Every day, the seven National Primate Research Centers (NPRCs) conduct and enable collaborative research studies to improve human and animal health. For more than five years now, we’ve been sharing our latest news and scientific advancements with you via NPRC.org and @NPRCnews (X), and there’s more coming your way. 

To ensure the NPRCs provide the topics of most interest to our readers and followers, we looked back at your favorite stories to help us move forward. Your top interests span behavior and psychology, infectious disease and neuroscience and brain disorders research. We will continue to share news that represents what you have most enjoyed, and we will also bring you information that reflects the breadth and depth of research across the NPRC network.   

We appreciate our readers and followers, and encourage you to take another look at your favorite blogs about NPRC research, to share the information with your family, friends and colleagues, and to continue connecting with us via NPRC.org, @NPRCnews and, now, on the new NPRC LinkedIn account. Via these resources, you’ll always be able to access the latest news on NPRC research that is helping people across generations and around the world live longer, healthier lives.   

Behavior and Psychology 

1. The Effects of Wildfire Smoke Exposure in Early Pregnancy 

A study by California NPRC and UC Davis researchers investigated the effects of wildfire smoke exposure on infant monkeys during early pregnancy. The study found that exposure led to increased inflammation, reduced stress response, memory deficits and a more passive temperament in the monkeys. The findings suggest environmental changes during pregnancy can have lasting effects on offspring.  

Infectious Disease 

2. A Deadly Relationship: Stopping the Progression of Tuberculosis in HIV Patients   

Researchers at the Southwest National Primate Research Center have discovered chronic immune activation in the lungs plays a crucial role in the progression of tuberculosis (TB) and HIV co-infection. This dysfunction hampers the body’s ability to fight off infections. The study suggests the need to develop treatments targeting chronic immune activation alongside antiretroviral therapy (ART). TB and HIV are global pandemics that reinforce each other, affecting a significant portion of the world’s population. The findings offer hope for improved treatment strategies in the next decade. 

3. New Possible Correlation Between Lyme Disease and Lewy Body Dementia  

At Tulane National Primate Research Center, researchers discovered intact spirochetes of Borrelia burgdorferi, the bacterium that causes Lyme disease, in the central nervous system of a 69-year-old woman who received multiple rounds of antibiotic treatment. The presence of this bacterium coupled with her persistent neurological decline raises the possibility of a correlation between Lyme disease and Lewy body dementia. This finding highlights the bacterium’s persistence despite targeted therapy and emphasizes the need for further research to comprehend its role in severe neurological conditions. 

4. Are DNA Vaccinations a Perennial Answer to the Flu?  

Researchers at the Washington National Primate Research Center are developing a universal flu vaccine that could protect against all strains of the influenza virus. Using a DNA vaccine administered through the skin, the team has achieved promising results in macaques, providing 100% protection against a previous flu virus. This approach could eliminate the need for annual flu shots and be quickly deployed during pandemics. The researchers believe this technology could also be effective against other viruses and outbreaks. 

Neuroscience & Brain Disorders 

5. Past Social Experiences May Affect Brain’s Response to Oxytocin

A study at the Emory (formerly Yerkes) National Primate Research Center and Emory University showed the response of neurons to oxytocin, a chemical involved in social bonding, can vary based on an individual’s past experiences. Using female prairie voles, the researchers examined the nucleus accumbens, a brain region related to pair bonding. They found that oxytocin reduced neuron firing before bonding and increased it afterward, when triggered. The study also revealed a connection between oxytocin signals and endocannabinoids, affecting defensive interactions. These findings provide insights into how prior experiences influence oxytocin’s impact on brain circuits. 

6. NPRC Study May Have Found Link That Causes Anxiety and Depression  

Researchers at the Wisconsin National Primate Research Center and the University of Wisconsin-Madison have discovered brain pathways in juvenile monkeys that could contribute to anxiety and depression later in life. By studying the connections between specific brain regions, they found a correlation between synchronization and anxious temperament. These findings may lead to better treatment approaches and help identify gene alterations associated with anxiety. 

