease companies, including Assembly Biosciences, Naurex and others, guiding companies as the founding CEO through clinical development, IPOs and strategic exits.

“Our goal is to take lead candidates from the TREAT-AD pipeline and move it toward clinical trials,” Small said. “That’s where our team steps in with the next stages of drug development.”

Dolby Family Ventures is also a major investment partner of Monument Biosciences, Small said. The venture firm was created in honor of Dolby Laboratories founder Ray Dolby, who died of Alzheimer’s disease. The firm funds dozens of companies focused on disease-modifying treatments for Alzheimer’s disease and depression.

Tim Richardson. Photo by Liz Kaye, Indiana University

TREAT-AD, which launched in 2019 and received a five-year grant renewal in December 2024 from the National Institute on Aging, narrowed down a list of hundreds of potential drug targets for Alzheimer’s disease to a portfolio of five that are promising potential new therapies.

Monument Biosciences set up an exclusive licensing arrangement with the IU Innovation and Commercialization Office to develop drug targets discovered through TREAT-AD into potential therapeutics for clinical trials. Richardson said the center’s portfolio of targets focuses on the neuro-inflammatory component of Alzheimer’s disease, a novel way of approaching the disease. potential therapeutics for clinical trials. Richardson said the center’s portfolio of targets focuses on the neuro-inflammatory component of Alzheimer’s disease, a novel way of approaching the disease.

“TREAT-AD hopes to take Alzheimer’s disease treatments to the next level by focusing on microglia, a specialized type of immune cell primarily responsible for clearing amyloid and protecting the brain,” Richardson said.

One of the center’s most advanced projects is targeting a microglial-specific gene associated with Alzheimer’s disease, which the team received a five-year grant from the National Institute on Aging to study. The gene, INPP5D, encodes the protein SHIP1 and is also one of the top targets for Monument Biosciences, Richardson said, along with the gene PLCG2, an immune cell-specific gene that has also been rigorously studied by IU School of Medicine researchers.

“I don’t think we’ve been in a more exciting period for the potential of impacting Alzheimer’s patients with new innovation,” Palkowitz said. “Our hope is that what we’re doing through Monument Biosciences and having our roots in the research community at IU and the Indiana Biosciences Research Institute is going to make a big impact on the disease. We look forward to what the future holds.”

Sugar is everywhere, hidden in drinks, snacks, and even foods we think of as healthy. For decades, it has been at the center of debates on obesity, diabetes, and heart health. But now, the World Health Organization (WHO) is sounding the alarm on another consequence of our sugar-heavy diets: tooth decay.According to the agency, removing or even sharply reducing sugar intake could protect billions worldwide from the world’s most common noncommunicable disease.

What WHO has said

WHO estimates that over 2.5 billion people currently live with dental caries, including more than 2 billion adults with cavities in permanent teeth and over half a billion children with decayed baby teeth.

The agency identifies free sugars—those added to processed foods and drinks, or naturally present in items like syrups, honey, and fruit juices—as the key dietary risk factor. Its recommendation is firm: limit free sugar intake to less than 10% of daily calories, and ideally under 5%, to significantly lower the risk of decay across a lifetime.

Understanding dental caries

Dental caries, often referred to as tooth decay or cavities, is more than a cosmetic concern. It is a disease process where the structure of the tooth is gradually destroyed by acid produced when bacteria in plaque metabolize sugar. The first signs may be mild sensitivity, but if left untreated, decay can lead to persistent toothache, pain while chewing, and visible pits or holes.Advanced cases cause infection, tooth loss, and even difficulty eating, speaking, or sleeping, which can take a serious toll on overall health and quality of life.

How it develops

Tooth decay develops through a continuous cycle. After consuming sugary foods or drinks, bacteria in plaque break down those sugars into acids. These acids attack the enamel—the hard protective layer of the tooth—weakening it over time. If the cycle continues unchecked, cavities form and progress deeper, eventually reaching the inner tooth structures.

The real culprit

While multiple factors can contribute to poor dental health, WHO is clear that sugar is the main driver of caries worldwide. Hidden sugars in sodas, packaged juices, breakfast cereals, sauces, and even so-called health bars mean that many people exceed safe levels without realizing it.And it is not just cavities, that one needs to worry about. Diets high in free sugars contribute to obesity, type 2 diabetes, and cardiovascular disease.

