Linda Richards | |
---|---|
Born | Australia |
Citizenship | Australian |
Alma mater | University of Melbourne, Walter and Eliza Hall Institute |
Awards | Australian Neuroscience Society Nina Kondelos Prize (2010) |
Scientific career | |
Fields | Neuroscience |
Institutions | Queensland Brain Institute |
Doctoral advisor | Perry Bartlett |
Linda Richards is an Australian researcher at Queensland Brain Institute (QBI) at the University of Queensland.
Richards undertook undergraduate studies at Monash University, and at the University of Melbourne, where she was awarded a Bachelor of Science in 1990.[ citation needed ] Her PhD, researching the determination of neuronal lineage of in the developing spinal cord, was conferred in 1995 from the laboratory of Perry Bartlett, at the Walter and Eliza Hall Institute of Medical Research in Melbourne. [1] [ better source needed ]
Richards began her postdoctoral training at the Salk Institute of Biological Studies, in the laboratory of Professor Dennis O'Leary. In 1997 she established her own laboratory at the University of Maryland medical school. In 2005 she returned to Australia, taking up a position at the University of Queensland, where she was appointed Associate Professor in the QBI, and the School of Biomedical Sciences. She was subsequently promoted to Professor in 2010.[ citation needed ]
Richards has been the Chair of the Department of Neuroscience at the Washington University in St. Louis since 2021. [2] Richards is also the head of the Cortical Development and Axon Guidance Laboratory at the QBI. The laboratory researches the cellular and molecular mechanisms which regulate the formation and development of the corpus callosum. The research focus of her laboratory to study the development of the cortical midline in animal models and in human tissue. [3] In particular, she is involved in researching a phenomenon where the corpus callosum is absent (agenesis) or disformed (dysgenesis) in the developing brain. [4] This condition affects 1 in 4000 people, and is associated with 50 different human congenital disorders. [5]
Richards also acts as scientific advisor for the Australian Disorders of the Corpus Callosum. [6]
Richards has published over 220 articles. Most cited articles include Agenesis of the corpus callosum: genetic, developmental and functional aspects of connectivity (2007), [12] Neuropilin-1 conveys semaphorin and VEGF signaling during neural and cardiovascular development (2003), [13] and De novo generation of neuronal cells from the adult mouse brain (1992). [14]
In 2006, Richards founded the Australian-New Zealand Brain Bee Challenge. This a competition for secondary students interested in neuroscience. The goal is to educate students and teachers about neuroscience and to encourage students from rural Australia and New Zealand to become involved in neuroscience. [15]
Colpocephaly is a cephalic disorder involving the disproportionate enlargement of the occipital horns of the lateral ventricles and is usually diagnosed early after birth due to seizures. It is a nonspecific finding and is associated with multiple neurological syndromes, including agenesis of the corpus callosum, Chiari malformation, lissencephaly, and microcephaly. Although the exact cause of colpocephaly is not known yet, it is commonly believed to occur as a result of neuronal migration disorders during early brain development, intrauterine disturbances, perinatal injuries, and other central nervous system disorders. Individuals with colpocephaly have various degrees of motor disabilities, visual defects, spasticity, and moderate to severe intellectual disability. No specific treatment for colpocephaly exists, but patients may undergo certain treatments to improve their motor function or intellectual disability.
The corpus callosum, also callosal commissure, is a wide, thick nerve tract, consisting of a flat bundle of commissural fibers, beneath the cerebral cortex in the brain. The corpus callosum is only found in placental mammals. It spans part of the longitudinal fissure, connecting the left and right cerebral hemispheres, enabling communication between them. It is the largest white matter structure in the human brain, about 10 in (250 mm) in length and consisting of 200–300 million axonal projections.
The longitudinal fissure is the deep groove that separates the two cerebral hemispheres of the vertebrate brain. Lying within it is a continuation of the dura mater called the falx cerebri. The inner surfaces of the two hemispheres are convoluted by gyri and sulci just as is the outer surface of the brain.
Agenesis of the corpus callosum (ACC) is a rare birth defect in which there is a complete or partial absence of the corpus callosum. It occurs when the development of the corpus callosum, the band of white matter connecting the two hemispheres in the brain, in the embryo is disrupted. The result of this is that the fibers that would otherwise form the corpus callosum are instead longitudinally oriented along the ipsilateral ventricular wall and form structures called Probst bundles.
Pachygyria is a congenital malformation of the cerebral hemisphere. It results in unusually thick convolutions of the cerebral cortex. Typically, children have developmental delay and seizures, the onset and severity depending on the severity of the cortical malformation. Infantile spasms are common in affected children, as is intractable epilepsy.
The anterior commissure is a white matter tract connecting the two temporal lobes of the cerebral hemispheres across the midline, and placed in front of the columns of the fornix. In all but five species of mammal the great majority of fibers connecting the two hemispheres travel through the corpus callosum, which in humans and all non-monotremes is more than 10 times larger than the anterior commissure. Other routes of communication pass through the hippocampal commissure or, indirectly, via subcortical connections. Nevertheless, the anterior commissure is a significant pathway that can be clearly distinguished in the brains of all mammals.
