News

Researchers Find Temporary Anxiety Impacts Learning

Monday, April 21, 2025

A brief episode of anxiety may have a bigger influence on a person’s ability to learn what is safe and what is not. The research recently published in Nature Science of Learning used a virtual reality game that involved picking flowers with bees in some of the blossoms that would sting the participant—simulated by a mild electrical stimulation on the hand.

Researchers worked with 70 neurotypical participants between the ages of 20 and 30. Claire Marino, a research assistant in the ZVR Lab, and Pavel Rjabtsenkov, a Neuroscience graduate student at the University of Rochester School of Medicine and Dentistry, were co-first authors of the study that found that the people who learned to distinguish between the safe and dangerous areas—where the bees were and were not—showed better spatial memory and had lower anxiety, while participants who did not learn the different areas had higher anxiety and heightened fear even in safe areas. Surprisingly, they discovered that temporary feelings of anxiety had the biggest impact on learning and not a person’s general tendency to feel anxious.

“These results help explain why some people struggle with anxiety-related disorders, such as PTSD, where they may have difficulty distinguishing safe situations from dangerous ones,” said the senior author of this study, Benjamin Suarez-Jimenez, PhD, associate professor of Neuroscience and Center for Visual Science at the Del Monte Institute of Neuroscience at the University of Rochester. “The findings suggest that excessive anxiety disrupts spatial learning and threat recognition, which could contribute to chronic fear responses. Understanding these mechanisms may help improve treatments for anxiety and stress-related disorders by targeting how people process environmental threats.”

Suarez-Jimenez explains that it is now important to understand if individuals with psychopathologies of anxiety and stress have similar variations in spatial memory. Adding an attention-tracking measure, like eye-tracking, to future studies could help determine whether a focus on potential threats impacts broader environmental awareness.

Additional authors include Caitlin Sharp, Zonia Ali, Evelyn Pineda, Shreya Bavdekar, Tanya Garg, Kendal Jordan, Mary Halvorsen, Carlos Aponte, and Julie Blue of the University of Rochester Medical Center, and Xi Zhu, PhD, of Columbia University Irving Medical Center. The research was supported by the National Institute of Mental Health, Wellcome Trust Fellowship, and the European Research Council Grant.

Modulating the Brain’s Immune System May Curb Damage in Alzheimer’s

Thursday, April 17, 2025

New research suggests that calming the brain’s immune cells might prevent or lessen the damaging inflammation seen in Alzheimer’s disease. The study points to the key role of the hormone and neurotransmitter norepinephrine, and this new understanding could pave the way for more focused treatments that start earlier and are tailored to the needs of each person.

“Norepinephrine is a major signaling factor in the brain and affects almost every cell type. In the context of neurodegenerative diseases such as Alzheimer’s disease, it has been shown to be anti-inflammatory,” said Ania Majewska, PhD, with the Del Monte Institute for Neuroscience at the University of Rochester, and senior author of the study, which appears in the journal Brain, Behavior, and Immunity. “In this study, we describe how enhancing norepinephrine’s action on microglia can mitigate early inflammatory changes and neuronal injury in Alzheimer’s models.”

Brain Chemicals & Immune Cells

The research, which was conducted in mice, included teams from two labs, combining research programs studying the complex role of the brain’s immune system and the role of inflammation in Alzheimer's. Led by Linh Le, PhD, a graduate student in both labs, the researchers focused on norepinephrine, a chemical in the brain that helps control inflammation. In our brains, immune cells called microglia usually help keep things in balance. Microglia have a receptor called β2AR, which acts like a “switch” and directs the cells to respond to norepinephrine and calm down inflammation.

In Alzheimer’s disease and as we age, this calming switch becomes less active, especially in areas of the brain where harmful protein clumps called amyloid plaques build up. As these plaques form, the nearby microglia lose more of their β2AR receptors, making it harder for them to fight inflammation.

When scientists removed or blocked the receptor, the brain’s damage worsened: more plaques, increased inflammation, and more harm to brain cells. On the other hand, when they stimulated or "turned up" the receptor, the harmful effects were reduced. Interestingly, the results appeared to depend on factors like the animal’s sex and how early the treatment started.

Joan Wright Goodman Dissertation Fellowship Recipient

Friday, April 11, 2025

Thomas Delgado has been awarded a Joan Wright Goodman Dissertation Fellowship for 2025-2026!  This fellowship was endowed by Joan Wright Goodman, PhD class of 1952, to support doctoral students across disciplines in the sciences.  It is one of the University’s most competitive dissertation fellowships and is given to students who display exceptional ability and promise.

Congratulations to Thomas. We are very proud of this achievement. Keep up the good work.

The great brain clearance and dementia debate

Wednesday, April 9, 2025

Scientists have known about a link between poor sleep and an increased risk of dementia for decades. Maiken Nedergaard, codirector of the Center for Translational Neuromedicine, says that people who report six hours or less of sleep a night are more likely to develop dementia later. “Sleep disturbances very often precede the first sign of dementia by many years.”

