Major progress on identify Alzheimer’s before symptoms arise

A blood test to detect the brain changes of early Alzheimer’s disease has moved one step closer to reality. Researchers from Washington University School of Medicine in St. Louis report that they can measure levels of the Alzheimer’s protein amyloid beta in the blood and use such levels to predict whether the protein has accumulated in the brain. The findings represent a key step toward a blood test to diagnose people on track to develop the devastating disease before symptoms arise

When combined with age and genetic risk factor, test is 94% accurate

Up to two decades before people develop the characteristic memory loss and confusion of Alzheimer’s disease, damaging clumps of protein start to build up in their brains. Now, a blood test to detect such early brain changes has moved one step closer to clinical use.

Researchers from Washington University School of Medicine in St. Louis report that they can measure levels of the Alzheimer’s protein amyloid beta in the blood and use such levels to predict whether the protein has accumulated in the brain. When blood amyloid levels are combined with two other major Alzheimer’s risk factors – age and the presence of the genetic variant APOE4 – people with early Alzheimer’s brain changes can be identified with 94% accuracy, the study found.

The findings, published Aug. 1 in the journal Neurology, represent another step toward a blood test to identify people on track to develop Alzheimer’s before symptoms arise. Surprisingly, the test may be even more sensitive than the gold standard – a PET brain scan – at detecting the beginnings of amyloid deposition in the brain.

Such a test may become available at doctors’ offices within a few years, but its benefits will be much greater once there are treatments to halt the disease process and forestall dementia. Clinical trials of preventive drug candidates have been hampered by the difficulty of identifying participants who have Alzheimer’s brain changes but no cognitive problems. The blood test could provide a way to efficiently screen for people with early signs of disease so they can participate in clinical trials evaluating whether drugs can prevent Alzheimer’s dementia.

“Right now we screen people for clinical trials with brain scans, which is time-consuming and expensive, and enrolling participants takes years,” said senior author Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology. “But with a blood test, we could potentially screen thousands of people a month. That means we can more efficiently enroll participants in clinical trials, which will help us find treatments faster, and could have an enormous impact on the cost of the disease as well as the human suffering that goes with it.”

The test, an earlier version of which first was reported two years ago, uses a technique called mass spectrometry to precisely measure the amounts of two forms of amyloid beta in the blood: amyloid beta 42 and amyloid beta 40. The ratio of the two forms goes down as the amount of amyloid beta deposits in the brain goes up.

The current study involved 158 adults over age 50. All but 10 of the participants in the new study were cognitively normal, and each provided at least one blood sample and underwent one PET brain scan. The researchers classified each blood sample and PET scan as amyloid positive or negative, and found that the blood test from each participant agreed with his or her PET scan 88 percent of the time, which is promising but not accurate enough for a clinical diagnostic test.

In an effort to improve the test’s accuracy, the researchers incorporated several major risk factors for Alzheimer’s. Age is the largest known risk factor; after age 65, the chance of developing the disease doubles every five years. A genetic variant called APOE4 raises the risk of developing Alzheimer’s three- to fivefold. And gender also plays a role: Two out of three Alzheimer’s patients are women.

When the researchers included these risk factors in the analysis, they found that age and APOE4 status raised the accuracy of the blood test to 94%. Sex did not significantly affected the analysis.

“Sex did affect the amyloid beta ratio, but not enough to change whether people were classified as amyloid positive or amyloid negative, so including it didn’t improve the accuracy of the analysis,” said first author Suzanne Schindler, MD, PhD, an assistant professor of neurology.

Further, the results of some people’s blood tests initially were considered false positives because the blood test was positive for amyloid beta but the brain scan came back negative. But some people with mismatched results tested positive on subsequent brain scans taken an average of four years later. The finding suggests that, far from being wrong, the initial blood tests had flagged early signs of disease missed by the gold-standard brain scan.

There is growing consensus among neurologists that Alzheimer’s treatment needs to begin as early as possible, ideally before any cognitive symptoms arise. By the time people become forgetful, their brains are so severely damaged no therapy is likely to fully heal them. But testing preventive treatments requires screening thousands of healthy people to find a study population of people with amyloid build-up and no cognitive problems, a slow and expensive process.

