The brain computer interface (BCI) device can be used by inexperienced patients to play games within just a few sessions.
Category: neuroscience – Page 185
Neurodevelopmental disorders (NDDs) are a group of disorders in which the development of the central nervous system (CNS) is disturbed, resulting in different neurological and neuropsychiatric features, such as impaired motor function, learning, language or non-verbal communication. Frequent comorbidities include epilepsy and movement disorders. Advances in DNA sequencing technologies revealed identifiable genetic causes in an increasingly large proportion of NDDs, highlighting the need of experimental approaches to investigate the defective genes and the molecular pathways implicated in abnormal brain development. However, targeted approaches to investigate specific molecular defects and their implications in human brain dysfunction are prevented by limited access to patient-derived brain tissues. In this context, advances of both stem cell technologies and genome editing strategies during the last decade led to the generation of three-dimensional (3D) in vitro-models of cerebral organoids, holding the potential to recapitulate precise stages of human brain development with the aim of personalized diagnostic and therapeutic approaches. Recent progresses allowed to generate 3D-structures of both neuronal and non-neuronal cell types and develop either whole-brain or region-specific cerebral organoids in order to investigate in vitro key brain developmental processes, such as neuronal cell morphogenesis, migration and connectivity. In this review, we summarized emerging methodological approaches in the field of brain organoid technologies and their application to dissect disease mechanisms underlying an array of pediatric brain developmental disorders, with a particular focus on autism spectrum disorders (ASDs) and epileptic encephalopathies.
Neurodevelopmental disorders (NDDs) encompass a range of frequently co-existing conditions that include intellectual disability (ID), developmental delay (DD), and autism spectrum disorders (ASDs) (Heyne et al., 2018; Salpietro et al., 2019). ASDs represent a complex set of behaviorally defined phenotypes, characterized by impairments in social interaction, communication and restricted or stereotyped behaviors (Chen et al., 2018). Epilepsy and NDDs frequently occur together, and when refractory seizures are accompanied by cognitive slowing or regression, patients are considered to have an epileptic encephalopathy (EE) (Scheffer et al., 2017). Both ID and ASDs are clinically and etiologically heterogeneous and a unifying pathophysiology has not yet been identified for either the disorder as a whole or its core behavioral components (Myers et al., 2020). Family and twin studies suggest high (0.65–0.91) heritability (Chen et al.
Academics are proposing a new and improved way to help researchers discover when consciousness emerges in human infancy.
When over the course of development do humans become conscious? When the seventeenth-century French philosopher René Descartes was asked about infant consciousness by his critics, he eventually suggested that infants might have thoughts, albeit ones that are simpler than those of adults. Hundreds of years later, the issue of when human beings become conscious is a question which remains a challenge for psychologists and philosophers alike.
But now, in response to a recent article in Trends in Cognitive Sciences, two academics from the University of Birmingham have suggested an improved way to help scientists and researchers identify when babies become conscious.
For several years, Jimo Borjigin, a professor of neurology at the University of Michigan, had been troubled by the question of what happens to us when we die.
New research into the dying brain suggests the line between life and death may be less distinct than previously thought by Alex Blasdel.
Electroconvulsive therapy is more effective than ketamine at treating severe depression, according to a new meta-analysis.
Professor Jürgen Götz and Dr Pranesh Padmanabhan from the Queensland Brain Institute comment on the successful human trial by the WVU Rockefeller Neuroscience Institute which found a five-fold reduction of amyloid-β in Alzheimer’s patients.
The latest trial results underscore the safety of using…
The potentially powerful combination of ultrasound and antibodies for the treatment of Alzheimer’s disease is the focus of a News & Views article by UQ’s Queensland Brain Institute (QBI) researchers.
😗😁😘 year 2023.
The world’s first supercomputer capable of simulating networks at the scale of the human brain has been announced by researchers at the International Centre for Neuromorphic Systems (ICNS) at Western Sydney University.
DeepSouth uses a neuromorphic system which mimics biological processes, using hardware to efficiently emulate large networks of spiking neurons at 228 trillion synaptic operations per second — rivalling the estimated rate of operations in the human brain.
ICNS Director, Professor André van Schaik says DeepSouth stands apart from other supercomputers as it is purpose-built to operate like networks of neurons, requiring less power and enabling greater efficiencies. This contrasts with supercomputers optimised for more traditional computing loads, which are power hungry.
Closed-loop electrical stimulation of the internal capsule of participants undergoing intracranial epilepsy monitoring improved the participants’ performance on a cognitive conflict task, and performance could be decoded from electrode activity.
Two progressively degenerative diseases, amyotrophic lateral sclerosis (ALS, commonly known as Lou Gehrig’s disease) and frontotemporal dementia (FTD, recently in the news with the diagnoses of actor Bruce Willis and talk show host Wendy Williams), are linked by more than the fact that they both damage nerve cells critical to normal functioning—the former affecting nerves in the brain and spinal cord leading to loss of movement, the latter eroding the brain regions controlling personality, behavior and language.
Research studies have repeatedly shown that in patients with ALS or FTD, the function of TAR DNA-binding protein 43, more commonly called TDP-43, becomes corrupted. When this happens, pieces of the genetic material called ribonucleic acid (RNA) can no longer be properly spliced together to form the coded instructions needed to direct the manufacture of other proteins required for healthy nerve growth and function.
The RNA strands become riddled with erroneous code sequences called “cryptic exons” that instead affect proteins believed to be associated with increased risk for ALS and FTD development.