Food is more than the energy that fuels our bodies it is preventive medicine. Maybe not a cheesy chimichanga, but the type of food that is loaded with vitamins and proteins can maximize the benefits to the human body.

We need to look at the functional properties of food more closely so we can achieve the desired outcome, said Justin Siegel, associate professor of chemistry, biochemistry and molecular medicine, and faculty director for the Innovation Institute for Food and Health. Instead of focusing on the quantity of food which is a legitimate long-term concern globally lets hone in on creating quality food that possesses more active nutritional ingredients that deliver greater health benefits with every serving.

Siegel has a vision to transform the greater Sacramento region into the incubator pipeline for food science innovations. The initiative, dubbed Food Valley, would accelerate the commercialization of game-changing ideas across the food system by tapping into research, industry and policy. It would also prepare tomorrows food innovators and entrepreneurs through experiential learning programs.

Food Valley aims to patent its food innovations through developing technologies. These concepts can be grown into companies and potentially be a launchpad for Aggie entrepreneurs.

Siegel became interested in biotechnology as a kid. More recently, he thought about the possibilities of using biotech to disrupt the food systems industry. He co-founded PVP Biologics, a food biotech company, in 2016. PVP created a pill called KumaMax, which could help those who have celiac disease. KumaMax is currently in clinical trials, awaiting FDA approval.

Food Valley is about letting people experience freedom in what they are able to eat especially as it pertains to food allergies and restrictions, Siegel said. With modern technology we can both see the exact molecules that make up our food and manipulate those molecules to change how they interact with someones body.

No centralized hub for food innovations exists yet. Siegel said he believes UCDavis has the right ingredients to emerge as the leader.

Twenty years ago, this was science fiction, he said. Now we can do things we never thought possible. There is going to be a hub for food innovation, and UCDavis should be the place it happens.

This is one of several Big Ideas, forward-thinking, interdisciplinary programs and projects that will build upon the strengths of UCDavis to positively impact the world for generations to come. Learn more at bigideas.ucdavis.edu.

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06 September 2019, Berlin: After a group music therapy session in a dementia residential community ... [+] in Berlin-Neuklln, which is looked after by the Unionhilfswerk, one resident holds hands. In Germany, the number of people suffering from dementia is increasing. Although the sick forget more and more, music can reawaken certain memories - at least for a moment. (to dpa "Dit one does not forget" - with music memories awaken) Photo: Christoph Soeder/dpa (Photo by Christoph Soeder/picture alliance via Getty Images)

Alzheimers is a devastating diagnosis for people suffering from the disease, as well as their families, but a group of researchers feels that they are one step closer to finding a cure.

Alzheimer's disease (AD) affects about 5.7 million people in the US and is the leading cause of age-related dementia today. Many people suffering from AD face a myriad of challenges including the lack of effective treatments, reliable biomarkers, or preventive strategies. Unfortunately, several promising drug candidates in the past have failed in clinical trials so researchers are still searching for new preventions or therapies to combat the development of AD. But there seems to be hope with a new vaccine that may proceed to clinical trials after successful animal testing.

A new paper in the journalAlzheimer's Research & Therapyis opening the door for further research in 2020, with medical researchers at the Institute for Molecular Medicine and University of California, Irvine (UCI) working with a successful vaccine formulated on adjuvants(1) developed by Flinders University Professor Nikolai Petrovsky in South Australia.

The causes of AD, in part, are believed to be tied to the role two proteins in the brain;

It is these two proteins that the US-led research team is looking to develop effective immunotherapy for via a new vaccine to remove brain plaques and tau protein tangles.

As explained in the research teams report, Alzheimer disease (AD) is characterised by the accumulation of beta-amyloid (A) plaques and neurofibrillary tangles composed of hyperphosphorylated(2) tau, which together lead to neurodegeneration and cognitive decline, continuing that, Current therapeutic approaches have primarily aimed to reduce pathological aggregates of either A or tau, yet phase 3 clinical trials of these approaches have thus far failed to delay disease progression in humans. The researchers contend that combinatorial therapies that concurrently target both A and tau might be needed for effective disease modification.

The research teams claims that recent success in their tests with mice supports progression to human trials in years to come, sparking hope in he field. "Our approach is looking to cover all bases and get past previous roadblocks in finding a therapy to slow the accumulation of A/tau molecules and delay AD progression in a the rising number of people around the world," says Professor Petrovsky.

However, one downside of the potential vaccine is thatit could not currently be used as a preventive measure in healthy subjects due to the need for frequent (monthly) administration of high concentrations of immunotherapeutic drugs, which are a class of drugs targeting the immune system to either kickstart or suppress immune function.

However, if future human trials are successful, the new paper concludes that the new combined vaccination approach could potentially be used to induce strong immune responses to both of the hallmark pathologies of AD in a broad population base of vaccinated subjects with high MHC (major histocompatibility complex(3)) class II gene polymorphisms, stating that, This synergistic model suggests that combinatorial/multi-target therapies directed at the accumulation of both amyloid and tau pathologies may be more effective in the treatment of AD than previously tested unimodal approaches.

