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Huberman Lab · 2026-02-02 · Andrew Huberman (host), Read Montague

How Dopamine & Serotonin Shape Decisions, Motivation & Learning | Dr. Read Montague

48 research-tied claims examined: 5 contradicted 1 overstated 6 context 30 supported 6 unverified

30 Supported by research
0:05:39Read Montaguesupportedhigh

Dopamine fluctuations encode temporal difference errors—the difference between successive expectations—before reaching a terminal outcome.

"There's been no reinforcing feedback. It hasn't rained yet because it's not Saturday yet. I'm making a prediction about Saturday. But there's a difference between this expectation and that expectation. Those differences are encoded by dopamine. It's called the temporal difference error. Um, and dopamine seems to code that before you ever get to the terminal return." (said at 0:05:39)

The speaker accurately describes the core premise of the temporal difference reinforcement learning (TDRL) model of dopamine function. In TDRL models, midbrain dopamine neurons fire in response to temporal difference prediction errors—the difference between successive temporal expectations/predictions of future outcomes—updating value representations at intermediate time steps before the terminal outcome or reward is ever reached.

0:10:15Read Montaguesupportedmoderate

Temporal difference reward prediction error algorithms are biologically implemented across diverse species ranging from honeybees and sea slugs to humans.

"What is clear to me from data is an algorithm based on that is installed in bee brains, sea slug brains, all the way up to human brains. There are these temporal difference reward prediction errors." (said at 0:10:15)

Temporal difference (TD) reinforcement learning models and reward prediction error (RPE) mechanisms have been extensively demonstrated and computationally modeled across phylogenetic taxa. Seminal computational and neurobiological work (notably by Montague, Dayan, Sejnowski, and Schultz) demonstrated that invertebrate conditioning (such as octopaminergic VUMmx1 neuron signaling during honeybee foraging and classical/operant conditioning in Aplysia) and vertebrate mesencephalic dopamine signaling (in primates and humans) implement predictive reward prediction error algorithms consistent with temporal difference learning.

0:10:15Read Montaguesupportedvery low

In honeybee brains, temporal difference learning rules are mediated by octopamine rather than dopamine.

"In honeybee brains it's probably octopamine, not dopamine." (said at 0:10:15)

Published experimental and computational neurobiology demonstrates that appetitive reward conditioning in honeybees (Apis mellifera) is mediated by octopaminergic transmission (notably via VUMmx1 neurons), whereas dopamine mediates aversive conditioning and motor execution. Classic reinforcement learning models (e.g., Montague et al., based on Hammer's recordings in honeybees) established that octopaminergic signaling delivers the appetitive reinforcement/prediction signals analogous to dopamine in mammalian temporal difference models.

0:13:14Andrew Huberman (host)supportedmoderate

Red light and near-infrared light therapy sources have positive effects on muscle recovery, wound healing, acne, inflammation, mitochondrial function, and vision.

"Now, in addition to sunlight, red light and near-infrared light sources have been shown to have positive effects on improving numerous aspects of cellular and organ health, including faster muscle recovery, improved skin health and wound healing, improvements in acne, reduced pain and inflammation, even mitochondrial function, and improving vision itself." (said at 0:13:14)

The statement accurately reflects the published literature on red light and near-infrared photobiomodulation (PBM). The primary mechanism involves photon absorption by mitochondrial cytochrome c oxidase, boosting ATP production and modulating cellular signaling. Clinical and preclinical studies demonstrate positive outcomes across muscle recovery, wound repair, acne management, inflammation/pain reduction, and visual acuity in ocular conditions such as age-related macular degeneration.

0:18:57Read Montaguesupportedhigh

Simple expectation-outcome learning rules fail to account for higher-order conditioning where a secondary predictive cue is associated with a reward.