As part of the study, the researchers analyzed the enrollment process for a prominent Alzheimer’s prevention trial called the A4 study that used PET scans to confirm the presence of early Alzheimer’s brain changes in potential participants. They concluded that prescreening with a blood test followed by a PET scan for confirmation would have reduced the number of PET scans needed by two thirds. Unlike blood tests, which cost a few hundred dollars, each PET scan costs upward of $4,000. A single site can only run a few dozen PET brain scans a month, because PET scanners are primarily reserved for patient care, not research studies.

“If you want to screen an asymptomatic population for a prevention trial, you would have to screen, say, 10,000 people just to get 1,500 or 2,000 that would qualify,” Bateman said. “Reducing the number of PET scans could enable us to conduct twice as many clinical trials for the same amount of time and money. It’s not the $4,000 per PET scan that we’re worried about. It’s the millions of patients that are suffering while we don’t have a treatment. If we can run these trials faster, that will get us closer to ending this disease.”

Learn more: Blood test is highly accurate at identifying Alzheimer’s before symptoms arise

 

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Could immunotherapy be effective against pancreatic cancer?

ROHEENA PANNI
Pancreatic tumors were much smaller in mice that had been treated with compound ADH-503 (right, tumor outlined in yellow) than in untreated mice (left). Researchers at Washington University School of Medicine in St. Louis and Rush University in Chicago have found a compound that promotes a vigorous immune assault on pancreatic cancer. The findings suggest a way to improve immunotherapy for the deadly disease in patients.

Chemical compound extends survival by months, in mice

Pancreatic cancer is especially challenging to treat – only eight percent of patients are still alive five years after diagnosis. Chemotherapy and radiation therapy are of limited benefit, and even immunotherapy – which revolutionized treatment for other kinds of cancer by activating the body’s immune system to attack cancer cells – has been largely ineffective because pancreatic tumors have ways to dampen the immune assault.

Now, researchers at Washington University School of Medicine in St. Louis and Rush University in Chicago have found a chemical compound that promotes a vigorous immune assault against the deadly cancer. Alone, the compound reduces pancreatic tumor growth and metastases in mice. But when combined with immunotherapy, the compound significantly shrank tumors and dramatically improved survival in the animals.

The findings, published July 3 in Science Translational Medicine, suggest that the immune-boosting compound could potentially make resistant pancreatic cancers susceptible to immunotherapy and improve treatment options for people with the devastating disease.

“Pancreatic cancer is a highly lethal disease, and we are in desperate need of new therapeutic approaches,” said co-senior author David DeNardo, PhD, an associate professor of medicine and of pathology and immunology at Washington University School of Medicine. “In animal studies, this small molecule led to very marked improvements and was even curative in some cases. We are hopeful that this approach could help pancreatic cancer patients.”

On paper, immunotherapies for pancreatic cancer seem like a good idea. The technique works by releasing a brake on specialized immune cells called T cells so they can attack the cancer. In the past, researchers working in the lab found they could release the brake and prod T cells into killing pancreatic cancer cells. But when doctors tried to treat people with pancreatic cancer using immunotherapies, fewer than five percent of patients improved.

This failure of immunotherapy in pancreatic cancer has puzzled scientists. But T cells aren’t the only player in the immune assault on cancer. Myeloid cells, another kind of immune cell found in and around tumors, can either tamp down or ramp up the immune response. They tilt the playing field by releasing immune molecules that affect how many T cells are recruited to the tumor, and whether the T cells show up at the tumors activated and ready to kill, or suppressed and inclined to ignore the tumor cells. In pancreatic tumors, myeloid cells typically suppress other immune cells, undermining the effects of immunotherapy.

DeNardo, co-senior author Vineet Gupta, PhD, of Rush University, and colleagues realized that releasing the brake on T cells might not be enough to treat pancreatic cancer. Unleashing the power of immunotherapy might require also shifting the balance of myeloid cells toward those that activate T cells to attack.

The researchers identified a compound, called ADH-503, that interferes with the migration of myeloid cells. Normally, pancreatic tumors are teeming with myeloid cells that suppress the immune response. When the researchers gave the compound to mice with pancreatic cancer, the number of myeloid cells in and near the tumors dropped, and the remaining myeloid cells were of the kind that promoted, rather than suppressed, immune responses. This environment translated into greater numbers of cancer-killing T cells in the tumor, significantly slower tumor growth and longer survival.

