It was once thought that inflammation and immune responses in the brain were limited; that is was a so-called immune privileged organ. But there is increasing evidence to the contrary. New research has shown that immune cells called mucosal-associated invariant T cells (MAITs) can serve critical roles in the brain that reduce the levels of damaging reactive oxygen species, which prevents neuroinflammation, and protects learning and memory. The findings have been reported in Nature Immunology.
In this study, researchers genetically engineered mice so MAITs would no longer be produced. These mice were compared to a normal group and mice and while cognitive function was the same in both groups to start with, difference appeared as the mice approached middle age. The MAIT-deficient mice had difficulty forming new memories.
But even junk has hidden treasures. Studies found variations in these unsequenced regions were intricately involved in human health, from aging to conditions like cancer and developmental disorders like autism. In 2022, a landmark study finally resolved the genomic unknown, completely sequencing the remaining eight percent of undeciphered DNA remaining.
Now, scientists are discovering that some genetic sequences encode proteins that lack any obvious ancestors, what geneticists call orphan genes. Some of these orphan genes, the researchers surmise, arose spontaneously as we evolved, unlike others that we inherited from our primate ancestors. In a paper published Tuesday in the journal Cell Reports, researchers in Ireland and Greece found around 155 of these smaller versions of DNA sequences called open reading frames (or ORF) make microproteins potentially important to a healthy cell’s growth or connected to an assortment of ailments like muscular dystrophy and retinitis pigmentosa, a rare genetic disease affecting the eyes.
“This is, I think, the first study looking at the specific evolutionary origins of these small ORFs and their microproteins,” Nikolaos Vakirlis, a scientist at the Biomedical Sciences Research Center “Alexander Fleming” in Greece and first author of the paper, tells Inverse. It’s an origin, he says, that’s been mired in much question and mystery.
Researchers at the Netherlands Institute for Neuroscience have discovered that the energy management of inhibitory brain cells is different than that of excitatory cells in our brain. Why is that the case and what is the link with multiple sclerosis?
Brain cells are connected to each other by axons, the parts of the neuron that transmit electrical signals. To do this efficiently, axons are wrapped in myelin, a lipid-rich material which increases the speed at which electrical pulses are conducted. The importance of myelin becomes apparent in diseases such as multiple sclerosis (MS), where myelin is broken down, which has detrimental effects on brain function.
As a result of myelin loss, the conduction of electrical signals is disrupted, which also means that the energy costs of this process become much higher.
It has been shown in epidemiological studies that the immediate postnatal period has a significant influence on the development of our microbiota. A change in postnatal microbiota has long-term implications on neurocognitive outcomes and mental health. Currently, little is known about the molecular mechanisms underlying critical windows of microbial influence.
About the Study
A recentBrain, Behavior, and Immunitystudy investigated the role of the early-life gut microbiota in determining neurodevelopmental outcomes. The current study used a mouse model to evaluate the long-term impact of gut microbial disruption during the critical windows of development.
During deliberation, as we quietly consider our options, the neural activities representing the decision variables that reflect the goodness of each option rise in various regions of the cerebral cortex.1,2,3,4,5,6,7 If the options are depicted visually, we make saccades, focusing gaze on each option. Do the kinematics of these saccades reflect the state of the decision variables? To test this idea, we engaged human participants in a decision-making task in which they considered two effortful options that required walking across various distances and inclines. As they deliberated, they made saccades between the symbolic representations of their options. These deliberation period saccades had no bearing on the effort they would later expend, yet saccade velocities increased gradually and differentially: the rate of rise was faster for saccades toward the option that they later indicated as their choice. Indeed, the rate of rise encoded the difference in the subjective value of the two options. Importantly, the participants did not reveal their choice at the conclusion of deliberation, but rather waited during a delay period, and finally expressed their choice by making another saccade. Remarkably, vigor for this saccade dropped to baseline and no longer encoded subjective value. Thus, saccade vigor appeared to provide a real-time window to the otherwise hidden process of option evaluation during deliberation.
David Chalmers is a professor of philosophy and neural science at New York University, and an honorary professor of philosophy at the Australian National University. He is the co-director of the Center for Mind, Brain, and Consciousness, as well as the PhilPapers Foundation. His research focuses on the philosophy of mind, especially consciousness, and its connection to fields such as cognitive science, physics, and technology. He also investigates areas such as the philosophy of language, metaphysics, and epistemology. With his impressive breadth of knowledge and experience, David Chalmers is a leader in the philosophical community.
The central challenge for consciousness studies is to explain how something immaterial, subjective, and personal can arise out of something material, objective, and impersonal. This is illustrated by the example of a bat, whose sensory experience is much different from ours, making it difficult to imagine what it’s like to be one. Thomas Nagel’s “inconceivability argument” has its advantages and disadvantages, but ultimately it is impossible to solve the mind-body problem due to the subjective nature of experience. This is further explored by examining the concept of philosophical zombies, which are physically and behaviorally indistinguishable from conscious humans yet lack conscious experience. This has implications for the Hard Problem of Consciousness, which is the attempt to explain how mental states are linked to neurophysiological activity. The Chinese Room Argument is used as a thought experiment to explain why physicality may be insufficient to be the source of the subjective, coherent experience we call consciousness. Despite much debate, the Hard Problem of Consciousness remains unsolved. Chalmers has been working on a functional approach to decide whether large language models are, or could be conscious.
A large portion of people on the planet is infected with the parasite Toxoplasma. Now, a study headed by scientists at Stockholm University demonstrates how this tiny parasite spreads so successfully throughout the body, for example to the brain. The parasite infects immune cells and hijacks their identity. The research was recently published in the journal Cell Host & Microbe.
The various roles of immune cells in the body are very strictly regulated in order to combat infections. How Toxoplasma infects so many people and animal species and spreads so quickly has long been a mystery to scientists.
“We have now discovered a protein that the parasite uses to reprogram the immune system”, says Arne ten Hoeve, a researcher at the Department of Molecular Biosciences, Wenner-Gren Institute at Stockholm University.
Researchers discovered a new daily rhythm in a kind of synapse that dampens brain activity using a mouse model. These neural connections, known as inhibitory synapses, are rebalanced as we sleep to allow us to consolidate new information into lasting memories. The results, which were published in the journal PLOS Biology, may help explain how subtle synaptic changes improve memory in humans. Researchers from the National Institute of Neurological Disorders and Stroke (NINDS), which is part of the National Institutes of Health, led the study.
“Inhibition is important for every aspect of brain function. But for over two decades, most sleep studies have focused on understanding excitatory synapses,” said Dr. Wei Lu, senior investigator at NINDS. “This is a timely study to try to understand how sleep and wakefulness regulate the plasticity of inhibitory synapses.”
Kunwei Wu, Ph.D., a postdoctoral fellow in Dr. Lu’s lab, investigated what occurs at inhibitory synapses in mice during sleep and wakefulness. Electrical recordings from neurons in the hippocampus, a brain region involved in memory formation, revealed a previously unknown pattern of activity. During wakefulness, steady “tonic” inhibitory activity increased but fast “phasic” inhibition decreased. They also discovered a far larger activity-dependent enhancement of inhibitory electrical responses in awake mouse neurons, suggesting that wakefulness, rather than sleep, might strengthen these synapses to a greater extent.