"So for example, if I show a light and train on a reward with an outcome and I use that expectation-outcome learning rule, it won't chain back to something that predicts a light. Suppose a sound predicts a light and we know the light predicted the outcome. Now I ask the question, well, what happens to the sound? Well, we know people learn. They'll associate the sound with the outcome. It's Pavlovian. Yeah. But those learning rules won't do that. They learn the wrong thing." (said at 0:18:57)

The speaker's claim is supported. Classical expectation-outcome learning rules (such as the standard Rescorla-Wagner delta rule) update associative strength purely on the basis of primary reward/unconditioned stimulus (US) presentation and outcome expectation. When a novel cue (CS2 / sound) is paired with an established predictive cue (CS1 / light) in the absence of the primary unconditioned reward, simple outcome-expectation learning rules fail: because expected reward is positive but actual unconditioned reward is zero, the model computes a negative prediction error, predicting conditioned inhibition or extinction of CS1 rather than chaining reward value back to CS2 (second-order conditioning). This well-known limitation motivated extensions like temporal difference learning and dual-system models (e.g., PVLV).

0:22:33Read Montaguesupportedhigh

DeepMind's AlphaGo Zero utilized Sutton and Barto's reinforcement learning algorithm to train entirely from scratch without expert human gameplay input.

"That algorithm that I just described with my hands waving is the same thing that David Silver and the DeepMind guys did when they made the world champion Go-playing program and it beat the world champion. And that particular game had expert advice built into it, okay? And they removed all that and then they trained it from scratch. It's called AlphaGo Zero." (said at 0:22:33)

AlphaGo Zero (developed by David Silver and the DeepMind team) replaced the human-expert data and supervised training utilized in the original AlphaGo with pure reinforcement learning from self-play, starting from random play without any expert human gameplay input.

0:27:02Read Montaguesupportedlow

Dopamine signals can operate on multiple timescales, with fast fluctuations encoding expectation changes and slower-changing envelope signals correlating with overall motivational state.

"And if you were doing an experiment, you were trying to look at dopamine, depending on the time scale you looked at, you might see little changes in it that correlated with fluctuating expectations. And you might see something as a kind of an envelope, a slower changing thing, which is the kind of experiment you might do in an experimental psychology setup. And that would look like it correlated with motivation with all these little wandering things going on underneath." (said at 0:27:02)

Electrophysiological and neurochemical recordings in animal models demonstrate that dopamine signals operate across multiple distinct timescales. Rapid (phasic) subsecond fluctuations encode momentary reward prediction errors and expectation updates, while slower baseline/envelope dynamics correlate with motivational state, behavioral vigor, and sustained task engagement.

0:38:15Read Montaguesupportedvery low

A 2004 paper by David Redish framed addiction as a computational disease where drugs blocking dopamine reuptake provide dopamine signals that the brain cannot anticipate.

"there was a paper in 2004 by David Redish talking about, um, addiction as a computational disease gone awry where you keep feeding system, um, a level of dopamine by putting a drug in that blocks its reuptake that it can't anticipate, right?" (said at 0:38:15)

A 2004 paper by A. David Redish published in Science titled 'Addiction as a computational process gone awry' presented a temporal-difference reinforcement learning (TDRL) computational model of addiction. In the model, drugs cause a noncompensable dopamine increase (such as by blocking reuptake) that the learning system cannot predict or drive to zero, leading to compulsive over-selection of drug-taking actions.

  • supports: Addiction as a computational process gone awry. (Science (New York, N.Y.) 2004) · cited 545x in the literature
    "These natural learning systems can be modeled through temporal-difference reinforcement learning (TDRL), which requires a reward-error signal that has been hypothesized to be carried by dopamine. TDRL learns to predict reward by driving that reward-error signal to zero. By adding a noncompensable drug-induced dopamine increase to a TDRL model, a computational model of addiction is constructed that over-selects actions leading to drug receipt." (abstract, passage verified)
    pubmedfull study (doi)
0:39:24Andrew Huberman (host)supportedhigh

ADHD medications such as Ritalin and Adderall increase brain levels of both dopamine and norepinephrine.

"These drugs, almost all of them, right, whether or not it's Ritalin or Adderall or these other drugs, they raise levels of dopamine and norepinephrine—" (said at 0:39:24)

The primary pharmacological mechanism of stimulant ADHD medications such as methylphenidate (Ritalin) and amphetamines (Adderall) is well-established. Methylphenidate acts predominantly as a dopamine and norepinephrine transporter inhibitor, whereas amphetamine acts as both a transporter inhibitor and a releasing agent; both mechanisms reliably elevate extracellular levels of dopamine and norepinephrine in brain regions such as the prefrontal cortex and striatum.

