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Category: neuroscience – Page 853

To paraphrase Churchill’s words following the Second Battle of El Alamein: Google’s announcement about their new venture to extend human life, Calico, is not the end, nor even the beginning of the end, but it is, perhaps, the end of the beginning.

(MORE: Google vs. Death)

Since the dawn of civilization, humanity has been enslaved by the knowledge that no lifestyle choice, no medicine, no quirk of fate can enable anyone to live for more than a few decades without suffering progressive, inexorable decline in physical and mental function, leading inevitably to death. So soul-destroying has this knowledge been, for almost everyone, that we have constructed our entire society and world view around ways to put it out of our minds, mostly by convincing ourselves that the tragedy of aging is actually a good thing. And why not? After all, why be preoccupied about something one cannot affect?

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Protein Chrdl1 appears to regulate brain plasticity.

Researchers from the Salk Institute have discovered that a protein called Chrdl1, secreted by astrocytes, is responsible for driving synapse maturation and limiting brain plasticity later in life [1].

Abstract

In the developing brain, immature synapses contain calcium-permeable AMPA glutamate receptors (AMPARs) that are subsequently replaced with GluA2-containing calcium-impermeable AMPARs as synapses stabilize and mature. Here, we show that this essential switch in AMPARs and neuronal synapse maturation is regulated by astrocytes. Using biochemical fractionation of astrocyte-secreted proteins and mass spectrometry, we identified that astrocyte-secreted chordin-like 1 (Chrdl1) is necessary and sufficient to induce mature GluA2-containing synapses to form. This function of Chrdl1 is independent of its role as an antagonist of bone morphogenetic proteins (BMPs). Chrdl1 expression is restricted to cortical astrocytes in vivo, peaking at the time of the AMPAR switch. Chrdl1 knockout (KO) mice display reduced synaptic GluA2 AMPARs, altered kinetics of synaptic events, and enhanced remodeling in an in vivo plasticity assay.

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Human neurons are much larger than those of model organisms mice and rats, so it’s been unclear whether it’s size that makes a difference in our brain’s computational power. Now, in a study appearing October 18 in the journal Cell, researchers show that unlike those of other animals, human neurons employ highly compartmentalized signaling. Human dendrites—the tree-like branching structures that function as neurons’ antennas—process electrical signals differently than dendrites in rodents, the most common model systems for studying neuronal properties.

“The human neuron is basically like a rat neuron, but because it’s so much longer, signals have much farther to travel. The human dendrites thus have a different input-output function” from rats, says senior author Mark Harnett, the Fred and Carole Middleton Career Development Assistant Professor in the Department of Brain and Cognitive Sciences at the Massachusetts Institute of Technology. “Dendrites farther away from the cell body have fewer ion channels, which control signal processing. That was something we absolutely did not expect.”

Harnett, who studies how the biophysical features of neurons shape information processing in the brain, believes our longer, bigger dendritic arbors endow human neurons and their respective circuits with enhanced computational abilities.

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Neuroscientists are debating the nature and meaning of neural activity during the critical moment of working memory when people must hold information in mind.

Scientists present dueling theories in the high-stakes quest to understand how we hold and juggle multiple pieces of information in mind.

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Researchers healed mice with a genetic metabolic disorder that also affects humans by using a new editing tool to target and correct genetic mutations.

Some babies are born with the metabolic disorder phenylketonuria and need a special diet so that the amino acid phenylalanine doesn’t accumulate in the body. Excess phenylalanine delays mental and motor development. If left untreated, the children may develop mental disabilities.

The cause of this metabolic disorder is a mutation in a gene that provides the blueprint for the enzyme phenylalanine hydroxylase (Pah). The enzyme, which is produced by the cells of the liver, metabolizes phenylalanine.

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Speaking from beyond the grave, Professor Stephen Hawking has told a new generation growing up in an increasingly insular world: ‘Remember to look up at the stars and not down at your feet.’

The eminent cosmologist, who had motor neurone disease and died in March, had his final public thoughts broadcast at a special event to launch his last book, Brief Answers To The Big Questions.

Prof Hawking’s words of advice and defiance, echoing from an Imax screen at London’s Science Museum, brought tears to the eyes of his daughter Lucy.

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Today on The Neuroethics Blog is a post by Adina L. Roskies, Professor of Philosophy and chair of the Cognitive Science Program and Helman Family Distinguished Professor at Dartmouth College, entitled “What can neuroscience tell us about ethics?”

By Adina L. Roskies Image courtesy of Bill Sanderson, Wellcome Collection What can neuroscience tell us about ethics? Some say nothing – ethics is a normative discipline that concerns the way the world should be, while neuroscience is normatively insignificant: it is a descriptive science which tells us about the way the world is. This seems in line with what is sometimes called “Hume’s Law”, the claim that one cannot derive an ought from an is (Cohon, 2018). This claim is contentious and its scope unclear, but it certainly does seem true of demonstrative arguments, at the least. Neuroethics, by its name, however, seems to suggest that neuroscience is relevant for ethical thought, and indeed some have taken it to be a fact that neuroscience has delivered ethical consequences. It seems to me that there is some confusion about this issue, and so here I’d like to clarify the ways in which I think neuroscience can be relevant to ethics.

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Fletcher told the ABC the guidelines were developed in consultation with people living with autism, researchers and doctors, and had been approved by the National Health and Medical Research Council.

“It does not change what the NDIS does and indeed it may well be that there are people who, today, would not be diagnosed who will be diagnosed,” he said. “That will be a judgment for clinicians and medical profession and the NDIS will continue to do what it does, which is make an assessment of the impairment that somebody suffers as a result of a disability. Is it likely to be permanent and lifelong? Is it significant? What impact does it have on the functioning?”

Dr Wenn Lawson, the co-chair of the Australian Autism Research Council, said a consistent assessment and diagnosis process for autism meant people would be able to access more appropriate supports.

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Some of Allen’s philanthropy has taken a scientific bent: Allen founded the Allen Institute for Brain Science in 2003, pouring $500 million into the non-profit that aims to give scientists the tools and data they need to probe how brain works. One recent project, the Allen Brain Observatory, provides an open-access “catalogue of activity in the mouse’s brain,” Saskia de Vries, senior scientist on the project, said in a video. That kind of data is key to piecing together how the brain processes information.

Microsoft co-founder Paul Allen died today from complications with non-Hodgkin’s lymphoma. He was 65. Allen said earlier this month that he was being treated for the disease.

Allen was a childhood friend of Bill Gates, and together, the two started Microsoft in 1975. He left the company in 1983 while being treated for Hodgkin’s lymphoma and remained a board member with the company through 2000. He was first treated for non-Hodgkin’s lymphoma in 2009, before seeing it go into remission.

In a statement given to ABC News, Gates said he was “heartbroken by the passing of one of my oldest and dearest friends.” He went on to commend his fellow co-founder for his life after Microsoft:

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