Drs. Ania Majewska and Monique Mendes in a podcast for NINDS on F applications
Monday, March 1, 2021
Dr. Ania Majewska and NGP alum, Dr. Monique Mendes, will be featured in The National Institute of Neurological Disorders and Stroke’s Building Up the Nerve podcast on 3/5/2021. In this episode, our grantee guests discuss how they involved their mentor(s)/sponsor(s) in the application process to ensure the training plan reflects their individual needs and the mentor is able to provide the appropriate level of support and expertise to achieve those training goals.
The podcast features Jaroslaw Aronowski, PhD, Professor, UTHealth McGovern Med School; Alexis S. Mobley, MS, PhD Candidate, UTHealth McGovern Med School; Ania Majewska, PhD, Professor, University of Rochester; Monique Mendes, PhD, Postdoctoral Researcher, Stanford University; Mark Wu, MD, PhD, Professor, Johns Hopkins University; Margaret Ho, PhD, Postdoctoral Fellow, Johns Hopkins University School of Medicine.
Spread the word.Read More: Drs. Ania Majewska and Monique Mendes in a podcast for NINDS on F applications
Two faculty members received Sloan Awards for research on how the brain perceives the world.
Wednesday, February 17, 2021
Two University of Rochester researchers in the Department of Brain and Cognitive Sciences are being honored with a celebrated award for their contributions to and leadership in the scientific community.
Martina Poletti and Manuel Gomez-Ramirez, both assistant professors of brain and cognitive sciences and of neuroscience, are among this year’s recipients of Sloan Research Fellowships. Awarded annually by the Alfred P. Sloan Foundation since 1955, the fellowships recognize young scientists for their independent research accomplishments, creativity, and potential to become leaders in the scientific community. Each fellowship carries a $75,000, two-year award. This year, 128 scientists across the US and Canada were awarded fellowships. Gomez-Ramirez and Poletti are the University’s fourth and filth Sloan fellows in the last three years.Read More: Two faculty members received Sloan Awards for research on how the brain perceives the world.
New Research Sheds Light on Vision Loss in Batten Disease
Friday, February 5, 2021
Progressive vision loss, and eventually blindness, are the hallmarks of juvenile neuronal ceroid lipofuscinosis (JNCL) or CLN3-Batten disease. New research shows how the mutation associated with the disease could potentially lead to degeneration of light sensing photoreceptor cells in the retina, and subsequent vision loss.
“The prominence and early onset of retinal degeneration in JNCL makes it likely that cellular processes that are compromised in JNCL are critical for health and function of the retina,” said Ruchira Singh, Ph.D., an associate professor in the Department of Ophthalmology and Center for Visual Science and lead author of the study which appears in the journal Communications Biology. “It is important to understand how vision loss is triggered in this disease, what is primary and what is secondary, and this will allow us to develop new therapeutic strategies.”
Batten disease is caused by a mutation in the CLN3 gene, which is found on chromosome 16. Most children suffering from JNCL have a missing part in the gene which inhibits the production of certain proteins. Rapidly progressive vision loss can start in children as young as 4, who eventually go on to develop learning and behavior problems, slow cognitive decline, seizures, and loss of motor control. Most patients with the disease die between the ages of 15 and 30.
It has been well established that vision loss in JNCL is due to degeneration of the light-sensing tissue in the retina. The vision loss associated with JNCL can precede other neurological symptoms by many years in some instances, which often leads to patients being misdiagnosed with other more common retinal degenerations. However, one of the barriers to studying vision loss in Batten disease is that mouse models of CLN3 gene mutation do not produce the retinal degeneration or vision loss found in humans. Additionally, examination of eye tissue after death reveals extensive degeneration of retinal cells which does not allow researchers to understand the precise mechanisms that lead to vision loss.
