Toggle light / dark theme

๐€๐ฅ๐ณ๐ก๐ž๐ข๐ฆ๐ž๐ซโ€™๐ฌ ๐ƒ๐ข๐ฌ๐ž๐š๐ฌ๐ž


One of the main features of Alzheimerโ€™s disease is that the ฮฒ-amyloid peptide, a molecule found inside neurons that has many diverse functions, begins to fold incorrectly and accumulates. This process, which ends up causing neuronal death, is linked to a series of other cellular alterations, making it difficult to determine whether they are the cause or the consequence. An example is the case of the deregulation of a type of dynorphin.

Dynorphins are the bodyโ€™s own opioid peptides, which play a key role in many brain pathways. They are located in different areas of the brain, such as the hippocampus, amygdala or hypothalamus, and are involved in memory processes, emotion control, stress and pain, and among other processes. In addition, several studies have shown their involvement in epilepsy, stroke, addictions, depression and schizophrenia.

Now, in a study published in the Computational and Structural Biotechnology Journal, a research group led by ร€lex Perรกlvarez-Marรญn, researcher in the Department of Biochemistry and Molecular Biology and the UAB Institut de Neurociรจncies, has studied from computer models and which interactions may exist between ฮฒ-amyloid peptide and big dynorphin, to determine its role in ฮฒ-amyloid accumulation.

๐’๐ญ๐ฎ๐๐ฒ ๐ฎ๐ง๐ฏ๐ž๐ข๐ฅ๐ฌ ๐ง๐ž๐ฎ๐ซ๐š๐ฅ ๐ฉ๐š๐ญ๐ก๐ฐ๐š๐ฒ ๐ฉ๐ซ๐จ๐ฆ๐จ๐ญ๐ข๐ง๐  ๐ซ๐ž๐ ๐ž๐ง๐ž๐ซ๐š๐ญ๐ข๐จ๐ง ๐š๐Ÿ๐ญ๐ž๐ซ ๐ญ๐ซ๐š๐ฎ๐ฆ๐š๐ญ๐ข๐œ ๐ข๐ง๐ฃ๐ฎ๐ซ๐ข๐ž๐ฌ

