Terraforming Mars

Neurons have the right shape for deep learning

Deep learning has brought about machines that can ‘see’ the world more like humans can, and recognize language. And while deep learning was inspired by the human brain, the question remains: Does the brain actually learn this way? The answer has the potential to create more powerful artificial intelligence and unlock the mysteries of human intelligence.

In a study published in eLife, CIFAR Fellow Blake Richards and his colleagues unveiled an algorithm that simulates how deep learning could work in our brains. The network shows that certain mammalian neurons have the shape and electrical properties that are well-suited for deep learning. Furthermore, it represents a more biologically realistic way of how real brains could do deep learning.

Research was conducted by Richards and his graduate student Jordan Guerguiev, at the University of Toronto, Scarborough, in collaboration with Timothy Lillicrap at Google DeepMind. Their algorithm was based on neurons in the neocortex, which is responsible for higher order thought.

“Most of these neurons are shaped like trees, with ‘roots’ deep in the brain and ‘branches’ close to the surface,” says Richards. “What’s interesting is that these roots receive a different set of inputs than the branches that are way up at the top of the tree.”

Using this knowledge of the neurons’ structure, Richards and Guerguiev built a model that similarly received signals in segregated compartments. These sections allowed simulated neurons in different layers to collaborate, achieving deep learning.

“It’s just a set of simulations so it can’t tell us exactly what our brains are doing, but it does suggest enough to warrant further experimental examination if our own brains may use the same sort of algorithms that they use in AI,” Richards says.

This research idea goes back to AI pioneers Geoffrey Hinton, a CIFAR Distinguished Fellow and founder of the Learning in Machines & Brains program, and program Co-Director Yoshua Bengio, and was one of the main motivations for founding the program in the first place. These researchers sought not only to develop artificial intelligence, but also to understand how the human brain learns, says Richards.

In the early 2000s, Richards and Lillicrap took a course with Hinton at the University of Toronto and were convinced deep learning models were capturing “something real” about how human brains work. At the time, there were several challenges to testing that idea. Firstly, it wasn’t clear that deep learning could achieve human-level skill. Secondly, the algorithms violated biological facts proven by neuroscientists.

Now, Richards and a number of researchers are looking to bridge the gap between neuroscience and AI. This paper builds on research from Bengio’s lab on a more biologically plausible way to train neural nets and an algorithm developed by Lillicrap that further relaxes some of the rules for training neural nets. The paper also incorporates research from Matthew Larkam on the structure of neurons in the neocortex. By combining neurological insights with existing algorithms, Richards’ team was able to create a better and more realistic algorithm simulating learning in the brain.

The tree-like neocortex neurons are only one of many types of cells in the brain. Richards says future research should model different brain cells and examine how they could interact together to achieve deep learning. In the long-term, he hopes researchers can overcome major challenges, such as how to learn through experience without receiving feedback.

“What we might see in the next decade or so is a real virtuous cycle of research between neuroscience and AI, where neuroscience discoveries help us to develop new AI and AI can help us interpret and understand our experimental data in neuroscience,” Richards says.

Just thought you should know I was browsing Archive Of Our Own and came across an actual fanfic about PIE. The fandom was listed as "languages (anthropomorphic)" and it had pairings such as "Mycenaean Greek/Minoan", "Gothic/Gaulic Latin" and "Pregermanic/Maglemosian". I just about died.

oh my god???!?

Psychologists and child development specialists have also come up with ways to support shy kids. The key, said Sandee McClowry, a psychologist at New York University, is to nudge children out of their comfort zones without trying to change their fundamental natures.

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New path into bipolar disorder comes to light

Bipolar disorder (BD) is a multifactorial brain disorder in which patients experience radical shifts in mood and undergo periods of depression followed by periods of mania. It has been known for some time that both environmental and genetic factors play important roles in the disease. For instance, exposure to high levels of stress for long periods, especially during childhood, is one factor associated with development of BD.  

