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Stem cell patch reverses brain damage in fetuses with spina bifida

A patch made of stem cells from donor placentas has been used to treat fetuses in the womb with a severe form of spina bifida as part of a world-first trial. The novel approach seems to have reversed a brain complication associated with the congenital condition at least as effectively as the go-to treatment, but is expected to enable more children to walk over the long term.

The mother of one of the babies, who is now 4 years old, says she expected that her son Toby would require a wheelchair when he was diagnosed with the condition in the womb. “But Toby is healthy [and] has hit all of his milestones – he’s walking, running and jumping – and has no problems with bladder control, which is rare for people with the condition,” she says.

Spina bifida – which affects about 1 in every 2,800 births in the US every year – occurs when a baby’s spine and spinal cord do not fully develop in the womb. In the most severe form of the condition, called myelomeningocele, the spinal cord and its surrounding tissue protrude out of a gap in the vertebrae, which often impairs mobility and bowel and bladder control. The cause of spina bifida is unknown, but folic acid deficiency during pregnancy raises the risk.

One of the standard treatments involves surgery in the womb that tucks the spinal cord and the surrounding tissue back into the vertebrae, before sewing up the skin to form a tight seal. “But many children still end up unable to walk and there’s [usually] no improvement in bowel or bladder control,” says Diana Farmer at the University of California, Davis.

This led Farmer and her colleagues to wonder if the addition of stem cells could help by promoting the growth and repair of spinal tissue. To find out, they recruited six pregnant women carrying fetuses with myelomeningocele.

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Noninvasive monitoring of gene expression in primate brains

Gene therapy has been successfully used to treat a number of diseases, including immune deficiencies, hereditary blindness, hemophilia and, recently, Huntington’s disease, a fatal neurological disorder.

An advance reported in the journal Neuron adds to the technique’s growing track record of evidence supporting the view that it could unlock powerful, personalized therapies: researchers found that released markers of activity (RMAs) ⎯ engineered proteins designed to cross the blood-brain barrier and persist in the blood for hours at a time, providing a reliable and noninvasive way to get information about gene expression in the brain ⎯ work just as well in monkeys as they do in mice.

Alongside precision, RMA technology is also capacious and adaptable: Different serum markers can be designed to track multiple genes across different brain regions. ScienceMission sciencenewshighlights.

Physicist: I Believe You Can Enhance Your Consciousness—And Expand Your Perception Into a “Different Realm”

But what if our biological makeup limits how creative we can be? Maybe the timing of the clock that governs our introspections forces our intuitive periods—or the times of uncertainty—to be too brief. Could we use our quantum technologies to extend the wavelike processing inside our brains? I am here inspired by Aldous Huxley, who suggested in his famous book, The Doors of Perception, that drugs could alter our consciousness, revealing true reality. But rather than using drugs, I envision quantum chips designed to suppress the “noise” that induces introspection, allowing a longer interference period for our intuitive thoughts to develop. This has the potential to be far more potent than what Huxley could ever have imagined.

For my idea to work, we would first have to understand where and how these superpositions are stored and manipulated in the brain. The British physicist Roger Penrose, PhD, has speculated that this occurs within microtubules, which are dynamic, hollow, rod-like components of the eukaryotic cytoskeleton that are responsible for things such as intercellular transport. Despite some circumstantial evidence, we do not have a strong reason to believe that microtubules are capable of quantum interference, but they are certainly worth further investigation. Once we understand how our brain uses quantum effects, we could then design a quantum chip that interfaces with the relevant biological components. Theoretically, the device would be able to upload superposition states to store them for longer periods and shield them from collapse, helping us to enhance our creative wavelike thinking.

One wonders what kind of power would be unleashed by doing this. I imagine the change would not be purely quantitative, so that we merely become faster calculators or quicker problem solvers, although even that would be amazing. Instead, I think the change could be qualitative, expanding our perception into a completely different realm, effectively creating a new species. We might theoretically become more powerful than modern humans, just as we currently are with respect to other apes. Quantum-enhanced humans would see further domains of reality that would otherwise remain hidden forever from us ordinary humans.

Identifying Key Regulators in Odorant Receptor Trafficking

JNeurosci: Lu and Matsunami analyzed gene activity to find proteins that help odor-detecting receptors reach the cell surface. They identified three helper genes—Gfy, Clgn, and Syt1—that support receptor function as olfactory cells mature.