Then, the researchers – including first author Roheena Panni, MD, resident in general surgery at Washington University and Barnes-Jewish Hospital, and co-author William Hawkins, MD, the Neidorff Family and Robert C. Packman Professor of Surgery at Washington University School of Medicine – investigated whether creating this same environment could make pancreatic tumors susceptible to standard immunotherapy. First, they treated mice with a so-called PD-1 inhibitor, a standard immunotherapy used to treat other kinds of cancer. Unsurprisingly, they saw no effect. But when the researchers gave the mice the immunotherapy in conjunction with ADH-503, the tumors shrank and the mice survived significantly longer. In some experiments, all the tumors disappeared within a month of treatment, and all the mice survived for four months, when the researchers stopped monitoring them. In comparison, all the untreated mice died within six weeks.

Gupta noted that while pancreatic cancer is the third leading cause of cancer-related death in the United States, only about three percent of clinical trials for cancer immunotherapies target pancreatic cancer.

“Unlocking the promise of immunotherapies for pancreatic cancer requires a new approach,” Gupta said. “We believe these data demonstrate that targeting myeloid cells can help overcome resistance to immunotherapies.”

The strategy of boosting antitumor immune activity by shifting the balance of myeloid cells improved the effectiveness of other pancreatic cancer therapies as well, the researchers said. Mice treated with chemotherapy or radiation therapy both fared significantly better when ADH-503 was added to the regimen.

“You can’t make a one-to-one translation between animal studies and people, but this is very encouraging,” DeNardo said. “More study is needed to understand if the compound is safe and effective in people, which is why Gossamer Bio, Inc., is starting phase I safety studies in people later this year at Washington University and other sites.”

Learn more: Immune-boosting compound makes immunotherapy effective against pancreatic cancer

 

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Aging delayed . . . in mice for now

via Washington University School of Medicine

An enzyme in blood of young mice extends life span

New research has identified a novel approach to staving off the detrimental effects of aging, according to a study from Washington University School of Medicine in St. Louis.

The study suggests that a protein that is abundant in the blood of young mice plays a vital role in keeping mice healthy. With age, levels of this protein decline in mice and people, while health problems such as insulin resistance, weight gain, cognitive decline and vision loss increase. Supplementing older mice with the protein obtained from younger mice appears to slow this decline in health and extend the life spans of older mice by about 16 percent.

The study is published June 13 in the journal Cell Metabolism.

The circulating protein is an enzyme called eNAMPT, which is known to orchestrate a key step in the process cells use to make energy. With age, the body’s cells become less and less efficient at producing this fuel — called NAD — which is required to keep the body healthy. Washington University researchers have shown that supplementing eNAMPT in older mice with that of younger mice appears to be one route to boosting NAD fuel production and keeping aging at bay.

“We have found a totally new pathway toward healthy aging,” said senior author Shin-ichiro Imai, MD, PhD, a professor of developmental biology. “That we can take eNAMPT from the blood of young mice and give it to older mice and see that the older mice show marked improvements in health — including increased physical activity and better sleep — is remarkable.”

Imai has long studied aging, using mice as stand-ins for people. Unlike other studies focused on transfusing whole blood from young mice to old mice, Imai’s group increased levels of a single blood component, eNAMPT, and showed its far-reaching effects, including improved insulin production, sleep quality, function of photoreceptors in the eye, and cognitive function in performance on memory tests, as well as increased running on a wheel. Imai’s group also has shown other ways to boost NAD levels in tissues throughout the body. Most notably, the researchers have studied the effects of giving oral doses of a molecule called NMN, the chemical eNAMPT produces. NMN is being tested in human clinical trials.

“We think the body has so many redundant systems to maintain proper NAD levels because it is so important,” Imai said. “Our work and others’ suggest it governs how long we live and how healthy we remain as we age. Since we know that NAD inevitably declines with age, whether in worms, fruit flies, mice or people, many researchers are interested in finding anti-aging interventions that might maintain NAD levels as we get older.”

Imai’s research has shown that the hypothalamus is a major control center for aging throughout the body, and it is directed in large part by eNAMPT, which is released into the blood from fat tissue. The hypothalamus governs vital processes such as body temperature, thirst, sleep, circadian rhythms and hormone levels. The researchers have shown that the hypothalamus manufactures NAD using eNAMPT that makes its way to the brain through the bloodstream after being released from fat tissue. They also showed that this eNAMPT is carried in small particles called extracellular vesicles. As levels of eNAMPT in the blood decline, the hypothalamus loses its ability to function properly, decreasing life span.

