Immune cells in the brain that go rogue contribute to the death of neurons, so getting rid of them may slow the progression of neurodegenerative conditions like amyotrophic lateral sclerosis
Category: neuroscience – Page 45
Creating CAR-T Cells Using Current Alzheimer’s Antibodies
A team of researchers has biologically engineered T cells with currently available Alzheimer’s drugs in order to directly attack the characteristic amyloid plaques of Alzheimer’s disease.
Building on the current paradigm
Most Alzheimer’s treatments used in the clinic are-mabs, monoclonal antibodies that are designed to attack the amyloid beta plaques that accumulate in the brains of people with Alzheimer’s. However, while they have been found to have enough meaningful benefits in clinical trials to be approved by the FDA, they are not a cure, and some analyses question their effectiveness [1].
A unified framework combining linear and 3D molecular features for robust drug-protein interaction prediction
Robust drug-protein interaction prediction tool.
The researchers develop PointDPI to predict drug-protein interactions (DPIs) by integrating linear and 3D molecular structures.
PointDPI preserves intermolecular relationships and predicts key regulatory sites, outperforming several state-of-the-art methods.
Four predicted drug-protein interactions (DPIs) are experimentally validated at both mRNA and protein levels, highlighting the therapeutic potential of adenosine in inflammatory diseases, ondansetron and etodolac in neurological diseases, and neuroprotective action for dopamine. sciencenewshighlights ScienceMission https://sciencemission.com/rug-protein-interaction
Sun et al. develop PointDPI to predict drug-protein interactions (DPIs) by integrating linear and 3D molecular structures. PointDPI preserves inter-molecular relationships and predicts key regulatory sites, outperforming several state-of-the-art methods.
Scientists discover new gatekeeper cell in the brain
VIB and Ghent University researchers have identified and characterized a previously unknown cellular barrier in the brain, which sheds new light on how the brain is protected from the rest of the body. In a study published in Nature Neuroscience, the scientists also reveal a new pathway by which the immune system can impact the brain.
Prof. Roosmarijn Vandenbroucke (VIB–UGent Center for Inflammation Research), said, “These findings reveal how vulnerable and protectable the brain is, opening new perspectives for more targeted interventions in brain disorders.”
The brain is protected from the rest of the body by multiple barriers that maintain a stable, tightly regulated environment and defend it against harmful substances and pathogens. The most well-known of these barriers is the blood-brain barrier, but another critical interface is the choroid plexus, a small structure found within the brain’s fluid-filled spaces, which produces cerebrospinal fluid.
Driven electrolytes are agile and active at the nanoscale
Technologies for energy storage as well as biological systems such as the network of neurons in the brain depend on driven electrolytes that are traveling in an electric field due to their electrical charges. This concept has also recently been used to engineer synthetic motors and molecular sensors on the nanoscale or to explain biological processes in nanopores. In this context, the role of the background medium, which is the solvent, and the resulting hydrodynamic fluctuations play an important role. Particles in such a system are influenced by these stochastic fluctuations, which effectively control their movements.
“When we imagine the environment inside a driven electrolyte at the nanoscale, we might think of a calm viscous medium in which ions move due to the electric field and slowly diffuse around. This new study reveals that this picture is wrong: the environment resembles a turbulent sea, which is highly nontrivial given the small scale,” explains Ramin Golestanian, who is director of the Department of Living Matter Physics at MPI-DS, and author of the study published in Physical Review Letters.
The research uncovers how the movement of the ions creates large-scale fluctuating fluid currents that stir up the environment and lead to fast motion of all the particles that are immersed in the environment, even if they are not charged.
Aging brains pile up damaged synaptic proteins in microglia
It is increasingly clear, though, that the loss of synapses—the flexible and adaptive relay stations central to our brains’ ability to think, learn, and remember—is central to the rise of cognitive decline and dementia in old age.
Now, researchers have discovered clues that may tie synapse loss to another hallmark of brain aging: the declining ability of brain cells to break down and recycle damaged proteins.
Published in Nature, the study shows that synaptic proteins are particularly susceptible to this age-related garbage-disposal problem: In old age, synaptic proteins break down much more slowly, they become more likely to pile up into the tangled clumps of protein characteristic of neurodegenerative disease, and they are more likely to make their way into microglia, immune cells that prune away damaged synapses.
Those findings are the latest in a series of discoveries that suggest new links between the brain’s waste management systems, microglia, and neurodegeneration—and they could yield new insights into human brain aging and neurodegeneration, said the study’s lead author. ScienceMission sciencenewshighlights.
A glaucoma drug may help prevent opioid relapse
An existing drug currently used to treat glaucoma, altitude sickness, and seizures may also have the potential to prevent relapse in opioid use disorder, according to a study by researchers at University of Iowa Health Care. The work is published in the journal Neuropsychopharmacology.
The UI researchers led by John Wemmie, MD, Ph.D., focused on the drug known as acetazolamide (AZD) because it blocks the activity of a brain enzyme called carbonic anhydrase 4 (CA4). Wemmie’s team had previously discovered that inhibiting CA4 in the whole brain, or just in its reward center (the nucleus accumbens), of mice, significantly reduced the brain changes that occurred after cocaine withdrawal. In addition, blocking the CA4 enzyme reduced drug-seeking behavior and relapse in the mice.
“What makes this approach promising is that it works in a completely different way from current treatments,” says Wemmie, a professor of psychiatry in the UI Carver College of Medicine. “Instead of targeting opioid receptors, AZD targets a different pathway involved in drug-induced synaptic changes and drug-seeking behavior. This could open the door to new therapies that help people stay in recovery by addressing the brain’s long-term response to drug use.”
Strategies for blood–brain barrier rejuvenation and repair
The blood–brain barrier (BBB) is a dynamic interface that tightly regulates the transport of substances from the blood into the brain. BBB dysfunction can occur with ageing and is a hallmark of many major diseases but is underappreciated as a therapeutic target. Here, Searson and Banks review studies on BBB repair and rejuvenation, highlighting common mechanisms across disorders and potential strategies for pharmacological intervention.