Summary: Critical aspects of hippocampal function can be reversed in old age, or compensated for throughout life, with the help of neural stem cells. Source: TU DresdenWe all will experience it.
Category: neuroscience – Page 859
We all will experience it at some point, unfortunately: The older we get the more our brains will find it difficult to learn and remember new things
What the reasons underlying these impairments are is yet unclear but scientists at the Center for Regenerative Therapies of TU Dresden (CRTD) wanted to investigate if increasing the number of stem cells in the brain would help in recovering cognitive functions, such as learning and memory, that are lost during ageing.”
https://tu-dresden.de/tu-dresden/newsportal/news/verjuengung…en-maeusen
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Ein jeder wird es irgendwann erleben: Je älter wir werden, desto schwieriger wird es für unser Gehirn, neue Dinge zu lernen und sich an sie zu erinnern. Die Gründe hinter diesen Beeinträchtigungen sind oft unklar. Nun haben Wissenschaftler des Zentrums für Regenerative Therapien der TU Dresden (CRTD) untersucht, ob eine Erhöhung der Anzahl von Hirnstammzellen helfen würde, kognitive Funktionen wie Lernen und Gedächtnis wiederzuerlangen, die im Laufe des Alterns verloren gehen.
Die Forschungsgruppe von Prof. Federico Calegari hat dazu eine im eigenen Labor entwickelte Methode verwendet: Im Gehirn alter Mäuse stimulierten die Wissenschaftler den dort vorhandenen kleinen Pool neuronaler Stammzellen so, dass sich die Menge dieser Stammzellen und damit auch die Anzahl der aus ihnen erzeugten Gehirnzellen erhöhte. Das Team beobachtete, dass diese zusätzlichen Neuronen überleben und sogar neue Kontakte zu benachbarten Zellen knüpfen können. In einem nächsten Schritt untersuchten die Wissenschaftler eine wichtige Aufgabe des Gehirns, die ähnlich wie bei der Maus auch beim Menschen im Laufe des Alterns verloren geht: die Navigationsfähigkeit.
Missing protein in brain causes behaviors mirroring autism
Scientists at Rutgers University-Newark have discovered that when a key protein needed to generate new brain cells during prenatal and early childhood development is missing, part of the brain goes haywire—causing an imbalance in its circuitry that can lead to long-term cognitive and movement behaviors characteristic of autism spectrum disorder.
“During brain development, there is a coordinated series of events that have to occur at the right time and the right place in order to establish the appropriate number of cells with the right connections,” said Juan Pablo Zanin, Rutgers-Newark research associate and lead author on a paper published in the Journal of Neuroscience.” Each of these steps is carefully regulated and if any of these steps are not regulated correctly, this can impact behavior.”
Zanin has been working with Wilma Friedman, professor of cellular neurobiology in the Department of Biological Sciences, studying the p75NTR protein—needed to regulate cell division—to determine its exact function in brain development, gain a better understanding of how this genetic mutation could cause brain cells to die off and discover whether there is a genetic link to autism or neurological diseases like Alzheimer’s.
Nanoparticles deliver ‘suicide gene’ therapy to pediatric brain tumors growing in mice
Johns Hopkins researchers report that a type of biodegradable, lab-engineered nanoparticle they fashioned can successfully deliver a “suicide gene” to pediatric brain tumor cells implanted in the brains of mice. The poly(beta-amino ester) nanoparticles, known as PBAEs, were part of a treatment that also used a drug to kill the cells and prolong the test animals’ survival.
In their study, described in a report published January 2020 in the journal Nanomedicine: Nanotechnology, Biology and Medicine, the researchers caution that for safety and biological reasons, it is unlikely that the suicide gene herpes simplex virus type I thymidine kinase (HSVtk)—which makes tumor cells more sensitive to the lethal effects of the anti-viral drug ganciclovir—could be the exact therapy used to treat human medulloblastoma and atypical teratoid/rhabdoid tumors (AT/RT) in children.
So-called “suicide genes” have been studied and used in cancer treatments for more than 25 years. The HSVtk gene makes an enzyme that helps restore the function of natural tumor suppression.
Dendritic action potentials and computation in human layer 2/3 cortical neurons
A new unique signal discovered within the brain might be what makes us human:
https://science.sciencemag.org/content/367/6473/83
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A special developmental program in the human brain drives the disproportionate thickening of cortical layer 2/3. This suggests that the expansion of layer 2/3, along with its numerous neurons and their large dendrites, may contribute to what makes us human. Gidon et al. thus investigated the dendritic physiology of layer 2/3 pyramidal neurons in slices taken from surgically resected brain tissue in epilepsy patients. Dual somatodendritic recordings revealed previously unknown classes of action potentials in the dendrites of these neurons, which make their activity far more complex than has been previously thought. These action potentials allow single neurons to solve two long-standing computational problems in neuroscience that were considered to require multilayer neural networks.
Science, this issue p. 83
The active electrical properties of dendrites shape neuronal input and output and are fundamental to brain function. However, our knowledge of active dendrites has been almost entirely acquired from studies of rodents. In this work, we investigated the dendrites of layer 2 and 3 (L2/3) pyramidal neurons of the human cerebral cortex ex vivo. In these neurons, we discovered a class of calcium-mediated dendritic action potentials (dCaAPs) whose waveform and effects on neuronal output have not been previously described. In contrast to typical all-or-none action potentials, dCaAPs were graded; their amplitudes were maximal for threshold-level stimuli but dampened for stronger stimuli. These dCaAPs enabled the dendrites of individual human neocortical pyramidal neurons to classify linearly nonseparable inputs—a computation conventionally thought to require multilayered networks.
Cancer-like metabolism makes brain grow
The size of the human brain increased profoundly during evolution. A certain gene that is only found in humans triggers brain stem cells to form a larger pool of stem cells. As a consequence, more neurons can arise, which paves the way to a bigger brain. This brain size gene is called ARHGAP11B and so far, how it works was completely unknown. Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden now uncovered its mode of action. They show that the ARHGAP11B protein is located in the powerhouse of the cell—the mitochondria—and induces a metabolic pathway in the brain stem cells that is characteristic of cancer cells.
The research group of Wieland Huttner, a founding director of the Max Planck Institute of Molecular Cell Biology and Genetics, has been investigating the molecular mechanisms underlying the expansion of the brain during mammalian evolution for many years. In 2015, the group reported a key role for a gene that is only present in humans and in our closest extinct relatives, the Neanderthals and Denisovans. This gene, named ARHGAP11B, causes the so-called basal brain stem cells to expand in number and to eventually increase the production of neurons, leading to a bigger and more folded brain in the end. How the gene functions within the basal brain stem cells has been unknown so far.
Takashi Namba, a postdoctoral scientist in the research group of Wieland Huttner, wanted to find the answer to this question, together with colleagues from the Max Planck Institute, the University Hospital Carl Gustav Carus Dresden, and the Department of Medical Biochemistry at the Semmelweis University, Budapest. He found that the ARHGAP11B protein is located in mitochondria, the organelles that generate most of the cell’s source of chemical energy and hence are often referred to as the powerhouse of the cell. Takashi Namba explains the results: We found that ARHGAP11B interacts with a protein in the membrane of mitochondria that regulates a membrane pore. As a consequence of this interaction, the pores in the membrane are closing up, preventing calcium leakage from the mitochondria. The resulting higher calcium concentration causes the mitochondria to generate chemical energy by a metabolic pathway called glutaminolysis.