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Iron & the brain: Where and when neurodevelopmental disabilities may begin during pregnancy

Monday, March 6, 2023

Study finds possible cellular origin for impairments associated with gestational iron deficiency

The cells that make up the human brain begin developing long before the physical shape of the brain has formed. This early organizing of a network of cells plays a major role in brain health throughout the course of a lifetime. Numerous studies have found that mothers with low iron levels during pregnancy have a higher risk of giving birth to a child that develops cognitive impairments like autism, attention deficit syndrome, and learning disabilities. However, iron deficiency is still prevalent in pregnant mothers and young children.

The mechanisms by which gestational iron deficiency (GID) contributes to cognitive impairment are not fully understood. The laboratory of Margot Mayer- Proschel, PhD, a professor of Biomedical Genetics and Neuroscience at the University of Rochester Medical Center, was the first to demonstrated that the brains of animals born to iron-deficient mice react abnormally to excitatory brain stimuli, and that iron supplements giving at birth does not restore functional impairment that appears later in life. Most recently, her lab has made a significant progress in the quest to find the cellular origin of the impairment and have identified a new embryonic neuronal progenitor cell target for GID. This study was recently published in the journal Development.

“We are very excited by this finding,” Mayer-Proschel said, who was awarded a $2 million grant from the National Institute of Child Health & Human Development in 2018 to do this work. “This could connect gestational iron deficiency to these very complex disorders. Understanding that connection could lead to changes to healthcare recommendations and potential targets for future therapies.”

Can hearing loss be reversed? Research in Patricia White's lab reveals clues that could regrow the cells that help us hear

Monday, February 13, 2023

Taking a bite of an apple is considered a healthy choice. But have you ever thought about putting in earplugs before your favorite band takes the stage?

Just like your future body will thank you for the apple, your future ears (specifically your cochlear hair cells) will thank you for protecting them. The most common cause of hearing loss is progressive because these hair cells—the primary cells to detect sound waves—cannot regenerate if damaged or lost. People who have repeated exposure to loud noises, like military personnel, construction workers, and musicians, are most at risk for this type of hearing loss. But, it can happen to anyone over time (even concert goers).

On the other hand, birds and fish can regenerate these hair cells, and now researchers at the Del Monte Institute for Neuroscience are getting closer to identifying the mechanisms that may promote this type of regeneration in mammals, as explained in research recently published in Frontiers in Cellular Neuroscience.

“We know from our previous work that expression of an active growth gene, called ERBB2, was able to activate the growth of new hair cells (in mammals), but we didn’t fully understand why,” said Patricia White, PhD, professor of Neuroscience and Otolaryngology at the University of Rochester Medical Center. The 2018 study led by Jingyuan Zhang, PhD, a postdoctoral fellow in the White lab at the time, found that activating the growth gene ERBB2 pathway triggered a cascading series of cellular events by which cochlear support cells began to multiply and activate other neighboring stem cells to become new sensory hair cells.

Researchers identify neurons that "learn" to smell a threat

Tuesday, January 24, 2023

Whether conscious of it or not, when entering a new space, we use our sense of smell to assess whether it is safe or a threat. In fact, for much of the animal kingdom, this ability is necessary for survival and reproduction. Researchers at the Del Monte Institute for Neuroscience at the University of Rochester are finding new clues to how the olfactory sensory system aids in threat assessment and have found neurons that “learn” if a smell is a threat.

Julian Meeks, PhD

“We are trying to understand how animals interact with smell and how that influences their behavior in threatening social and non-social contexts,” said Julian Meeks, PhD, principal investigator of the Chemosensation and Social Learning Laboratory. “Our recent research gives us valuable tools to use in our future work and connects specific sets of neurons in our olfactory system to the memory of threatening smells.”

Kerry O'Banion speaks with Medical News Today

Wednesday, January 18, 2023

Gut-brain connection: 3 fatty acids may be linked to tau-mediated damage

As the prevalence of Alzheimer’s disease (AD) continues to increase, the search for ways to treat and prevent it is ever more pressing. Newly licensed treatments, such as aducanumab and lecanemab, that clear beta-amyloidTrusted Source from the brain are a positive development, but they are expensive and controversial.

Many researchers are now focusing on other areas, one of which is the effect of the microbiomeTrusted Source — microbes, particularly bacteria, that inhabit the gut — on neurodegenerative disorders.

. "There is growing recognition of a gut-brain axis and evidence that the microbiome of individuals varies with disease status," said O'Banion. "The biggest issue is understanding whether gut changes are due to disease or contribute to disease (or both)."

Maiken Nedergaard's lab just discovered a new part of the brain's waste disposal system

Thursday, January 5, 2023

New Scientist, January 5

The new structure is a fourth membrane, lying on top of the innermost membrane, called the subarachnoid lymphatic-like membrane (SLYM). The SLYM hadn’t been noticed before, partly because the membrane disintegrates when the brain is removed from the skull in post-mortems, says Maiken Nedergaard, a professor of neurology and of neurosurgery and codirector of the Center for Translational Neuromedicine, who helped discover the structure. It is also too thin to be seen in living people via brain-scanning machines.

Newly Discovered Anatomy Shields and Monitors Brain

Thursday, January 5, 2023

From the complexity of neural networks to basic biological functions and structures, the human brain only reluctantly reveals its secrets.  Advances in neuro-imaging and molecular biology have only recently enabled scientists to study the living brain at level of detail not previously achievable, unlocking many of its mysteries.  The latest discovery, described today in the journal Science, is a previously unknown component of brain anatomy that acts as both a protective barrier and platform from which immune cells monitor the brain for infection and inflammation.

The new study comes from the labs of Maiken Nedergaard, co-director of the Center for Translational Neuromedicine at University of Rochester and the University of Copenhagen and Kjeld Møllgård, M.D., a professor of neuroanatomy at the University of Copenhagen.  Nedergaard and her colleagues have transformed our understanding of the fundamental mechanics of the human brain and made significant findings in the field of neuroscience, including detailing the many critical functions of previously overlooked cells in the brain called glia and the brain’s unique process of waste removal, which the lab named the glymphatic system.

“The discovery of a new anatomic structure that segregates and helps control the flow of cerebrospinal fluid (CSF) in and around the brain now provides us much greater appreciation of the sophisticated role that CSF plays not only in transporting and removing waste from the brain, but also in supporting its immune defenses,” said Nedergaard. 

The study focuses on the series of membranes that encase the brain, creating a barrier from the rest of the body and keeping the brain bathed in CSF.  The traditional understanding of what is collectively called the meningeal layer identifies the three individual layers as dura, arachnoid, and pia matter.