Scientists have created one of the most detailed 3D images of the synapse.
A synapse is a specialized junction between nerve cells that allows for the transfer of electrical or chemical signals, through the release of neurotransmitters by the presynaptic neuron and the binding of receptors on the postsynaptic neuron. It plays a key role in communication between neurons and in various physiological processes including perception, movement, and memory.
A five-year “adversarial collaboration” of consciousness theorists led to a stagy showdown in front of an audience. It crowned no winners — but it can still claim progress.
Human Brain Project researchers from Forschungszentrum Jülich and the University of Cologne (Germany) have uncovered how neuron densities are distributed across and within cortical areas in the mammalian brain. They have unveiled a fundamental organizational principle of cortical cytoarchitecture: the ubiquitous lognormal distribution of neuron densities.
Numbers of neurons and their spatial arrangement play a crucial role in shaping the brain’s structure and function. Yet, despite the wealth of available cytoarchitectonic data, the statistical distributions of neuron densities remain largely undescribed. The new Human Brain Project (HBP) study, published in the journal Cerebral Cortex, advances our understanding of the organization of mammalian brains.
Analyzing the datasets and the lognormal distribution.
Abstract. Numbers of neurons and their spatial variation are fundamental organizational features of the brain. Despite the large corpus of cytoarchitectonic data available in the literature, the statistical distributions of neuron densities within and across brain areas remain largely uncharacterized. Here, we show that neuron densities are compatible with a lognormal distribution across cortical areas in several mammalian species, and find that this also holds true within cortical areas. A minimal model of noisy cell division, in combination with distributed proliferation times, can account for the coexistence of lognormal distributions within and across cortical areas. Our findings uncover a new organizational principle of cortical cytoarchitecture: the ubiquitous lognormal distribution of neuron densities, which adds to a long list of lognormal variables in the brain.
Short-lived proteins control gene expression in cells to carry out a number of vital tasks, from helping the brain form connections to helping the body mount an immune defense. These proteins are made in the nucleus and are quickly destroyed once they’ve done their job.
Despite their importance, the process by which these proteins get broken down and removed from cells once they are no longer needed has eluded scientists for decades—until now.
In a cross-departmental collaboration, researchers from Harvard Medical School identified a protein called midnolin that plays a key role in degrading many short-lived nuclear proteins. The study shows that midnolin does so by directly grabbing the proteins and pulling them into the cellular waste-disposal system, called the proteasome, where they are destroyed.
A speech-to-text brain–computer interface that records spiking activity from intracortical microelectrode arrays enabled an individual who cannot speak intelligibly to achieve 9.1 and 23.8% word error rates on a 50-and 125,000-word vocabulary, respectively.
In the study, published August 8, 2023 in Cell Reports, the researchers demonstrate that transplanting hematopoietic stem and progenitor cells was effective in rescuing multiple signs and symptoms of Alzheimer’s in a mouse model of the disease. Mice that received healthy hematopoietic stem cells showed preserved memory and cognition, reduced neuroinflammation and significantly less β-amyloid build-up compared to other Alzheimer’s mice.
Future studies will further explore how the healthy transplanted cells produced such significant improvements, and whether similar transplant strategies can be used to alleviate Alzheimer’s symptoms in humans.
“Alzheimer’s disease poses a major emotional and economic burden on our society, yet there is no effective treatment available,” said Cherqui. “We are excited to see such promising preclinical results from hematopoietic stem cell therapy and look forward to developing a new therapeutic approach for this devastating disease.”
Co-authors of the study include: Alexander Silva, Jay Sharma, Jacqueline Nguyen, Donald P. Pizzo and Debashis Sahoo, all at UC San Diego, as well as Denise Hinz at the La Jolla Institute for Immunology.
Dr. Joni L. Rutter, Ph.D., (https://ncats.nih.gov/director/bio) is the Director of the National Center for Advancing Translational Sciences (NCATS — https://ncats.nih.gov/) at the U.S. National Institutes of Health (NIH) where she oversees the planning and execution of the Center’s complex, multifaceted programs that aim to overcome scientific and operational barriers impeding the development and delivery of new treatments and other health solutions. Under her direction, NCATS supports innovative tools and strategies to make each step in the translational process more effective and efficient, thus speeding research across a range of diseases, with a particular focus on rare diseases.
By advancing the science of translation, NCATS helps turn promising research discoveries into real-world applications that improve people’s health. The NCATS Strategic Plan can be found at — https://ncats.nih.gov/strategicplan.
In her previous role as the NCATS deputy director, Dr. Rutter collaborated with colleagues from government, academia, industry and nonprofit patient organizations to establish robust interactions with NCATS programs.
Prior to joining NCATS, Dr. Rutter served as the director of scientific programs within the All of Us Research Program, where she led the scientific programmatic development and implementation efforts to build a national research cohort of at least 1 million U.S. participants to advance precision medicine. During her time at NIH, she also has led the Division of Neuroscience and Behavior at the National Institute on Drug Abuse (NIDA). In this role, she developed and coordinated research on basic and clinical neuroscience, brain and behavioral development, genetics, epigenetics, computational neuroscience, bioinformatics, and drug discovery. Dr. Rutter also coordinated the NIDA Genetics Consortium and biospecimen repository.
“Microglia exhibit both maladaptive and adaptive roles in the pathogenesis of neurodegenerative diseases and have emerged as a therapeutic target for central nervous system (CNS) disorders, including those affecting the retina,” wrote the researchers. “Replacing maladaptive microglia, such as those impacted by aging or over-activation, with exogenous microglia that enable adaptive functions has been proposed as a potential therapeutic strategy for neurodegenerative diseases. To investigate the potential of microglial cell replacement as a strategy for retinal diseases, we first employed an efficient protocol to generate a significant quantity of human-induced pluripotent stem cells (hiPSC)-derived microglia.”
“Our understanding of microglia function comes predominantly from rodent studies due to the difficulty of sourcing human tissue and isolating the microglia from these tissues. But there are genetic and functional differences between microglia in mice and humans, so these studies may not accurately represent many human conditions,” explained lead author Wenxin Ma, a PhD, biologist at the Retinal Neurophysiology Section, National Eye Institute, National Institutes of Health.
“To address this concern, researchers have been growing human microglia from human stem cells. We wanted to take this a step further and see if we could transplant human microglia into the mouse retina, to serve as a platform for screening therapeutic drugs as well as explore the potential of microglia transplantation as a therapy itself,” added senior author Wai Wong, vice president of retinal disease, Janssen Research and Development.