7. The Drinking Gene: Could Alcoholism Be Inherited?  

Research conducted at Oregon National Primate Research Center has identified a gene, GPR39, as a potential target for developing medication to prevent and treat alcoholism. By modifying protein levels encoded by this gene in mice, the researchers observed a significant reduction in alcohol consumption. They also found a link between alcohol and the activity of this gene. The study draws attention to the importance of cross-species approaches to identify drugs for treating alcohol use disorder. Further investigations are under way to determine if the same mechanism applies to humans. These findings offer potential insights for developing drugs to address chronic alcoholism and mood disorders. 

Oxytocin is a hormone that plays a critical role in social bonding and attachment. In recent years, researchers have been studying the effects of intranasal oxytocin, a non-invasive treatment that reduces social impairment in several neurological and behavioral disorders, such as autism.  

However, the long-term effects and efficacy of the treatment are currently under examination. Studies conducted by Dr. Karen Bales’ lab at the California National Primate Research Center reveal that chronic intranasal oxytocin produces sex-specific biological and behavioral responses in titi monkeys, a monogamous nonhuman primate.  

The researchers found that all OT-treated monkeys engaged more in social interactions but differed in their social behavior by sex. The males exhibited more social interest in unfamiliar animals, while females directed their interest toward their parents.  

The monkeys were divided into two groups: one received a daily dose of intranasal OT, while the other received saline for six months. The treatment group exhibited more prosocial behavior in their home enclosure immediately following their dose than the control group. 

Researchers also examined neural effects and social behavior during adolescence and into adulthood one-year after treatment ended. As adults, males from the treatment group maintained some prosocial effects. They also scored higher on several measures of affiliative behavior than the control group. Females, however, experienced a slight delay in forming a bond with their new mate. 

The researchers observed that chronic treatments during adolescence altered their behavior long-term, and these behavioral changes were different for males and females. These findings emphasize the complexity of the treatment and lay an essential foundation for more research on its use in humans. 

A collaborator on the project, Dr. Suma Jacob from the University of Minnesota Medical School, explained that “there is more research to be done on oxytocin, how it works, its effects, and feedback systems.”

Oxytocin, a brain chemical known for promoting social bonding and nurturing behavior, has been used in several studies to potentially treat disorders such as autism, but with inconsistent results. 

Yerkes National Primate Research Center Division Chief Larry Young and his research colleagues in Yerkes’ Division of Behavioral Neuroscience and Psychiatric Disorders as well as Emory’s Center for Translational Social Neuroscience found the dynamic response of neurons to oxytocin may vary depending on the past social experiences of the individual. 

The study was conducted in female prairie voles because they form lifelong bonds with their partners and focused on the nucleus accumbens because it plays an important role in the brain for pair bonding. Tissue from the nucleus accumbens was exposed to TGOT, a drug that mimics oxytocin signals. 

Robert Liu, PhD, professor of biology and director of Emory’s Neuroscience graduate program compared the electrical responses of neurons to oxytocin signals to an analog television, before and after the television is tuned to a station. “Before the animal forms a pair bond, oxytocin reduces the static noise: the neurons in the nucleus accumbens fire spontaneously less often,” said Liu. “But after an animal has been exposed to a partner, it increases the clarity of the signal from the station: the neurons gradually fire with greater strength – but only when electrically triggered.”

In an unexpected turn, researchers found that after bonding, oxytocin signals became coupled to endocannabinoids, molecules produced within the brain resembling the psychoactive substances found in cannabis. By blocking the endocannabinoids, the scientists could interfere with some aspects of the prairie voles pair interactions. 

Blocking endocannabinoid signals increased the likelihood the female vole would display a defensive upright posture, a sign of rejection, in the presence of their partner, but not toward a stranger. However, the pair-bonded animals still spent more time with their partner than a stranger. This reaction shows endocannabinoid signaling is modulating defensive interactions, rather than pair bonding. 

The study suggests the way oxytocin modulates brain circuits changes with prior experience, which may help explain inconsistent results from human studies involving oxytocin.

Alzheimer’s disease (AD) is a progressive, neurodegenerative disease that destroys memory and other important mental functions. AD affects more than 44 million people worldwide and more than six million Americans. Given this prevalence, studying AD is a high priority, and researchers have been searching for better ways to learn more about the disease.

