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Category: neuroscience – Page 809

‘Amazing Natural Experiment’: In This Amazonian Tribe, Brains Don’t Age Like Ours

The Tsimane, an indigenous people who live in the Bolivian peripheries of the Amazon rainforest, lead lives that are very different to ours. They seem to be much healthier for it.

This tribal and largely isolated population of forager-horticulturalists still lives today by traditional ways of farming, hunting, gathering, and fishing – continuing the practices of their ancestors, established in a time long before industrialization and urbanization transformed most of the world.

For the Tsimane, the advantages are considerable. A study published in 2017 found that they effectively have the healthiest hearts in the world, with the lowest reported levels of coronary artery disease of any population ever recorded.

Computer simulations of the brain can predict language recovery in stroke survivors

At Boston University, a team of researchers is working to better understand how language and speech is processed in the brain, and how to best rehabilitate people who have lost their ability to communicate due to brain damage caused by a stroke, trauma, or another type of brain injury. This type of language loss is called aphasia, a long-term neurological disorder caused by damage to the part of the brain responsible for language production and processing that impacts over a million people in the US.

“It’s a huge problem,” says Swathi Kiran, director of BU’s Aphasia Research Lab, and College of Health & Rehabilitation Sciences: Sargent College associate dean for research and James and Cecilia Tse Ying Professor in Neurorehabilitation. “It’s something our lab is working to tackle at multiple levels.”

For the last decade, Kiran and her team have studied the brain to see how it changes as people’s improve with speech . More recently, they’ve developed new methods to predict a person’s ability to improve even before they start therapy. In a new paper published in Scientific Reports, Kiran and collaborators at BU and the University of Texas at Austin report they can predict recovery in Hispanic patients who speak both English and Spanish fluently—a group of aphasia patients particularly at risk of long-term language loss—using sophisticated computer models of the brain. They say the breakthrough could be a game changer for the field of speech therapy and for stroke survivors impacted by aphasia.

Expression of human‐specific ARHGAP11B in mice leads to neocortex expansion and increased memory flexibility

Generation of an ARHGAP11B-transgenic mouse line.

To generate a stable transgenic mouse line that expresses an ARHGAP11B protein, we first determined the temporal and spatial expression patterns of human ARHGAP11A and human ARHGAP11B mRNAs by qPCR of foetal human neocortical tissue at various developmental stages (gestational weeks 12–21; Fig EV1A and B) and by analysing previously published RNA-seq data sets of defined isolated NPC and neuron populations (Florio et al, 2015) (Fig EV1C and D), respectively. As the expression patterns of ARHGAP11A and ARHGAP11B mRNAs were found to be similar, we decided to generate the transgenic mouse line by converting one allele of the mouse Arhgap11a gene into a mutant mouse ARHGAP11B gene (mARHGAP11B), using the CRISPR/Cas9 genome editing technology (for details, see Materials and Methods). In m ARHGAP11B, the 55 nucleotides of Arhgap11a that in humans would be deleted from the ARHGAP11B mRNA by splicing using the new splice-donor site are replaced by the 141 nucleotides encoding the human-specific 47-amino acid sequence plus three nucleotides to generate a translational stop codon (Fig EV1E). Unless indicated otherwise, the ARHGAP11B-transgenic mice obtained (referred to as 11B mice hereafter) were used as heterozygous animals, that is, with one mouse Arhgap11a allele being replaced by m ARHGAP11B. The resulting ARHGAP11B protein will be expressed in developing mouse neocortex under the control of the native mouse Arhgap11a promotor.

Sonothermogenetics for noninvasive and cell-type specific deep brain neuromodulation

Critical advances in the investigation of brain functions and treatment of brain disorders are hindered by our inability to selectively target neurons in a noninvasive manner in the deep brain.

This study aimed to develop sonothermogenetics for noninvasive, deep-penetrating, and cell-type-specific neuromodulation by combining a thermosensitive ion channel TRPV1 with focused ultrasound (FUS)-induced brief, non-noxious thermal effect.

The sensitivity of TRPV1 to FUS sonication was evaluated in vitro. It was followed by in vivo assessment of sonothermogenetics in the activation of genetically defined neurons in the mouse brain by two-photon calcium imaging. Behavioral response evoked by sonothermogenetic stimulation at a deep brain target was recorded in freely moving mice. Immunohistochemistry staining of ex vivo brain slices was performed to evaluate the safety of FUS sonication.