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Researchers may have found a way to prevent Duchenne muscular dystrophy-related heart disease, the leading cause of death in patients living with the disease.

The study examines the role of Connexin-43 (Cx43), a protein that regulates heart function. The researchers found that Cx43 was dysfunctional in both human and mouse Duchenne muscular dystrophy (DMD) hearts, so they modified the Cx43 protein in the hopes of alleviating heart disease.

They discovered that altering the Cx43 protein through a process called phosphorylation protected DMD mice against irregular heart beat and late-stage failure.

DMD, a genetic disorder characterized by progressive muscle degeneration, is the most common type of muscular dystrophy, affecting about one in 5,000 males and typically beginning at about age 4. The average life expectancy is 26.

For many DMD patients, the heart muscles gradually break down, leading to death. Our findings may help give hope to millions of patients, says study coauthor Diego Fraidenraich, an assistant professor of cell biology and molecular medicine at Rutgers University New Jersey Medical School.

Medical advances have managed to slow down the disease progression in most muscles in the body, but there are yet to be any discoveries that target or prevent deterioration of the DMD heart, which remains the number one killer among these patients, says coauthor Eric Himelman, a PhD candidate. Therapies based on our finding may help prolong the lives of muscular dystrophy and other heart disease patients.

Next steps include developing drugs that directly target Cx43 in DMD hearts, with a goal of potentially introducing clinical trials using Cx43 modification as a therapy for DMD patients.

The study appears in the Journal of Clinical Investigation. Another study in JCI Insight also examined Cx43 activity in the heart.

The National Institutes of Health, the Muscular Dystrophy Association, and the American Heart Association funded the work.

Additional researchers are from Rutgers, the Fred Hutchinson Cancer Research Center, New York University, and Baylor College of Medicine.

Source: Rutgers University

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Research focuses on precisely how the disease develops in the brain

Anne Fagan, PhD, supervises staff scientist Matthew R. Amos as he analyzes samples for molecular signs of Alzheimer's disease. Fagan leads one arm of a long-running, international Alzheimers study aimed at understanding how the disease develops and progresses. Researchers at Washington University School of Medicine in St. Louis have received $29 million to continue the study known as the Dominantly Inherited Alzheimer Network for another five years.

For more than a decade, Washington University School of Medicine in St. Louis has led an international effort to better understand Alzheimers disease by studying people with rare genetic mutations that cause the disease to develop in their 50s, 40s or even 30s. The researchers have shown that the disease begins developing two decades or more before peoples memories begin to fade, as damaging proteins silently accumulate in the brain.

Now, the National Institute on Aging of the National Institutes of Health (NIH) has committed $29 million to support the effort known as the Dominantly Inherited Alzheimer Network (DIAN) for another five years, pending availability of funds. With the new funding, the network will add three new research initiatives to investigate more closely the changes that occur in the brain as the disease develops, which could lead to new ways to diagnose or treat Alzheimers.

The extraordinary accomplishments of the DIAN investigators and participants over the past decade have set the stage to understand the molecular changes that can cause Alzheimers disease, said DIAN director Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology. The three new scientific projects will provide deep insights into how Alzheimers disease begins and progresses to dementia.

DIAN follows families with genetic mutations that all but guarantee that those who inherit the mutations will develop Alzheimers disease at young ages. While devastating for families, this genetic form of Alzheimers disease creates a rare opportunity for researchers to look for brain changes long before symptoms appear in people who carry such mutations, compared with their relatives who dont have the mutation.

Although the study follows only people with a rare genetic form of Alzheimers, its findings could apply to the millions of people living with the much more common late-onset Alzheimers, which appears after age 65. The brain changes that lead to memory loss and confusion are thought to be much the same in early- and late-onset Alzheimers.

Since the network was established in 2008, DIAN researchers have established 19 sites in eight countries representing North and South America, Europe, Asia and Australia with another five sites in four Latin American countries in the works. People from families with genetic forms of Alzheimers take part in observational studies to track changes to their brains over time. The network also has established a clinical trials unit to test investigational therapies to prevent or treat the disease.

Participants undergo assessments of their memory and thinking skills, provide DNA for genetic analysis, undergo brain scans, and give blood and cerebrospinal fluid so researchers can look for molecular signs of Alzheimers disease. With the help of such participants, researchers have begun to piece together a timeline of the brain changes that culminate in cognitive decline and dementia. First, the protein amyloid beta starts forming plaques in the brain up to two decades before symptoms arise. Later, tangles of tau protein form, and the brain begins to shrink. Only then do signs of confusion and forgetfulness appear.