In an intriguing finding, Imai and first author Mitsukuni Yoshida, a doctoral student in Imai’s lab, showed that levels of eNAMPT in the blood were highly correlated with the number of days the mice lived. More eNAMPT meant a longer life span, and less meant a shorter one.

The researchers also showed increased life span with delivering eNAMPT to normal old mice. All mice that received saline solution as a control had died before day 881, about 2.4 years. Of the mice that received eNAMPT, one is still alive as of this writing, surpassing 1,029 days, or about 2.8 years.

“We could predict, with surprising accuracy, how long mice would live based on their levels of circulating eNAMPT,” Imai said. “We don’t know yet if this association is present in people, but it does suggest that eNAMPT levels should be studied further to see if it could be used as a potential biomarker of aging.”

The study also found sex differences in levels of eNAMPT, with female mice consistently showing higher levels of the enzyme.

“We were surprised by the dramatic differences between the old mice that received the eNAMPT of young mice and old mice that received saline as a control,” Imai said. “These are old mice with no special genetic modifications, and when supplemented with eNAMPT, their wheel-running behaviors, sleep patterns and physical appearance — thicker, shinier fur, for example — resemble that of young mice.”

Learn more: Aging delayed in older mice given blood component from young mice

 

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Can drug resistance in tuberculosis be reversed?

Mycobacterium tuberculosis – the bacteria shown here in a colorized electron micrograph – cause tuberculosis, the most lethal infectious disease in the world. Researchers at Washington University School of Medicine in St. Louis and Umea University in Sweden have found a compound that can prevent and even reverse antibiotic resistance in TB bacteria.

About 1.5 million people died of tuberculosis (TB) in 2017, making it the most lethal infectious disease worldwide. A growing rise in drug-resistant TB is a major obstacle to successfully treating the illness.

Now, researchers at Washington University School of Medicine in St. Louis and Umea University in Sweden have found a compound that prevents and even reverses resistance to isoniazid, the most widely used antibiotic for treating tuberculosis.

The research, published the week of May 6 in Proceedings of the National Academy of Sciences, was conducted in bacteria growing in the lab, setting the stage for future studies in animals and people.

Using the compound in conjunction with isoniazid potentially could restore the antibiotic’s effectiveness in people with drug-resistant tuberculosis. The compound also may bolster the antibiotic’s power to kill TB bacteria – even those sensitive to drugs – which means doctors could start thinking about cutting down the onerous six-month treatment regimen they prescribe today.

“It is very hard for people to comply with such a long regimen,” said co-senior author Christina Stallings, PhD, an associate professor of molecular microbiology at the School of Medicine. “It’s four drugs. They have side effects. It’s no fun. The longer people have to be on antibiotics, the more issues with patient compliance you get, and that can lead to drug resistance and treatment failure. Here, we’ve found a compound that sensitizes bacteria to an antibiotic, prevents drug resistance from arising, and even reverses drug resistance – at least in the lab. If we can turn this compound into a drug for people, it could make our current therapies more effective and be really beneficial for fighting this pandemic.”

Tuberculosis is caused by the bacterium Mycobacterium tuberculosis. Once inside the body, the bacteria morph into a tougher form that can withstand more stress and is harder to kill. Rather than look for new and better antibiotics, Stallings and co-first authors Kelly Flentie, PhD, a former postdoctoral researcher at Washington University, and Gregory Harrison, a graduate student, decided to look for compounds that prevent the bacteria from toughening up. When put in a low-oxygen environment to mimic the stressful conditions TB bacteria encounter inside the body, the bacteria come together and form a thin film called a biofilm that is resilient to not only low-oxygen conditions but also to antibiotics and other stressors.

With the help of co-senior author Fredrik Almqvist, PhD, a professor of chemistry at Umea University, they screened 91 compounds that share a core chemical structure that inhibits biofilms in other bacterial species. The researchers found one compound, called C10, that did not kill the TB bacteria but prevented them from forming a biofilm.

Further experiments showed that blocking biofilm formation with C10 made the bacteria easier to kill with antibiotics and even curbed the development of antibiotic resistance. The researchers needed only a fraction of the amount of isoniazid to kill the TB bacteria when C10 was included than with isoniazid alone. In addition, one out of 1 million TB bacteria spontaneously become resistant to isoniazid when grown under typical laboratory conditions. But when the researchers grew TB bacteria with isoniazid and the compound, the drug-resistant mutant bacteria never arose.