Now, researchers at the Wisconsin National Primate Research Center and other institutions at UW-Madison have shown rhesus monkeys can be a new, translational model for studying late-onset Alzheimer’s disease. “Age is a major risk factor for late-onset Alzheimer’s disease (AD) but seldom features in laboratory models of the disease,” the researchers write in the scientific publication Aging Cell.

The researchers studied brain tissues from transgenic mice, old monkeys with age-related amyloid plaques and post-mortem brain tissue from donors who were aged 72 to 96 and diagnosed with AD after death. This approach provides an alternative to the most common approaches to modeling AD, which tend to use young mice in which plaques and tangles are genetically imposed and seldom include age as part of the study design.

The new study design, however, shows the aged environment impacts inflammatory processes linked to neurodegeneration. In the monkeys and humans, where plaques develop as a function of age, each demonstrated differences from mice in the immediate vicinity of amyloid plaques, but were similar to each other.

In all three species, the authors discovered new structures enriched in mitochondria surround the plaques, and the presence of these plaques influences metabolism. In the monkeys and humans, said Dr. Ricki Colman of the WNPRC, “this mitochondrial dysfunction appears to be suggestive of Alzheimer’s disease.”

The published study concludes that, given the clear parallels between amyloid plaques in monkeys and humans, further studies in nonhuman primate models are warranted. Monkey models are more likely to translate to human disease than mouse studies and could help advance treatments for AD.

Parkinson’s disease is a slowly progressive chronic neurologic condition, causing a gradual loss of the nerve cells producing the neurotransmitter dopamine in the brain. While there are no standard diagnostic tests for Parkinson’s, the diagnosis is clinical and based on findings of a neurological exam and information provided by the patient. Tremors occur in about 70% of those living with Parkinson’s, typically appearing on one side of the body, in a hand or a foot, while relaxed or at rest.*

The primary and most potent medication used to treat Parkinson’s disease is Levodopa, which helps restore balance, reduce shaking, and manage other motor issues patients experience. Overall, this treatment is radically helpful for those suffering, but erratic involuntary movements often emerge as a side effect of this drug over time.

“Levodopa is amazing, it works like magic, but it has side effects. If we can eliminate these side effects, it could change the life of patients with Parkinson’s,” says Marcel Daadi, Ph.D., an associate professor at Texas Biomed and lead paper author.

Dyskinesia is a common side effect in patients with Parkinson’s disease. It is not a symptom of the disease itself. Still, it typically emerges about five years into taking Levodopa. And like human patients, primates develop Dyskinesia after receiving Levodopa.

A study commenced at Texas Biomedical Research Institute (Texas Biomed) to help make strides in the reduction of Dyskinesia in humans. During this time, Daadi and collaborators administered the compound PD13R (created by medicinal chemists at Temple University) to the marmoset animal model of Parkinson’s. When treated with PD13R, primates experienced relief from uncontrolled movements as their Dyskinesia dropped by more than 85%, a measurement made by with the help of wearable activity monitors.

*https://parkinsonrockies.org/live-well/diagnosis-and-symptoms/?gclid=Cj0KCQiA8vSOBhCkARIsAGdp6RTNBEB0jvY01T0sel6voKUxEkV3GrikEtZbWVghPiKl5jk1CToebVQaAvtIEALw_wcB

Pelizaeus-Merzbacher disease is an inherited condition involving the brain and spinal cord, resulting in reduced neurological function. Those affected by the disease (an estimated 1 in 100,000 people) typically experience weak muscle tone, involuntary movements of the eyes, and delayed motor skill development.

In 2016 the Oregon National Primate Research Center (ONPRC)  received a $4 million grant from the National Institutes of Health (NIH) to develop a genomic database for rhesus macaques. Today, the database contains the genomic sequences of over 2,000 monkeys, which has enabled researchers to identify thousands of genetic variants identical to those known to cause human disorders.

Anne Lewis, D.V.M., Ph.D., head of pathology services at ONPRC, observed three young rhesus macaques displaying symptoms, including tremors and motor dysfunction, which were similar to those seen in  human  Pelizaeus-Merzbacher patients. Scientists at ONPRC were able to match her observations with data in the rhesus macaque genome database, helping other scientists to apply therapies to an animal model that closely matches the disease impacting humans. Additional research, led by scientists at Oregon Health & Science University (ONPRCs affiliated institution), could help develop new therapies to treat Pelizaeus-Merzbacher disease.