New research published in Frontiers in Behavioral Neuroscience connects the dots between two genes involved in the brain’s response to environmental stimuli — called EGR3 and BDNF — and may explain the impaired resilience of BD patients to respond to events, including stress. The study not only provides new insights into the biology of BD, but also suggests that EGR3 could be a potential drug target.

Immediate early genes (IEGs) are a class of genes that respond very rapidly to environmental stimuli, including stress. IEGs respond to a stressor by activating other genes that lead to neuronal plasticity — that is, a change in form and function o brain cells in response to changes in the environment. Ultimately, the process of neuronal plasticity gives the brain the ability to learn from and adapt to new experiences.

One type of protein induced by IEGs is the so-called Early Growth Response (EGR) proteins, which translate environmental influence into long-term changes in the brain. These proteins are found throughout the brain and are highly produced in response to environmental changes such as stressful stimuli and sleep deprivation. Without the action played out by these proteins, brain cells and the brain itself cannot appropriately respond to the many stimuli that are constantly received from the environment.

Effective neuronal plasticity also depends on regulatory factors called neurotrophins that promote development and survival of brain cells. Brain-derived neurotrophic factor (BDNF), the neurotrophin mostly found in the brain, has been extensively investigated in BD patients and has been suggested as a hallmark of BD. Indeed, some studies have shown that serum levels of BDNF are reduced in BD patients during periods of depression, hypomania, or mania. Other studies have shown that regardless of mood state, BD patients present reduced levels of BDNF. Overall, changes in BDNF levels seem to be a characteristic found in BD patients that may contribute to the pathophysiology of the disease.

The new study by an international team of researchers from Universidade Federal do Rio Grande do Sul in Brazil, University of Arizona College of Medicine in the United States and McMaster University in Canada connects the dots between these two players to explain the impaired cellular resilience observed in BD that in the grand scheme of things may relate to the impaired resilience presented by BD patients to respond to events, including stress.

In a previous study by the group in 2016, one type of IEG gene known as EGR3, that normally responds to environmental events and stressful stimuli, was found to be repressed in the brain of BD patients. This suggests that when facing a stressor, the EGR3 in BD patients does not respond to the stimulus appropriately. Indeed, BD patients are highly prone to stress and have more difficulties dealing with stress or adapting to it if compared to healthy individuals. The research group is now suggesting that both EGR3 and BDNF may each play a critical role in the impaired cellular resilience seen in BD, and that each of these two genes may affect each other’s expression in the cell.

“We believe that the reduced level of BDNF that has been extensively observed in BD patients is caused by the fact that EGR3 is repressed in the brain of BD patients. The two molecules are interconnected in a regulatory pathway that is disrupted in BD patients,” says Fabio Klamt, leading author of the article.

The authors also add that the fact that EGR3 responds very quickly to environmental stimuli renders the molecule a potential drug target. “It is possible to imagine that EGR3 may be modulated in order to increase its expression and that of BDNF, which may have a positive impact on BD patients,” says Bianca Pfaffenseller, a scientist working at Hospital de Clínicas de Porto Alegre, in Brazil, and the first author of the study.

The idea that mental disorders should be seen as any other chronic disease in which the underlying biology plays an important role has replaced the old descriptions of mental illnesses as the result of bad psychological influences. As Nobel prize laureate Eric Kandel has said, “all mental processes are brain processes and therefore all disorders of mental functioning are biological diseases.” The perspective article authored by Fabio Klamt and colleagues supports this view by offering new insights into the underlying biology of this lifelong and devastating mental disorder affecting millions of people worldwide.

You are born with the ability to see whether people listen more often to the angel or the devil on their shoulder, based on the opacity of each- if they listen more to the angel, it’s more solid and the demon is more transparent, and vice versa. You recently met a guy online and you’re finally going to meet. You go in for a handshake and glance at his shoulders, but you can’t see the angel. Only a solid demon.

I love that you don't correct people thinking you are gay. Like you just roll with it. Or are you gay?

I have been straight for the last 22 years. But you know, there’s always tomorrow, amigo