“By combining C10, or something like it, with isoniazid we could enhance the potency of the antibiotic and block the TB bacteria from developing drug resistance,” Stallings said. “That means we might be able to shorten the treatment regimen.”

Most surprisingly, the compound even reversed drug resistance. TB bacteria with mutations in the gene katG can withstand isoniazid treatment. But such bacteria die when treated with isoniazid plus the compound, the researchers discovered. The bacteria had not lost their genetic resistance, but they’d lost the ability to survive when exposed to isoniazid, as long as it was given alongside C10.

“This was a totally unexpected finding,” Stallings said. “We had no idea we would be able to reverse drug resistance. But this could mean that with all those millions of isoniazid-resistant TB cases, if we use something like C10, we could give people the option of using isoniazid again.”

The compound is not ready to be used in people or even tested in animals, Stallings cautioned. This study was conducted on bacteria growing in a lab. The researchers are still figuring out whether the compound is safe and how it might be processed by the body.

“We have this great compound, and we’ve shown that it’s possible to prevent and reverse antibiotic resistance,” Stallings said. “But now we have to either improve on the compound itself so we can start testing it in animals, or figure out how it prevents biofilm formation so we can develop other drugs that target the pathway. We have a new strategy to treat TB, but it’s going to take time before it’s a reality.”

 

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Cavitation dose painting would allow precise delivery of a certain amount of drugs to an exact location

Researchers from the McKelvey School of Engineering and Washington University School of Medicine in St. Louis are one step closer to delivering precise amounts of medication to exact location, repurposing an existing imaging “painting” method. Cavitation images (left); PET images (middle); overlay of the two (right). (Courtesy: Hong Chen lab)

Researchers are integrating ultrasound imaging with ultrasound therapy to pave the way for a new kind of drug delivery

If traditional drug delivery were a type of painting, it might be akin to paintball. With good aim, a majority of the paint ends on the bullseye, but it also drips and splashes, carrying streams of paint across the target.

If the drug needs to enter the bloodstream and circulate throughout your body for treating disease wherever it may be, this paintball-like delivery system may work. But it won’t work for targeted and precise drug delivery.

A more acute delivery approach would look more like “painting by numbers,” a technique that would allow precise delivery of a certain amount of drugs to an exact location. Researchers at the McKelvey School of Engineering and the School of Medicine at Washington University in St. Louis are developing the tools necessary for such a drug delivery system, which they call cavitation dose painting.

Their research was published online this week in Scientific Reports.

Using focused ultrasound with its contrast agent, microbubbles, to deliver drugs across the blood-brain barrier (FUS-BBBD), the research team, led by Hong Chen, assistant professor of biomedical engineering at McKelvey School of Engineering, and assistant professor of radiation oncology at the School of Medicine, was able to overcome some of the uncertainty of drug delivery.

This method takes advantage of the microbubbles expanding and contracting when they interact with the ultrasound, essentially pumping the intravenously-delivered drug to wherever the ultrasound is pointing.

To determine where and how much of the drugs were being delivered, the researchers used nanoparticles tagged with radio labels to represent drug particles, then used positron emission tomography (PET) imaging to track their whereabouts and concentrations. They could then create a detailed image, showing where the nanoparticles were going and in what concentrations.

There’s one hitch, though.

“The problem is, PET imaging is expensive and associated with radioactive exposure,” Chen said.

So the team turned to passive cavitation imaging (PCI), an ultrasound imaging technique that has been under development by several groups for imaging the spatial distribution of microbubble cavitation, or the oscillation of microbubbles in the ultrasound field.

To determine whether PCI could also accurately determine the amount of drugs at a certain location, they correlated a PCI image with a PET image (which they knew can quantify the concentration of radioactive agents).

“We found there’s pixel by pixel correlation between the ultrasound imaging and the PET imaging,”  said Yaoheng Yang, the lead author of this study and a second-year PhD student in the Department of Biomedical Engineering. The PCI image, therefore, can be used to predict where a drug goes and how much drug is there. Hence, she called the new technique cavitation dose painting.

Going forward, Chen believes this method could drastically change the way some drugs are delivered. Using cavitation dose painting in tandem with focused ultrasound will allow doctors to deliver precise amounts of drugs to specific locations, for example, targeting different areas of a tumor with exactitude.

“I think this cavitation dose painting technique in combination with focused ultrasound-enabled brain drug delivery opens new horizons in spatially targeted and modulated brain drug delivery,” Chen said.

Learn more: A new method for precision drug delivery: painting

 

 

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