Brain’s Own Repair Mechanism: New Neurons May Reverse Damage in Huntington’s Disease

Monday, April 7, 2025

New research shows that the adult brain can generate new neurons that integrate into key motor circuits. The findings demonstrate that stimulating natural brain processes may help repair damaged neural networks in Huntington’s and other diseases.

“Our research shows that we can encourage the brain’s own cells to grow new neurons that join in naturally with the circuits controlling movement,” said Abdellatif Benraiss, PhD, a senior author of the study, which appears in the journal Cell Reports. “This discovery offers a potential new way to restore brain function and slow the progression of these diseases.” Benraiss is a research associate professor in the University of Rochester Medical Center (URMC) lab of Steve Goldman, MD, PhD, in the Center for Translational Neuromedicine.

It was long believed that the adult brain could not generate new neurons. However, it is now understood that niches in the brain contain reservoirs of progenitor cells capable of producing new neurons. While these cells actively produce neurons during early development, they switch to producing support cells called glia shortly after birth. One of the areas of the brain where these cells congregate is the ventricular zone, which is adjacent to the striatum, a region of the brain devastated by Huntington’s disease.

The idea that the adult brain retains the capacity to produce new neurons, called adult neurogenesis, was first described by Goldman and others in the 1980s while studying neuroplasticity in canaries. Songbirds, like canaries, are unique in the animal kingdom in their ability to lay down new neurons as they learn new songs. The research in songbirds identified proteins—one of which was brain-derived neurotrophic factor (BDNF)—that direct progenitor cells to differentiate and produce neurons.

Further research in Goldman’s lab showed that new neurons were generated when BDNF and another protein, Noggin, were delivered to progenitor cells in the brains of mice. These cells then migrated to a nearby motor control region of the brain—the striatum—where they developed into cells known as medium spiny neurons, the major cells lost in Huntington’s disease. Benraiss and Goldman also demonstrated that the same agents could induce new medium spiny neuron formation in primates.

10 small things neurologists wish you’d do for your brain

Thursday, April 3, 2025

There’s growing research linking air pollution exposure to cognitive decline; scientists think very fine, inhalable particles in the air could trigger chemical changes once they reach the brain, says Deborah Cory-Slechta, a professor of environmental medicine and of neuroscience. She adds that wearing an N95 or surgical mask and using indoor air filters on days when air quality is worse (including because of wildfire smoke) can minimize your exposure.

2025 University of Rochester Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student

Friday, February 14, 2025

Congratulations to our very own Sarah Yablonski, who is a recipient of the 2025 University of Rochester Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student.

Well-deserved Sarah!

What a fantastic accomplishment – keep on shining.

Student Spotlight: Aaron Huynh

Sunday, February 2, 2025

Aaron Huynh is a second-year student in the Neuroscience Graduate Program at the School of Medicine and Dentistry at the University of Rochester. He received his undergraduate degree in brain and cognitive sciences from the University of Rochester. He was a student in the biomedical research training program Post-baccalaureate Research Education Program (PREP) at the Medical Center. Huynh currently works in the lab of neurologist Ania Busza, MD, PhD, where his research focuses on ways to assess arm movement recovery in stroke patients over time.

"We're particularly interested in the acute setting," said Huynh. "We have an ongoing study that tracks the progress of stroke patients admitted to Strong [Memorial Hospital]. We use wireless sensors to collect electrical activity of muscles involved in simple movements from when they are admitted through six months post-stroke. We are using clinical measures and novel clinical and translational methods to identify ways to evaluate and hopefully improve motor recovery, specifically in the upper extremities. If we can find ways to develop individualized treatment, we hope that can improve people's quality of life and overall functioning."

70 countries have banned this pesticide. It’s still for sale in the US

Wednesday, January 22, 2025

The Washington Post, January 22

“The data is the data,” says Deborah Cory-Slechta, a professor of environmental medicine and of neuroscience. She says paraquat exposure is associated with the loss of dopamine neurons, which can cause slow and uncoordinated movements, tremors, and difficulty communicating, all of which are consistent with Parkinson’s disease.

“The evidence is very strong, both based on animal studies and on epidemiological evidence the fact that it kills dopamine neurons,” she said.

Brain Immune Cells May also be From Mars and Venus

Tuesday, January 21, 2025

Researchers find that microglia function differently in males versus females

A collision happens. Someone is hurt, a head injury, a concussion. Just as the first responders arrive to help the person, inside the brain, another “crew” of responders is busy clearing debris and repairing injured tissue.

This crew is called the microglia—the immune cells of the central nervous system. Microglia are imperative to maintaining neuronal function by clearing toxins in the brain and central nervous system. But if they are overactive, they can damage neurons instead and, in some cases, have been found to promote the progression of neurodegenerative diseases like Alzheimer’s and Parkinson’s.