How to prevent tooth decay?

The good news is that tooth decay is largely preventable. Cutting down on sugar is the most effective step, but it must be paired with daily oral hygiene, including brushing twice with fluoride toothpaste and flossing to remove plaque. Regular dental check-ups can help detect early signs before they progress to more serious problems. On a wider scale, WHO calls for public health policies such as taxing sugary drinks, reformulating processed foods, and educating families about sugar’s hidden presence in everyday diets.

COVID-19 infection appears to cause women’s blood vessels to age prematurely, potentially increasing their risk of heart disease, a new study says.

Women infected with COVID-19 experienced about five additional years of blood vessel aging, even if they had a mild case, according to results published Aug. 17 in the European Heart Journal.

If a woman landed in the intensive care unit with severe COVID, her blood vessels received up to 10 years of premature aging, results show.

“We know that COVID can directly affect blood vessels. We believe that this may result in what we call early vascular aging, meaning that your blood vessels are older than your chronological age and you are more susceptible to heart disease,” lead researcher Dr. Rosa Maria Bruno, a professor of clinical pharmacology at Université Paris Cité in France, said in a news release.

“If that is happening, we need to identify who is at risk at an early stage to prevent heart attacks and strokes,” Bruno added.

Men also experienced blood vessel aging as a result of COVID-19 infection, but the effect was not statistically significant among the participants studied, researchers report.

For the study, researchers tested 2,400 people from 16 countries recruited between September 2020 and February 2022.

The participants included people not infected by COVID-19, as well as COVID-19 patients who didn’t require hospitalization, were treated in a hospital or had an infection severe enough to require time in an intensive care unit.

Researchers assessed each person’s vascular age with a device that measures how quickly a wave of blood pressure travels between the carotid artery in the neck and the femoral arteries of the legs.

This measurement is called carotid-femoral pulse wave velocity. The higher this number, the stiffer and older a person’s blood vessels have become, researchers said.

Measurements taken six months and a year after a person’s COVID-19 infection showed that all three groups had stiffer arteries compared to those who were never infected:

The average increase in PWV was 0.55 meters per second for women who had mild COVID-19 and 0.6 meters per second for women hospitalized with COVID-19.

For women treated in an ICU, the average increase in PWV was 1.09 meters per second.

Researchers said an increase of about 0.5 meters per second is “clinically relevant” and equivalent to aging of around five years. For example, it would increase risk of heart disease by about 3% in a 60-year-old woman.

People who had persistent symptoms of long COVID-19, such as shortness of breath or fatigue, were more likely to have prematurely aged arteries, researchers said.

In fact, this effect on the arteries might help explain some of the long COVID-19 symptoms reported by as many as 40% of COVID-19 patients, Dr. Behnood Bikdeli, a cardiologist at Harvard Medical School, noted in an accompanying editorial.

“Vascular injury — marked by endothelial dysfunction, inflammation and coagulation abnormalities — is a key mechanism driving these complications,” Bikdeli wrote.

On the other hand, people who had been vaccinated against COVID-19 generally had arteries that were less stiff compared to the unvaccinated.

There are several potential explanations for why COVID-19 might cause premature stiffening in the arteries, Bruno said.

“The COVID-19 virus acts on specific receptors in the body, called the angiotensin-converting enzyme 2 receptors, that are present on the lining of the blood vessels,” she said. “The virus uses these receptors to enter and infect cells. This may result in vascular dysfunction and accelerated vascular aging.”

Bruno said the body’s inflammation and immune responses, defenses against infection, may also be involved.

Immune response might also explain the difference between women and men, she said.

“Women mount a more rapid and robust immune response, which can protect them from infection,” Bruno said. “However, this same response can also increase damage to blood vessels after the initial infection.”

Doctors should perform vascular aging tests on COVID-19 patients and treat those affected with drugs to lower their blood pressure and cholesterol, Bruno said. Lifestyle changes such as a healthy diet and regular exercise also can help protect their heart health.

“For people with accelerated vascular aging, it is important to do whatever possible to reduce the risk of heart attacks and strokes,” Bruno said.

The researchers plan to continue following participants to see whether their accelerated vascular aging actually leads to an increased risk of heart attack and stroke.

More information

The U.S. Centers for Disease Control and Prevention has more on long COVID.

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