URMC is a hub for Batten disease research. The Medical Center is home to the University of Rochester Batten Center (URBC), one of the nation’s premier centers dedicated to the study and treatment of this condition. The URBC is led by pediatric neurologist Jonathan Mink, M.D., Ph.D., who is a co-author of the study. Batten disease is also one of the key research projects that will be undertaken by the National Institute of Child Health and Human Development-supported University of Rochester Intellectual and Development Diseases Research Center.
To study Batten disease in patient’s own cells, the research team reengineered skin cells from patients and unaffected family members to create human-induced pluripotent stem cells. These cells, in turn, were used to create retinal cells which possessed the CLN3 mutation. Using this new human cell model of the disease, the new study shows for the first time that proper function of CLN3 is necessary for retinal pigment epithelium cell structure, the cell layer in the retina that nourishes light sensing photoreceptor cells in the retina and is critical for their survival and function and thereby vision.
Singh points out that understanding how RPE cell dysfunction contributes to photoreceptor cell loss in Batten disease is important first step, and it will enable researchers to target specific cell type in the eye using potential future gene therapies, cell transplantation, and drug-based interventions.
Additional co-authors of the study include Cynthia Tang, Jimin Han, Sonal Dalvi, Kannan Marian, Lauren Winschel, Celia Soto, Chad Galloway, Whitney Spencer, Michael Roll, Lisa Latchney, Erika Augustine, Vamsi Gullapalli, and Mina Chung with URMC, David Williams and Stephanie Volland with the University of California, Los Angeles, Vera Boniha with the Cleveland Clinic, and Tyler Johnson with Sanford Research. The research was supported with funding from the National Eye Institute BrightFocus Foundation, the David Bryant Trust, the Foundation of Fighting Blindness, the Knights Templar Eye Foundation, the Retina Research Foundation, and Research to Prevent Blindness.Read More: New Research Sheds Light on Vision Loss in Batten Disease
Brain changed by caffeine in utero, study finds
Thursday, February 4, 2021
New research finds caffeine consumed during pregnancy can change important brain pathways in baby.
New research finds caffeine consumed during pregnancy can change important brain pathways that could lead to behavioral problems later in life. Researchers in the Del Monte Institute for Neuroscience at the University of Rochester Medical Center (URMC) analyzed thousands of brain scans of nine and ten-year-olds, and revealed changes in the brain structure in children who were exposed to caffeine in utero.
“These are sort of small effects and it’s not causing horrendous psychiatric conditions, but it is causing minimal but noticeable behavioral issues that should make us consider long term effects of caffeine intake during pregnancy,” said John Foxe, Ph.D., director of the Del Monte Institute for Neuroscience, and principal investigator of the Adolescent Brain Cognitive Development or ABCD Study at the University of Rochester. “I suppose the outcome of this study will be a recommendation that any caffeine during pregnancy is probably not such a good idea.”
Elevated behavioral issues, attention difficulties, and hyperactivity are all symptoms that researchers observed in these children. “What makes this unique is that we have a biological pathway that looks different when you consume caffeine through pregnancy,” said Zachary Christensen, a M.D/Ph.D. candidate in the Medical Science Training Program and first author on the paper published in the journal Neuropharmacology. “Previous studies have shown that children perform differently on IQ tests, or they have different psychopathology, but that could also be related to demographics, so it's hard to parse that out until you have something like a biomarker. This gives us a place to start future research to try to learn exactly when the change is occurring in the brain.”
Investigators analyzed brain scans of more than 9,000 nine and ten-year-old participants in the ABCD study. They found clear changes in how the white matter tracks – which form connections between brain regions – were organized in children whose mothers reported they consumed caffeine during pregnancy.
Researchers analyzed the brain scans of more then 9,000 nine and ten-year-olds and found a change in important brain pathways in those whose mothers retrospectively reported consuming caffeine while pregnant.