During development, there are known sex-related differences in how microglia function. But into adulthood, there was thought to be less variation in how they behave. New research from the Del Monte Institute for Neuroscience at the University of Rochester finds that microglia function may not be as similar across sex as once thought. This discovery could have broad implications for how diseases like Alzheimer's and Parkinson's are approached and studied, and points to the necessity of having gender-specific research. It is already known that more women are diagnosed with Alzheimer’s and more men are diagnosed with Parkinson’s, but it’s unclear why.

“It is a fortuitous finding that has repercussions for what people are doing in the field, but also helps us understand microglia biology in a way that people may not have been expecting,” said Ania Majewska, PhD, professor of Neuroscience and the senior author of a study out today in Cell Reports that shows how microglia respond differently in adult male versus female mice when given an enzyme inhibitor to block its microglia survival receptor. “This research has a lot of ramifications for microglia biology and as a result all these diseases where microglia are important in a sex-specific manner.”

Pexidartinib or PLX3397 is an enzyme inhibitor commonly used to remove microglia in the lab setting to help researchers better understand the role of these cells in brain health, function, and disease. PLX3397 is also used to treat the rare disease tenosynovial giant cells tumors (TGCT), a condition that causes benign tumors to grow rapidly in the joints.

Researchers in the Majewska Lab were using PLX3397 in male versus female experiments but continued to run into difficulties, so they decided to take a different approach with the inhibitor. Instead of using it to ask other questions, they decided to better understand how microglia were responding to the drug in males versus females.

Biotin May Shield Brain from Manganese Damage, Study Finds

Tuesday, January 21, 2025

While manganese is essential in many bodily functions, both deficiency and excessive exposure can cause health issues. Maintaining a balanced diet typically provides sufficient manganese for most individuals; however, high levels of exposure can be toxic, particularly to the central nervous system. Chronic manganese exposure may result in a condition known as manganism, characterized by symptoms resembling Parkinson's disease, including tremors, muscle stiffness, and cognitive disturbances.

New research published in Science Signaling employs model systems and human nerve cells to show the mechanisms by which manganese inflicts damage to the central nervous system. The study also suggests that the vitamin biotin may be protective, potentially mitigating manganese-induced damage.

“Exposure to neurotoxic metals like manganese has been linked to the development of Parkinsonism,” said Sarkar Souvarish, PhD, an assistant professor at the University of Rochester Medical Center (URMC) Departments of Environmental Medicine and Neuroscience and lead author of the study. “In this study, we applied untargeted metabolomics using high-resolution mass spectrometry and advanced cheminformatics computing in a newly developed model of parkinsonism, leading us to the discovery of biotin metabolism as a modifier in manganese-induced neurodegeneration.”

Air pollution and brain damage: what the science says

Tuesday, January 14, 2025

Post-mortem studies of human brains provide direct evidence that numerous pollutants—including nanoparticles and toxic metals—accumulate in brain tissue. Deborah Cory-Slechta, a professor of environmental medicine and of neuroscience, says she suspects that the brain can’t cope with the resulting metal concentrations, noting that, for decades, pathologists have seen elevated levels of various metals in the brains of people with neurodegenerative diseases. She is now studying how the metals disrupt brain chemistry.

Common Sleep Aid May Leave Behind a Dirty Brain

Wednesday, January 8, 2025

Getting a good night’s sleep is a critical part of our daily biological cycle and is associated with improved brain function, a stronger immune system, and a healthier heart. Conversely, sleep disorders like insomnia and sleep apnea can significantly impact health and quality of life. Poor sleep often precedes the onset of neurodegenerative diseases and is a predictor of early dementia.

New research appearing in the journal Cell describes for the first time the tightly synchronized oscillations in the neurotransmitter norepinephrine, cerebral blood, and cerebrospinal fluid (CSF) that combine during non-rapid eye movement (non-REM) sleep in mice. These oscillations power the glymphatic system—a brain-wide network responsible for removing protein waste, including amyloid and tau, associated with neurodegenerative diseases.

New research appearing in the journal Cell describes for the first time the tightly synchronized oscillations in the neurotransmitter norepinephrine, cerebral blood, and cerebrospinal fluid (CSF) that combine during non-rapid eye movement (non-REM) sleep in mice. These oscillations power the glymphatic system—a brain-wide network responsible for removing protein waste, including amyloid and tau, associated with neurodegenerative diseases.

“As the brain transitions from wakefulness to sleep, processing of external information diminishes while processes such as glymphatic removal of waste products are activated,” said Maiken Nedergaard, MD, DMSc, co-director of the University of Rochester Center for Translational Neuromedicine and lead author of the study. “The motivation for this research was to better understand what drives glymphatic flow during sleep, and the insights from this study have broad implications for understanding the components of restorative sleep.”

The study also holds a warning for people who use the commonly prescribed sleep aid zolpidem. The drug suppressed the glymphatic system, potentially setting the stage for neurological disorders like Alzheimer’s, which are the result of the toxic accumulation of proteins in the brain.