Anirvan Ghosh is an American neuroscientist and Biotech executive.
Semaphorins are a class of secreted and membrane proteins that were originally identified as axonal growth cone guidance molecules. They primarily act as short-range inhibitory signals and signal through multimeric receptor complexes. Semaphorins are usually cues to deflect axons from inappropriate regions, especially important in the neural system development. The major class of proteins that act as their receptors are called plexins, with neuropilins as their co-receptors in many cases. The main receptors for semaphorins are plexins, which have established roles in regulating Rho-family GTPases. Recent work shows that plexins can also influence R-Ras, which, in turn, can regulate integrins. Such regulation is probably a common feature of semaphorin signalling and contributes substantially to our understanding of semaphorin biology.
Warren S. Brown is a professor of psychology in the Graduate School of Psychology at Fuller Theological Seminary and the founding director of the Travis Research Institute. Brown received his doctorate in Experimental Physiological Psychology from the University of Southern California (1971). Prior to Fuller, Brown spent 11 years as a research scientist at the UCLA Brain Research Institute. He was a founding member of the National Organization for Disorders of the Corpus Callosum, the International Research Consortium on the Corpus Callosum and Cerebral Connectivity (IRC5), and the International Society for Science and Religion. The "Warren and Janet Brown Scholarship", given at Fuller to support students in neuropsychological research, was created to honor Brown and his late wife.
Neuronal migration disorder (NMD) refers to a heterogenous group of disorders that, it is supposed, share the same etiopathological mechanism: a variable degree of disruption in the migration of neuroblasts during neurogenesis. The neuronal migration disorders are termed cerebral dysgenesis disorders, brain malformations caused by primary alterations during neurogenesis; on the other hand, brain malformations are highly diverse and refer to any insult to the brain during its formation and maturation due to intrinsic or extrinsic causes that ultimately will alter the normal brain anatomy. However, there is some controversy in the terminology because virtually any malformation will involve neuroblast migration, either primarily or secondarily.
Congenital mirror movement disorder(CMM disorder) is a rare genetic neurological disorder which is characterized by mirrored movement, sometimes referred to as associated or synkinetic movement, most often in the upper extremity of the body. These movements are voluntary intentional movements on one, ipsilateral, side of the body that are mirrored simultaneously by involuntary movements on the contralateral side.
Disconnection syndrome is a general term for a collection of neurological symptoms caused – via lesions to associational or commissural nerve fibres – by damage to the white matter axons of communication pathways in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.
Dual consciousness is a hypothesis or concept in neuroscience. It is proposed that it is possible that a person may develop two separate conscious entities within their one brain after undergoing a corpus callosotomy. The idea first began circulating in the neuroscience community after some split-brain patients exhibited alien hand syndrome (AHS), which led some scientists to believe that there must be two separate consciousnesses within the brain's left and right hemispheres in competition with one another once the corpus callosum is severed.
Andermann syndrome, also known as agenesis of corpus callosum with neuronopathy (ACCPN), Charlevoix disease and KCC3 axonopathy among other names, is a very rare neurodegenerative genetic disorder that damages the nerves used to control muscles and related to sensation and is often associated with agenesis of the corpus callosum.
David Anthony Keays is an Australian neuroscientist who studies magnetoreception and neurodevelopment. He is currently Chair of Organismal and Developmental Neurobiology at the Ludwig Maximilians University (LMU) in Munich, and a Principle Research Associate at the University of Cambridge. He was formerly a group leader at the Research Institute of Molecular Pathology (IMP) in Vienna, Austria,
Chenghua Gu is a Professor of Neurobiology at the Harvard Medical School where her research focuses on the Blood–brain barrier. She is also part of the Harvard Brain Science Initiative and has won numerous awards for her groundbreaking research on the brain's vascular component.
Chudley–Mccullough syndrome is a rare genetic disorder which is characterized by bilateral congenital hearing loss associated with brain malformations. It is a type of syndromic deafness.
Proud syndrome is a very rare genetic disorder which is characterized by severe intellectual disabilities, corpus callosum agenesis, epilepsy, and spasticity. It is a type of syndromic X-linked intellectual disability.
X-linked complicated corpus callosum dysgenesis is a genetic disorder characterized by dysplasia, hypoplasia or agenesis of the corpus callosum alongside variable intellectual disability and spastic paraplegia. Only 13 cases have been described in medical literature. Transmission is X-linked recessive. It is the mildest subtype of L1 syndrome.
Francisco Aboitiz is a Chilean neuroscientist, academic, and author. He is a professor at the Medical School and the Director of the Interdisciplinary Center for Neuroscience NeuroUC at Pontificia Universidad Católica (PUC) de Chile.
For distinguished service to medical research and education in the field of developmental neurobiology, and to community engagement in science.