A Massive New Gene Editing Project Is Out to Crush Alzheimer’s

The idea is simple: decades of research have found certain genes that seem to increase the chance of Alzheimer’s and other dementias. The numbers range over hundreds. Figuring out how each connects or influences another—if at all—takes years of research in individual labs. What if scientists unite, tap into a shared resource, and collectively solve the case of why Alzheimer’s occurs in the first place?

The initiative’s secret weapon is induced pluripotent stem cells, or iPSCs. Similar to most stem cells, they have the ability to transform into anything—a cellular genie, if you will. iPSCs are reborn from regular adult cells, such as skin cells. When transformed into a brain cell, however, they carry the original genes of their donor, meaning that they harbor the original person’s genetic legacy—for example, his or her chance of developing Alzheimer’s in the first place. What if we introduce Alzheimer’s-related genes into these reborn stem cells, and watch how they behave?

By studying these iPSCs, we might be able to follow clues that lead to the genetic causes of Alzheimer’s and other dementias—paving the road for gene therapies to nip them in the bud.

Neuralink Brain Chip Will End Language in Five to 10 Years, Elon Musk Says

In a recent interview, Elon Musk stated that the human language could possibly end within five to ten years. The CEO of Neuralink went to talk with Joe Rogan, implying that with the innovation of the brain chip the company is currently developing, humans won’t have to speak anymore using traditional languages.

Neuralink develops a chip that will soon be able to attach to the human brain. The chip’s invention aimed to communicate faster and conveniently. Through a single universal language, Elon Musk believes that the way we talk today will soon improve. The brain chip is expected to be completed to be developed within a few years, and by then, our communication could possibly evolve.

Elon Musk stated that the Neuralink chip’s success may take a while, but it should take five to ten years if the development will accelerate. He also added that the progress of the brain chip is on track, but with only to focus on their current objective, which is to help people minimize and prevent brain injuries, Express reported.

Elon Musk’s Brain Chip Completion on Progress, Initial Batch Will Solve Brain Injuries

The brain chip’s power was already displayed in a 2019 long-stream video by Neuralink. In the video published on the YouTube channel Monkey MindPong, a monkey with an active chip on its brain was shown playing a video game that is similar to a table tennis match. The astounding display of the monkey’s brain reaction toward the game left experts in awe.

Continue reading “Neuralink Brain Chip Will End Language in Five to 10 Years, Elon Musk Says” | >

BPA Exposure Below Regulatory Levels Can Impact Brain Development

Summary: A new mouse study reveals that exposure to BPA at levels 25 times lower than deemed safe has an impact on brain development.

Source: University of Calgary.

Humans are exposed to a bath of chemicals every day. They are in the beds where we sleep, the cars that we drive and the kitchens we use to feed our families. With thousands of chemicals floating around in our environment, exposure to any number is practically unavoidable. Through the work of researchers like Dr. Deborah Kurrasch, PhD, the implications of many of these chemicals are being thoroughly explored.

A Browsable Petascale Reconstruction of the Human Cortex

In January 2020 we released the fly “hemibrain” connectome — an online database providing the morphological structure and synaptic connectivity of roughly half of the brain of a fruit fly (Drosophila melanogaster). This database and its supporting visualization has reframed the way that neural circuits are studied and understood in the fly brain. While the fruit fly brain is small enough to attain a relatively complete map using modern mapping techniques, the insights gained are, at best, only partially informative to understanding the most interesting object in neuroscience — the human brain.

Today, in collaboration with the Lichtman Laboratory at Harvard University, we are releasing the “H01” dataset, a 1.4 petabyte rendering of a small sample of human brain tissue, along with a companion paper, “A connectomic study of a petascale fragment of human cerebral cortex.” The H01 sample was imaged at 4nm-resolution by serial section electron microscopy, reconstructed and annotated by automated computational techniques, and analyzed for preliminary insights into the structure of the human cortex. The dataset comprises imaging data that covers roughly one cubic millimeter of brain tissue, and includes tens of thousands of reconstructed neurons, millions of neuron fragments, 130 million annotated synapses, 104 proofread cells, and many additional subcellular annotations and structures — all easily accessible with the Neuroglancer browser interface.

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