 “This really sets us up for the possibility of doing gene therapies, or neural stem cell-based therapies in the developing brain,” said Larry Sherman, Ph.D., professor in the Division of Neuroscience at the ONPRC.

To learn more about genome sequencing at the NPRCs, please visit here.

About 30 percent of people who have severe anxiety and depression do not find sufficient relief in available medications and psychotherapy, causing them chronic, debilitating symptoms and a significant risk of suicide. To help end this debilitation, University of Wisconsin–Madison researcher Ned Kalin, MD, and his team are studying how to dial down overactive responses to potential threats.

The researchers are using an established method, called DREADDs (Designer Receptors Exclusively Activated by Designer Drugs), in monkeys at the Wisconsin National Primate Research Center (WiNPRC) to make small changes to genes in targeted cells to alter cell behavior. The idea is to coax neurons to produce a unique version of a protein, called a receptor. These “designer receptors” can receive chemical signals that regulate the cells’ function and affect how they communicate with other cells. Unlike other receptors in the brain that respond to naturally occurring chemical signals, the DREADDs only respond to a chemical not naturally present — a “designer” drug matched to the designer receptor.

“When such a drug interacts with DREADDs, you have the possibility of ‘fine-tuning’ the function of the brain cell that is now expressing this receptor,” says Patrick Roseboom, PhD, senior scientist and a lead study author.

The researchers injected a low dose of a psychiatric medication, Clozapine, in five monkeys to activate DREADDs in cells in the amygdala, the brain region responsible for regulating emotions. The researchers then tested the monkeys in a mildly stressful situation, placing them near an unfamiliar human, which is similar to how healthcare professionals assess anxiety levels in children. The researchers’ observations of the monkeys’ behavior and levels of stress hormones showed the most anxious monkeys freeze — becoming quiet and very still.

When the researchers gave the Clozapine before the stressful situation, the monkeys with the DREADDs experienced a significant reduction in freezing, while a control group without the DREADDS showed no change in behavior. 

The success of this proof-of-concept study is providing hope for using gene therapy and methods, such as DREADDs, to treat the millions of people who live with severe and treatment-resistant psychiatric illnesses. Read more about the NPRCs’ anxiety and depression research here.

Each year in the U.S., millions of people receive general anesthesia, and a small proportion of those patients actually regain some awareness during their medical procedures.

A recently published study about brain activity representing consciousness could help prevent that potential trauma as well as help scientists define which parts of the brain are key to the conscious mind. Such information could lead to more accurate measurements of patients undergoing anesthesia, improve treatment outcomes for people who have consciousness disorders and help people in comas maintain a continuous level of consciousness.

Yuri Saalmann, a University of Wisconsin-Madison psychology and neuroscience professor, and his research team recorded electrical activity in about 1,000 neurons surrounding each of 100 sites throughout the brains of a pair of monkeys at the Wisconsin National Primate Research Center (WiNPRC). The researchers recorded activity during several states of consciousness: under drug-induced anesthesia, light sleep, resting wakefulness and roused from anesthesia into a waking state through electrical stimulation of a spot deep in the brain.

To sift out characteristics that best indicate whether the monkeys were conscious or unconscious, the researchers used machine learning. They input their large pool of data into a computer, told the computer which state of consciousness had produced each pattern of brain activity and asked the computer which areas of the brain and patterns of electrical activity corresponded most strongly with consciousness.

Surprisingly, the results pointed away from the frontal cortex, which is the part of the brain healthcare professionals typically monitor to maintain patient safety while under general anesthesia and the part most likely to exhibit slow waves of activity long considered typical of unconsciousness.

“In the clinic now, they may put electrodes on the patient’s forehead,” says Mohsen Afrasiabi, an assistant scientist in Saalmann’s lab. “We propose that the back of the head is a more important place for those electrodes because we’ve learned the back of the brain and the deep brain areas are more predictive of state of consciousness than the front.”