URMC is one of 21-sites across the country collecting data for the ABCD study, the largest long-term study of brain development and child health. The study is funded by the National Institutes of Health. Ed Freedman, Ph.D., is the principal investigator of the ABCD study in Rochester and a co-author of the study.
“It is important to point out this is a retrospective study,” said Foxe. “We are relying on mothers to remember how much caffeine they took in while they were pregnant.”
Previous studies have found caffeine can have a negative effect on pregnancy. It is also known that a fetus does not have the enzyme necessary to breakdown caffeine when it crosses the placenta. This new study reveals that caffeine could also leave a lasting impact on neurodevelopment.
The researchers point out that it is unclear if the impact of the caffeine on the fetal brain varies from one trimester to the next, or when during gestation these structural changes occur.
“Current clinical guidelines already suggest limiting caffeine intake during pregnancy – no more than two normal cups of coffee a day,” Christensen said. “In the long term, we hope to develop better guidance for mothers, but in the meantime, they should ask their doctor as concerns arise.”
Inhaled paraquat enters brain, impairs sense of smell in male mice
Tuesday, February 2, 2021
Researchers funded by NIEHS reported that inhalation of the widely used pesticide paraquat reduced the sense of smell in male mice for several months after exposure. Moreover, the chemical entered the brain and other tissues. These results underscore the importance of studying the effects of inhalation of neurotoxicants, to protect public health.
Loss of sense of smell, or olfactory impairment, is an early sign of Parkinson's disease. The findings, published Dec. 29, 2020, in the journal Toxicological Sciences, suggest paraquat may contribute to such neurodegenerative diseases.
Researchers at the University of Rochester modeled an inhalation of low concentrations of paraquat. Using the university's Inhalation Core facility, they exposed mice to aerosolized paraquat. The team then measured levels of the pesticide in lung, kidney, and four regions of the brain — olfactory bulb, striatum, midbrain, and cerebellum.
"Inhalation can provide a direct route of entry to the brain," explained first author Timothy Anderson. "If you inhale something and it goes into your nose, it can actually enter the neurons responsible for sense of smell, and travel into the brain." Anderson is a graduate student at the University of Rochester lab of Deborah Cory-Slechta, Ph.D.,where the study was conducted. Cory-Slechta is deputy director of the university's NIEHS-funded Environmental Health Sciences Center.
Co-author Kevin Welle measured the highest brain levels in the olfactory bulb, suggesting paraquat entered the brain through nasal-olfactory neurons.
"The sex-dependent olfactory impairment observed after paraquat [PQ] inhalation exposure is intriguing and parallels important features of Parkinson's disease [PD], including early loss of sense of smell and greater prevalence in males," said Jonathan Hollander, Ph.D.,health scientist administrator in the NIEHS Genes, Environment, and Health Branch. Hollander oversees research grants for neurodegenerative diseases and other areas.
"Given that paraquat is a known risk factor for PD, and inhalation is a prevalent source of exposure, this study may lead to a more useful animal model of PQ-induced neurodegeneration," he added.Read More: Inhaled paraquat enters brain, impairs sense of smell in male mice
Motion got you feeling queasy? It may be all in your head... or your ears
Friday, January 29, 2021
New research from the University of Rochester Medical Center has detailed a part of the nervous system by which the brain can modify our sense of balance. The current study expands our understanding of how balance stimuli are received by the brain while also offering insights into potential drug targets in the ear, which may be leveraged for treating motion sickness and balance disorders.
“In my opinion, these data are one of the first steps in beginning to unravel the functional significance of the efferent vestibular system,” Joseph C. Holt, Ph.D., senior author of the study published in the journal Scientific Reports said. The efferent vestibular system (EVS) begins as a small collection of neurons that travel from the brainstem out to the ear where our sense of balance begins. While there is still little known about the function of the EVS, URMC researchers are uncovering more about the role these neurons may play in processing motion stimuli and maintaining our balance.Read More: Motion got you feeling queasy? It may be all in your head... or your ears