News

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.”

Understanding Autism: What It Is and What It Isn’t

Wednesday, April 9, 2025

Autism is complex and sometimes misunderstood. Myths and misinformation associated with autism can harm the autism community and perpetuate health disparities. Understanding autism starts with defining what it is—and what it isn’t.

Learn the facts from our experts Suzannah J. Iadarola, PhD, director of the Strong Center for Developmental Disabilities and associate professor of Pediatrics, and Emily Knight, MD, PhD, a clinician scientist in the Departments of Pediatrics, Developmental & Behavioral Pediatrics, and Neuroscience.

What is Autism?

Autism Spectrum Disorder (ASD) is a developmental difference that affects how people may perceive, experience, and interact with the world around them

While experiences vary widely, common characteristics include:

• Differences in social interaction and communication.
• Repetitive behaviors and focused interests.
• Sensory differences, including heightened sensitivities to sounds, lights, or textures; intense interest in sensory input; or both.

Is Autism a Mental Illness?

No, autism is not a mental illness—it is not an illness at all. Autism is a neurodevelopmental difference that primarily affects how a person thinks, perceives, and interacts with others.

It is important to know that some people with autism may experience co-occurring mental health conditions like anxiety and depression. These are separate from autism but are common within the neurodiverse community.

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.

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.