And while both low- and high-frequency activity can be present in unconscious states, complexity best indicates a waking mind. “You need more complexity to convey more information, which is why it’s related to consciousness,” says graduate student Michelle Redinbaugh. “If you have less complexity across these important brain areas, they can’t convey very much information. You’re looking at an unconscious brain.”

Read more about our consciousness research and how monkeys are helping improve patient care here.

Promising results from the Wisconsin National Primate Research Center (WiNPRC) are giving hope to the millions of people who live with Parkinson’s disease (PD). By grafting neurons from monkeys, WiNPRC researchers relieved the debilitating movement and depression symptoms associated with the disease.

The researchers used induced pluripotent stem cells from the monkeys’ own bodies to make dopaminergic neurons. which produce dopamine, a chemical that transmits signals between nerve cells. PD damages these neurons and disrupts the signals, making it progressively harder for people who have PD to coordinate their muscles for even simple movements and causing rigidity, slowness and tremors, which are the disease’s hallmark symptoms. Patients — especially those in earlier stages of Parkinson’s — are typically treated with drugs, such as L-DOPA, to increase dopamine production.

“Those drugs work well for many patients, but the effect doesn’t last,” says Marina Emborg, a Parkinson’s researcher at WiNPRC. “Eventually, as the disease progresses and their motor symptoms get worse, they are back to not having enough dopamine, and side effects of the drugs appear.”

To develop additional treatment options, the researchers used real-time magnetic resonance imaging (MRI)  to inject millions of dopamine-producing neurons and supporting cells into each monkey’s striatum, an area of the brain that is depleted of dopamine as a consequence of the ravaging effects of Parkinson’s.

Half the monkeys received cells from other monkeys (an allogenic transplant), and the other half received grafts made from their own induced pluripotent stem cells (called an autologous transplant). The allogeneic monkeys’ symptoms remained unchanged or worsened, but the autologous monkeys began making significant improvements within six months and even more within a year — dopamine levels doubled for some and tripled for others.

Emborg says examples of the improvements included the autologous animals moving more and grabbing food much faster and easier. She adds, “Although Parkinson’s is typically classified as a movement disorder, anxiety and depression are typical, too. Symptoms that resemble depression and anxiety — pacing, disinterest in others and even in favorite treats — abated after the autologous grafts grew in.”

These promising results add to the growing body of NPRC research into improving lives for people who live with PD. Read more about our PD research here.

Alzheimer’s disease (AD) affects more than 5.5 million Americans per year. This staggering prevalence makes it a high-priority disease for researchers to develop better treatments and even a cure. Researchers at California’s National Primate Research Center (CNPRC) are among those pursuing answers and believe the disease actually begins decades before the first signs of cognitive decline are triggered. 

Until recently, testing has primarily been done on transgenic mice that express a human version of amyloid or tau proteins, but these studies have proven to be difficult to translate into new medications for the human population. In contrast, nonhuman primate (NHP) models may yield new treatments by providing a closer biological link between the laboratory and clinic. 

“Humans and monkeys have two forms of the tau protein in their brains, but rodents only have one,” said Danielle Beckman, postdoctoral researcher at the CNPRC and first author on the paper. “We think the macaque is a better model, because it expresses the same versions of tau in the brain as humans do.”

Beckman and her team recommend adding an intermediate step for translational research: “If we can test therapies that work in mouse models prior to investing millions or billions of dollars into clinical trials, we really think it’s going to make an impact in having a new drug on the market. I think we really need to be open about new animal models for diseases.”

Visualization of biomarkers in the brain of NHP models may provide the key into the progression of Alzheimer’s disease. So far, teams have monitored signs of neuron death and performed positron emission tomography imaging. The effects of neurodegeneration were observed rapidly; within three months, end-stage tangles were present. And within 6 months, the progress of neurodegeneration increases markedly.

While it is still unknown whether the treated animals will present the full spectrum of Alzheimer’s Disease, including severe cognitive impairment, the initial observations have set the stage for the next steps in testing tau‐based therapeutics for AD patients. Research with monkeys is again proving critical to finding answers that can improve millions of lives worldwide. 

To learn more about the work happening at our research centers around the country, visit this link.