Daniel Dennett is one of the most influential philosophers in the world. He is an atheist, Darwinist and materialist. For him, we humans are nothing but a complex piece of matter subject to natural laws. He talks to Yves Bossart about our consciousness, illusions, freedom and faith.
German version: • Daniel Dennett im Gespräch über Geist…
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What makes one a person or a self? If he or she sees, hears, thinks and feels, is that a person or a self? How can separate perceptions bind together into a coherent mental unity of a single person or self?
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One of the variables in TD algorithms is called reward prediction error (RPE), which is the difference between the discounted predicted reward at the current state and the discounted predicted reward plus the actual reward at the next state. TD learning theory gained traction in neuroscience once it was demonstrated that firing patterns of dopaminergic neurons in the ventral tegmental area (VTA) during reinforcement learning resemble RPE5,9,10.
Implementations of TD using computer algorithms are straightforward, but are more complex when they are mapped onto plausible neural machinery11,12,13. Current implementations of neural TD assume a set of temporal basis-functions13,14, which are activated by external cues. For this assumption to hold, each possible external cue must activate a separate set of basis-functions, and these basis-functions must tile all possible learnable intervals between stimulus and reward.
In this paper, we argue that these assumptions are unscalable and therefore implausible from a fundamental conceptual level, and demonstrate that some predictions of such algorithms are inconsistent with various established experimental results. Instead, we propose that temporal basis functions used by the brain are themselves learned. We call this theoretical framework: Flexibly Learned Errors in Expected Reward, or FLEX for short. We also propose a biophysically plausible implementation of FLEX, as a proof-of-concept model. We show that key predictions of this model are consistent with actual experimental results but are inconsistent with some key predictions of the TD theory.
Can you pass me the whatchamacallit? It’s right over there next to the thingamajig.
Many of us will experience “lethologica”, or difficulty finding words, in everyday life. And it usually becomes more prominent with age.
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Join the late, renowned philosopher and cognitive scientist Daniel C Dennett on a captivating journey of intellectual exploration through his own life.
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The neurons that produce a sick feeling and food aversion are distinct from those that induce a feeling of fullness.
By Mariana Lenharo & Nature magazine
Next-generation anti-obesity drugs such as Wegovy can melt away weight — but they can also cause intolerable nausea. Now scientists have pinpointed a brain pathway that is involved in this common side effect, raising the prospect of effective weight-loss drugs that don’t make people sick1.
Toddlers engage more regions of their brains around 16-months to help them develop important cognitive skills enabling them to follow simple instructions and control impulses. Findings from the study, led by the Universities of Bristol and Oxford, and published in Imaging Neuroscience, suggests 16 months is a critical period for brain development.
A child’s first two years of life are crucial for developing cognitive skills, particularly executive functions that help adjust thoughts, actions, and behaviours for everyday life.
Inhibitory control is one important executive function. This particular skills allows individuals to stop themselves from doing something out of impulse, habit or temptation. It’s already known that inhibitory control begins to develop in infancy and grows into early childhood. However, until now, the brain mechanisms involved in its development were unclear.
A study investigating the effect of sleep on brain performance has found a link between an individual’s preference for morning or evening activity and their brain function, suggesting that self-declared “night owls” generally tend to have higher cognitive scores.
Researchers at Imperial College London looked at data from more than 26,000 people to find out how different aspects of sleep—including duration, patterns, and quality—affected mental sharpness and overall cognitive ability.
Using data from the extensive UK Biobank database, they analyzed information on U.K. adults who had completed a number of cognitive tests—including whether people described themselves as a “morning person” or an “evening person,” referring to which time of the day they felt more alert and productive.
Why did the experience of consciousness evolve from our underlying brain physiology? Despite being a vibrant area of neuroscience, current research on consciousness is characterised by disagreement and controversy – with several rival theories in contention.
A recent scoping review of over 1,000 articles identified over 20 different theoretical accounts. Philosophers like David Chalmers argue that no single scientific theory can truly explain consciousness.
We define consciousness as embodied subjective awareness, including self awareness. In a recent article published in Interalia (which is not peer reviewed), we argue that one reason for this predicament is the powerful role played by intuition.
To create one-time cures for Alzheimer’s disease, researchers are investigating the application of CRISPR-Cas9 gene-editing for novel therapies. Cutting and pasting genes is difficult with current technology, but CRISPR gene editing may help later stages or those individuals with hereditary mutations. Variants in the lipid transport protein apolipoprotein E (APOE4) have been associated with late-onset Alzheimer’s disease, with a three-to twelve-fold increase in risk.
Researchers engineered the Christchurch gene variation into mice bearing human APOE4 using CRISPR. After that, these mice were crossed, resulting in progeny that carried one or two copies of the modified variation.
The group discovered that mice bearing a single copy of the APOE4-Christchurch variation exhibited a partial defense against Alzheimer’s disease. The disease did not exhibit typical symptoms in mice carrying two copies. The work mimics the advantageous effects of the Christchurch mutation to propose possible treatment strategies for Alzheimer’s disease associated with APOE4.