๐™Ž๐™ฉ๐™ช๐™™๐™ž๐™š๐™จ ๐™š๐™ญ๐™ฅ๐™ก๐™ค๐™ง๐™ž๐™ฃ๐™œ ๐™ฉ๐™๐™š ๐™ฃ๐™š๐™ช๐™ง๐™–๐™ก ๐™ฅ๐™ง๐™ค๐™˜๐™š๐™จ๐™จ๐™š๐™จ ๐™ž๐™ฃ๐™ซ๐™ค๐™ก๐™ซ๐™š๐™™ ๐™ž๐™ฃ ๐™˜๐™š๐™ก๐™ก ๐™ง๐™š๐™œ๐™š๐™ฃ๐™š๐™ง๐™–๐™ฉ๐™ž๐™ค๐™ฃ ๐™–๐™ง๐™š ๐™ค๐™› ๐™˜๐™ง๐™ช๐™˜๐™ž๐™–๐™ก ๐™ž๐™ข๐™ฅ๐™ค๐™ง๐™ฉ๐™–๐™ฃ๐™˜๐™š, ๐™–๐™จ ๐™ฉ๐™๐™š๐™ฎ ๐™˜๐™ค๐™ช๐™ก๐™™ ๐™ฅ๐™–๐™ซ๐™š ๐™ฉ๐™๐™š ๐™ฌ๐™–๐™ฎ ๐™ฉ๐™ค๐™ฌ๐™–๐™ง๐™™๐™จ ๐™ฉ๐™๐™š ๐™™๐™š๐™ซ๐™š๐™ก๐™ค๐™ฅ๐™ข๐™š๐™ฃ๐™ฉ ๐™ค๐™› ๐™ข๐™ค๐™ง๐™š ๐™š๐™›๐™›๐™š๐™˜๐™ฉ๐™ž๐™ซ๐™š ๐™ฉ๐™ง๐™š๐™–๐™ฉ๐™ข๐™š๐™ฃ๐™ฉ๐™จ ๐™›๐™ค๐™ง ๐™ข๐™–๐™ฃ๐™ฎ ๐™ฅ๐™–๐™ฉ๐™๐™ค๐™ก๐™ค๐™œ๐™ž๐™š๐™จ ๐™–๐™จ๐™จ๐™ค๐™˜๐™ž๐™–๐™ฉ๐™š๐™™ ๐™ฌ๐™ž๐™ฉ๐™ ๐™ฉ๐™๐™š ๐™ข๐™ช๐™ฉ๐™–๐™ฉ๐™ž๐™ค๐™ฃ๐™จ ๐™ค๐™ง ๐™™๐™š๐™ฉ๐™š๐™ง๐™ž๐™ค๐™ง๐™–๐™ฉ๐™ž๐™ค๐™ฃ ๐™ค๐™› ๐™˜๐™š๐™ก๐™ก๐™จ. ๐™ˆ๐™ž๐™˜๐™ง๐™ค๐™œ๐™ก๐™ž๐™–, ๐™ฉ๐™๐™š ๐™—๐™ง๐™–๐™ž๐™ฃโ€™๐™จ ๐™ง๐™š๐™จ๐™ž๐™™๐™š๐™ฃ๐™ฉ ๐™ž๐™ข๐™ข๐™ช๐™ฃ๐™š ๐™˜๐™š๐™ก๐™ก๐™จ, ๐™—๐™š๐™˜๐™ค๐™ข๐™š ๐™–๐™˜๐™ฉ๐™ž๐™ซ๐™š ๐™ž๐™ฃ ๐™ง๐™š๐™จ๐™ฅ๐™ค๐™ฃ๐™จ๐™š ๐™ฉ๐™ค ๐™ฅ๐™–๐™ฉ๐™๐™ค๐™ก๐™ค๐™œ๐™ž๐™š๐™จ, ๐™จ๐™ค๐™ข๐™š๐™ฉ๐™ž๐™ข๐™š๐™จ ๐™ก๐™š๐™–๐™™๐™ž๐™ฃ๐™œ ๐™ฉ๐™ค ๐™˜๐™๐™ง๐™ค๐™ฃ๐™ž๐™˜ ๐™ž๐™ฃ๐™›๐™ก๐™–๐™ข๐™ข๐™–๐™ฉ๐™ž๐™ค๐™ฃ ๐™–๐™ฃ๐™™ ๐™ฉ๐™๐™š ๐™จ๐™˜๐™–๐™ง๐™ง๐™ž๐™ฃ๐™œ ๐™ค๐™› ๐™ฉ๐™ž๐™จ๐™จ๐™ช๐™š.


Studies exploring the neural processes involved in cell regeneration are of crucial importance, as they could pave the way towards the development of more effective treatments for many pathologies associated with the mutations or deterioration of cells. Microglia, the brainโ€™s resident immune cells, become active in response to pathologies, sometimes leading to chronic inflammation and the scarring of tissue.

Cell regeneration mechanisms thus regulate the reactivity of different glial cells, including microglia, preventing further damage and promoting recovery. While many past studies have explored the processes involved in inflammation, many questions about how the brain can successfully recover after injuries or pathologies remain unanswered.

Researchers at LMU Munich, Helmholtz Zentrum Munich, Johannes Gutenberg-Universitรคt (JGU), and other institutes in Germany have recently carried out a study on zebrafish aimed at better understanding the processes underpinning brain regeneration in both animals and humans. Their findings, published in Nature Neuroscience, unveiled a microglial state characterized by the accumulation of lipid droplets and TDP-43+, a RNA-binding protein, which delayed or prevented post-injury brain regeneration.

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 cellโ€™s growth or connected to an assortment of ailments like muscular dystrophy and retinitis pigmentosa, a rare genetic disease affecting the eyes.

โ€œThis is, I think, the first study looking at the specific evolutionary origins of these small ORFs and their microproteins,โ€ Nikolaos Vakirlis, a scientist at the Biomedical Sciences Research Center โ€œAlexander Flemingโ€ in Greece and first author of the paper, tells Inverse. Itโ€™s an origin, he says, thatโ€™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 , 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 .

As a result of myelin loss, the conduction of 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 recent Brain, Behavior, and Immunity study 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.