In addition to supporting ongoing research efforts, the grant funds three new projects:

The study described in this press release is supported by the National Institute on Aging of the National Institutes of Health (NIH) under award number U19AG032438. The grant from the National Institute on Aging provides 95.4% of the funding for this study, with the remainder provided by the Alzheimers Association (3.3%) and a consortium of pharmaceutical companies (1.3%). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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Culprit identified in bone loss from cancer therapy

Red and green lines represent new bone in this image of a normal mouse bone. Exposure to chemotherapy and radiation during cancer treatment leads to bone loss and increases the risk of osteoporosis and fractures. A new study from Washington University School of Medicine in St. Louis identifies the trigger for this bone loss and suggests ways to prevent it.

Bone loss that can lead to osteoporosis and fractures is a major problem for cancer patients who receive chemotherapy and radiation. Since the hormone estrogen plays an important role in maintaining bone health, bone loss is especially pronounced among postmenopausal women with breast cancer who are treated using therapies aimed at eliminating estrogen.

Men and children treated for other cancers also experience bone loss, suggesting that eliminating estrogen is not the only trigger leading to bone degeneration.

Studying mice, researchers from Washington University School of Medicine in St. Louis have found a driver of bone loss related to cancer treatment. They have shown that radiation and chemotherapy can halt cell division in bone, which results in a stress response referred to as senescence. According to the new study, cell senescence drives bone loss in female mice beyond that seen from the absence of estrogen alone. The researchers further found that this process occurs in males and females and is independent of cancer type. And perhaps most importantly, the researchers showed that such bone loss can be stopped by treating the mice with either of two investigational drugs already being evaluated in clinical trials.

The study appears Jan. 13 in Cancer Research, a journal of the American Association for Cancer Research.

Researchers have understood that this bone loss has to be due to more than just hormone loss, said senior author Sheila A. Stewart, PhD, a professor of cell biology & physiology. Cancer patients who receive chemotherapy and radiation lose a lot more bone than women with breast cancer treated with aromatase inhibitors, which eliminate estrogen. And children who have not yet gone through puberty, and arent making much estrogen, also lose bone. We wanted to understand what causes bone loss beyond a lack of estrogen and whether we can do anything to stop it.

Stopping bone loss could improve quality of life for cancer patients. Bone loss leads to an increased risk of fractures that continues many years after treatment. This loss of bone density makes it much more likely that patients will develop fractures in the pelvis, hips and spine, which affect mobility and increase the risk of death.

The researchers studied bone loss in mice treated with two common chemotherapy drugs doxorubicin and paclitaxel as well as in mice that received radiation to one limb, to understand whether the bone loss effects were similar in different types of cancer therapies. In all situations, the treatments induced the process of cellular senescence.

Senescence is a chronic stress response in a cell that stops it from dividing and also results in the release of many molecules, some of which we showed drive bone loss, said Stewart, who is also the associate director for basic sciences at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine.

The cells in mouse bones that were most affected by the cancer therapies included those responsible for bone remodeling. These are sets of cells that strike a vital balance between dismantling old bone and building new bone in its place. This balance is disturbed in conditions such as osteoporosis, in which the bone-building cells can no longer keep up with the bone-dismantling cells. The new study suggests that the balance is even more off-kilter following cancer therapy: Bone-building cell activity slows down, and the activity of cells that remove old bone actually accelerates.

The researchers showed they could prevent bone loss in the mice if they took steps to remove the cells that are no longer dividing, thus eliminating the molecular signals that the cells produce that drive bone loss. Toward possible therapies, Stewart and her colleagues then showed they could achieve a similar effect with two different types of compounds that block these molecular signals.

The investigational drugs, a p38MAPK inhibitor and a MK2 inhibitor, block different parts of the same pathway leading to bone loss. Stewart and her colleagues also published a study in 2018 showing that the two inhibitors slowed the growth of metastatic breast cancer in mice. The p38MAPK inhibitor is being tested in U.S. clinical trials for inflammatory diseases, such as chronic obstructive pulmonary disease (COPD). And the MK2 inhibitor is about to be evaluated as atherapy for rheumatoid arthritis.

Cancer patients at risk of bone loss often are treated with drugs for osteoporosis, including bisphosphonates and denosumab. Both have some undesirable side effects, such as muscle and bone pain and, because of the way they work, they may be less desirable for children whose bones are still growing.

The inhibitors we studied have extremely low toxicity, so we are interested in exploring whether they could be an improved option to stop bone loss in children receiving cancer therapy, Stewart said. Were also interested in pursuing a clinical trial to evaluate these drugs in women with metastatic breast cancer to see if we can slow metastatic growth and also preserve bone health in these patients.

This work was supported by the National Institutes of Health (NIH), grant numbers P30 AR074992, NS086741 and P30 CA91842; Washington University School of Medicine; and The Childrens Discovery Institute of Washington University and St. Louis Childrens Hospital, grant number CDI-CORE-2015-505.

Yao Z, Murali B, Ren Q, Luo X, Faget DV, Cole T, Ricci B, Thotala D, Monahan JB, van Deursen J, Baker D, Faccio R, Schwarz J, Stewart SA. Therapy-induced senescence drives bone loss. Cancer Research. Jan. 13, 2020.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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