0:57:42Andrew Huberman (host)supportedmoderate

Having a smartphone in the same room, even if placed face down on a table or in a bag, reduces cognitive performance compared to having the phone in another room.

"I'd read this paper that was published recently that said that if your phone is upside down on a table or in your bag in the same room, it lowers cognitive performance. Even if you're not aware of the phone, it's pulling resources. It's pulling resources. If it's in another room, it seems that your cognitive performance returns to its previously higher levels." (said at 0:57:42)

The speaker accurately describes the seminal 'brain drain' study by Ward et al. (2017) and the broader literature on smartphone presence. In these experimental paradigms, participants perform cognitive tasks while their smartphones are placed either face-down on a desk, in a bag/pocket, or in another room. The seminal study and subsequent meta-analyses demonstrate that the mere presence of a smartphone reduces available cognitive capacity (e.g., working memory and attention) relative to having the device in another room, supporting the hypothesis that inhibiting automatic attention toward the device consumes limited cognitive resources.

0:32:20Andrew Huberman (host)supportedhigh

Dopamine neurons in the retina regulate light adaptation.

"They're doing things totally unrelated to any of this. They're controlling adaptation of light levels." (said at 0:32:20)

Dopaminergic neurons in the retina (specifically dopaminergic amacrine cells) play an established, fundamental role in regulating light and dark adaptation. In response to light, these cells release dopamine, which acts via D1- and D2-family receptors to alter retinal circuitry—such as uncoupling rod-cone electrical synapses, shifting signal flow from rod-mediated night vision to cone-mediated daytime vision, and adjusting receptive field surround strength.

0:39:56Read Montaguesupportedhigh

Forager honeybees communicate the distance and direction of nectar sources relative to the sun to other bees in the hive using the waggle dance.

"So, when you're a forager bee, uh, you come back and you do a little dance in the hive, and it tells the hive, uh, other foragers where to go find the nectar source. Okay. And it's a, it's a whole language. People have worked that out. It tells you fly this far with the sun here, and there's a polarization—" (said at 0:39:56)

The speaker's claim accurately describes the established mechanism of the honeybee waggle dance communication system. Returning forager bees perform waggle dances inside the hive that encode a spatial vector to a resource (such as nectar or pollen). The duration of the waggle run conveys the distance to the food source, while the angle of the waggle run relative to gravity (on vertical combs) represents the azimuth angle of the food source relative to the sun (or celestial polarization patterns).

1:03:36Read Montaguesupportedvery low

Learning in rodents requires opponent signaling between dopamine and serotonin systems.

"At your own institution, Rob Malenka has a set of beautiful results in rodents where the learning that they see in the animal requires that kind of opponency. And I mean, it's a definitive experiment in the rodent." (said at 1:03:36)

The speaker accurately describes published work from Robert Malenka's laboratory demonstrating opponent signaling between dopamine and serotonin in rodent reinforcement learning. Using simultaneous genetic access, recording, and optogenetic manipulation of dopamine and serotonin neurons in mice, the study showed that rewards increase dopamine signaling while decreasing serotonin signaling in the nucleus accumbens. Optogenetically blunting both signals together profoundly disrupted associative learning and reinforcement, whereas reproducing both opponent responses was sufficient to drive the acquisition of new associations. Certainty is rated very low because the findings are derived exclusively from rodent animal models.

  • supports: Opponent control of reinforcement by striatal dopamine and serotonin. (Nature 2025) · cited 48x in the literature
    "Simultaneous recording of DA and 5HT axon activity, together with genetically encoded DA and 5HT sensor recordings, revealed that rewards increase DA signalling and decrease 5HT signalling in the NAc. Optogenetically dampening DA or 5HT reward responses individually produced modest behavioural deficits in an appetitive conditioning task, while blunting both signals together profoundly disrupted learning and reinforcement. Optogenetically reproducing DA and 5HT reward responses together was sufficient to drive the acquisition of new associations and supported reinforcement more potently than either manipulation did alone. Together, these results demonstrate that striatal DA and 5HT signals shape learning by exerting opponent control of reinforcement." (abstract, results, passage verified)
    pubmedfull study (doi)
1:08:16Read Montaguesupportedlow

Dopamine transporters can bind to extracellular serotonin and clear it into dopamine terminals when SSRIs block serotonin reuptake.

