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Category: neuroscience – Page 899

Most people have at some point echoed Macbeth’s complaint about the loss of “sleep that knits up the ravelled sleeve of care”. Sleep disorders, such as obstructive sleep apnoea (when breathing temporarily stops, causing both sleep disruption and lack of oxygen in blood) and sleep deprivation, have been associated with an increased risk of atherosclerosis and its harmful cardiovascular effects,. Atherosclerosis is characterized by the formation of ‘plaques’ in arteries, as white blood cells enter the artery wall, take up cholesterol and other substances from the blood and trigger an inflammatory response. However, the mechanisms linking sleep disruption and atherosclerosis have been largely unknown. Writing in Nature, McAlpine et al. show that persistent sleep disruption causes the brain to signal the bone marrow to increase the production of white blood cells.

McAlpine et al. studied mice that were prone to developing atherosclerosis. The authors induced sleep fragmentation by moving a bar intermittently across the bottom of the animals’ cages during their sleep period (Fig. 1), and compared these animals with animals that slept normally. They found that mice with sleep fragmentation had more-severe atherosclerosis, which was paralleled by increases in the production of white blood cells in the bone marrow and in the numbers of monocytes and neutrophils — two types of white blood cell — in the blood. These effects were absent if the bar was moved when the mice were fully awake. Stress activates the sympathetic nervous system (which is associated with the ‘fight-or-flight’ response), and such activation increases the production of white blood cells and atherosclerosis in other experimental settings. However, the authors did not find evidence for a role of sympathetic activation in their setting.

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Scientists think they’ve identified a previously unknown form of neural communication that self-propagates across brain tissue, and can leap wirelessly from neurons in one section of brain tissue to another – even if they’ve been surgically severed.

The discovery offers some radical new insights about the way neurons might be talking to one another, via a mysterious process unrelated to conventionally understood mechanisms, such as synaptic transmission, axonal transport, and gap junction connections.

“We don’t know yet the ‘So what?’ part of this discovery entirely,” says neural and biomedical engineer Dominique Durand from Case Western Reserve University.

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Deep-learning neural networks have come a long way in the past several years—we now have systems that are capable of beating people at complex games such as shogi, Go and chess. But is the progress of such systems limited by their basic architecture? Shimon Ullman, with the Weizmann Institute of Science, addresses this question in a Perspectives piece in the journal Science and suggests some ways computer scientists might reach beyond simple AI systems to create artificial general intelligence (AGI) systems.

Deep learning networks are able to learn because they have been programmed to create artificial neurons and the connections between them. As they encounter , new neurons and communication paths between them are formed—very much like the way the operates. But such systems require extensive training (and a feedback system) before they are able to do anything useful, which stands in stark contrast to the way that humans learn. We do not need to watch thousands of people in action to learn to follow someone’s gaze, for example, or to figure out that a smile is something positive.

Ullman suggests this is because humans are born with what he describes as preexisting network structures that are encoded into our neural circuitry. Such structures, he explains, provide growing infants with an understanding of the physical world in which they exist—a base upon which they can build more that lead to general intelligence. If computers had similar structures, they, too, might develop physical and social skills without the need for thousands of examples.

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There are a lot of people who like to claim themselves as “supremely logical.” The ones who insist that their every thought is controlled by reason and not emotions. Of course, this is incorrect. Outside of people with certain kinds of brain damage, people are not logical beings. Especially since there’s no definition of logic that fits the definition of what lot’s of people refer to as logic.

Why so many men online love to use “logic” to win an argument, and then disappear before they can find out they’re wrong.

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Genetic, epidemiologic, and biochemical evidence suggests that predisposition to Alzheimer’s disease (AD) may arise from altered cholesterol metabolism, although the molecular pathways that may link cholesterol to AD phenotypes are only partially understood. Here, we perform a phenotypic screen for pTau accumulation in AD-patient iPSC-derived neurons and identify cholesteryl esters (CE), the storage product of excess cholesterol, as upstream regulators of Tau early during AD development. Using isogenic induced pluripotent stem cell (iPSC) lines carrying mutations in the cholesterol-binding domain of APP or APP null alleles, we found that while CE also regulate Aβ secretion, the effects of CE on Tau and Aβ are mediated independent pathways. Efficacy and toxicity screening in iPSC- derived astrocytes and neurons showed that allosteric activation of CYP46A1 lowers CE specifically in neurons and is well tolerated by astrocytes. These data reveal that CE independently regulate Tau and Aβ and identify a druggable CYP46A1-CE-Tau axis in AD.

Van der Kant et al. performed a repurposing drug screen in iPSC-derived AD neurons and identified compounds that reduce aberrant accumulation of phosphorylated Tau (pTau). Reduction of cholesteryl ester levels or allosteric activation of CYP46A1 by lead compounds enhanced pTau degradation independently of APP and Aβ.

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Scientists at the University of Virginia School of Medicine have identified a potential explanation for the mysterious death of specific brain cells seen in Alzheimer’s, Parkinson’s and other neurodegenerative diseases.

The new research suggests that the may die because of naturally occurring in brain cells that were, until recently, assumed to be genetically identical. This variation – called “somatic mosaicism” – could explain why in the are the first to die in Alzheimer’s, for example, and why are the first to die in Parkinson’s.

“This has been a big open question in neuroscience, particularly in various neurodegenerative diseases,” said neuroscientist Michael McConnell of UVA’s Center for Brain Immunology and Glia, or BIG. “What is this selective vulnerability? What underlies it? And so now, with our work, the hypotheses moving forward are that it could be that different regions of the brain actually have a different garden of these [variations] in and that sets up different regions for decline later in life.”

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The so-called “zombie disease” has been reported in deer, elk, and moose across 24 US states, according to a new warning by the US Centers for Disease Control and Prevention (CDC).

As of January 2019, at least 251 counties across the US, from northern Montana to southern Texas, have reported CWD in free-ranging cervids, members of the deer family. Farther afield, there are similar concerns for reindeer in Norway, Finland, and, to a lesser extent, South Korea.

Scientifically known as chronic wasting disease (CWD), the contagious neurological disease gets its sensational nickname because of its effect on the brain of cervids, including North American elk or wapiti, red deer, mule deer, black-tailed deer, white-tailed deer, sika deer, reindeer, and moose. Deer that have been struck with the disease suffer from drastic weight loss, abnormal behavior, stumbling, drooling, lack of coordination, aggression, excessive thirst, and a fear of others.

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