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Odor detection in mammals is primarily mediated by odorant receptors (ORs), the largest family of G-protein-coupled receptors, expressed in olfactory sensory neurons (OSNs; [Buck and Axel, 1991][1]). However, most ORs exhibit little or no cell surface expression in nonolfactory cell types ([Lu et al., 2003][2]; [Hague et al., 2004][3]). While the accessory protein RTP1 and RTP2 enhance the expression of certain ORs, we hypothesized that additional proteins coregulated with RTP1 and RTP2 during OSN maturation may further enhance OR cell surface expression ([Saito et al., 2004][4]; [Zhuang and Matsunami, 2007][5]). To test this, we developed a computational pipeline based on publicly available single-cell transcriptomic data to create an interactive tool for exploring gene expression during OSN maturation.

One-question screen may flag hoarding in Alzheimer’s and other dementias

Researchers at the University of Colorado Anschutz have developed a simple, one-question screening tool that could help doctors quickly identify hoarding behaviors in patients with memory loss and other brain disorders. Early detection, they said, could lead to early intervention, helping to reduce safety risks, relieve caregiver stress and improve the quality of life for both patients and families.

The new tool was examined in a study published this month in The Journal of Neuropsychiatry and Clinical Neurosciences. The study was co-led by Peter Pressman, MD and Julia Schaffer, BA. The senior author is David Arciniegas, MD, professor of neurology at CU Anschutz.

“This was really born of shared observations in the memory clinic,” said Pressman, associate professor of neurology at Oregon Health & Science University who conducted the research while at CU Anschutz. “We noticed that hoarding was very common in these patients but it was not part of any screening protocols.”

Engineered protein markers read living brain gene activity in monkeys via blood

Gene therapy has been successfully used to treat a number of diseases, including immune deficiencies, hereditary blindness, hemophilia and, recently, Huntington’s disease, a fatal neurological disorder.

An advance reported in the journal Neuron adds to the technique’s growing track record of evidence supporting the view that it could unlock powerful, personalized therapies: Rice University bioengineer Jerzy Szablowski and collaborators in Vincent Costa’s lab at Emory University found that released markers of activity (RMAs) — engineered proteins designed to cross the blood-brain barrier and persist in the blood for hours at a time, providing a reliable and noninvasive way to get information about gene expression in the brain — work just as well in monkeys as they do in mice.

On the route from laboratory discovery to lifesaving treatment, large animal model studies are a critical part of the process. Most research never reaches this stage.

Bioengineered neuronal ‘circuit board’ mimics conditions of the human brain

A new bioengineered neuronal circuit board “BioConNet” allows scientists to artificially engineer human brain-like wiring at scale and can be used to engineer any possible circuit. The fully programmable, open-source system allows generation of large-scale circuits, while maintaining the ability to focus on single connections between neurons.

This is a key advance in engineering human-like neural circuits as it allows for a new level of wiring complexity compared to previous systems. BioConNet allows scientists increased control over wiring in the culture compared to existing methods such as organoids and commercially available systems. The research is published in the journal Advanced Healthcare Materials.

“By combining engineering and neurobiology with the most recent stem cell culture techniques, we can now create human-specific, functional, large-scale complex neural circuits in the lab,” said senior author, Dr. Andrea Serio, Reader in Neural Tissue Engineering, Group Leader at the UK Dementia Research Institute (UK DRI) at King’s and Senior Group Leader at the Crick.

High-Pressure Freezing EM Tomography of Entire Ribbon Synapses in the Retina

JNeurosci: Using advanced electron microscopy in rats, Zhang et al. captured 3D images of chemical synapses that perform visual computations in the retina. Their findings reveal how neural connections are structured for efficient visual signaling.

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In the retina, presynaptic active zones in photoreceptors and bipolar cells are distinguished by a plate-like “ribbon” linked to the plasma membrane (PM) and surrounded by dozens of synaptic vesicles (SVs) tethered to it. SVs at the base of the ribbon, closest to the PM, are thought to constitute the readily releasable vesicle pool (RRP), i.e., SVs primed to be released 1–2 ms following stimulation. The number of SVs in the RRP is a critical synaptic parameter that influences synaptic strength and varies with light levels to enable ribbon synapses to compute visual information. Physiological RRP measurements agree well with anatomical estimates obtained via electron microscopy (EM), although EM often employs chemical fixation, which causes exocytotic artifacts that may influence RRP size.

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