"The mechanisms that suck dopamine out of the spaces of your brain will also bind to serotonin and suck it out, not quite as well because it's tuned. It's called a dopamine transporter. And so, depending on what the downstream parts of your brain think, then in fact increasing serotonin could decrease the serotonin in the serotonin terminals by blocking the reuptake." (said at 1:08:16)

The claim states that dopamine transporters (DAT) can bind and uptake extracellular serotonin into dopamine terminals, particularly when serotonin selective reuptake inhibitors (SSRIs) block the primary serotonin transporter (SERT). Published neurochemical literature confirms that monoamine transporters display substrate promiscuity; specifically, DAT is capable of binding and clearing serotonin from extracellular fluid when extracellular serotonin levels rise or when SERT is inhibited. However, evidence supporting this mechanism comes primarily from review and preclinical neurochemical literature rather than direct clinical trial evidence in humans.

1:09:28Read Montaguesupportedvery low

A paper in Neuron with John Dani as senior author demonstrated that the dopamine transporter pathway takes serotonin into dopamine terminals in rodents after SSRI administration.

"There was a killer paper 20 years ago on that where they showed they gave rodents some common SSRI, they waited this number of weeks, and they went in there to say where is the serotonin... And what they showed was that the dopamine transporter pathway was the thing that was taking it into the dopamine terminals because that's where the dopamine transporters are... It was in a journal called Neuron. John Dani was the senior author." (said at 1:09:28)

A 2005 study published in Neuron with John A. Dani as the senior author (Zhou et al.) demonstrated in rodent striatal tissue that when extracellular serotonin (5-HT) is elevated by SSRIs (such as fluoxetine), the dopamine transporter (DAT) pathway takes up serotonin into striatal dopamine terminals, leading to corelease of dopamine and serotonin. Because this is preclinical mechanistic animal research, the GRADE certainty is very low.

  • supports: Corelease of dopamine and serotonin from striatal dopamine terminals. (Neuron 2005) · cited 192x in the literature
    "We found that when extracellular 5-HT is elevated by exogenous application or by using antidepressants (e.g., fluoxetine) to inhibit the 5-HT transporters, the extremely dense striatal DATs uptake 5-HT into dopamine terminals. Immunohistochemical results and measurements using fast cyclic voltammetry showed that elevated 5-HT is taken up by DATs into striatal dopamine terminals that subsequently release 5-HT and dopamine together." (abstract, results, passage verified)
    pubmedfull study (doi)
1:13:40Read Montaguesupportedlow

An Israeli study showed that judicial rulings differ significantly based on whether the judges had recently eaten a meal.

"There's an Israeli paper from I don't know, about 10 years ago, where they looked at judges and the judgments that were made if you hadn't eaten versus judgments that you made that you had eaten, and you really want a judge that's had a good lunch." (said at 1:13:40)

The speaker accurately describes a well-known 2011 study by Danziger et al. published in PNAS, which examined over 1,000 parole board decisions by Israeli judges. The researchers reported that the probability of a favorable parole ruling dropped from approximately 65% at the beginning of a session to near 0% before a food break (such as morning snack or lunch), and abruptly rebounded to about 65% immediately after the break. Because this was an observational study analyzing sequential court records rather than a randomized trial, the certainty of evidence for causality is graded as low.

1:03:12Read Montaguesupportedmoderate

Read Montague's research group is the only group that records sub-second levels of dopamine and serotonin concurrently in conscious human beings during behavioral tasks.

"We are the only group who records sub-second levels of dopamine and serotonin in conscious human beings while they do things: reward-motivated tasks, social interactions with other people, various kinds of visual perceptual tasks, looking at emotional pictures—positive, negative, and neutral—and whatnot." (said at 1:03:12)

Published neurochemical studies confirm that P. Read Montague's laboratory developed and pioneered the methodology (using fast-scan cyclic voltammetry and machine learning/elastic net electrochemistry during deep brain stimulation or neurosurgical procedures) to simultaneously record sub-second levels of dopamine and serotonin in awake, conscious humans performing cognitive, reward, and perceptual behavioral tasks.

1:21:17Andrew Huberman (host)supportedhigh

Supplementing with N-acetylcysteine (NAC) supports glutathione production and detoxification in the body.

"while also making an effort to eat more leafy greens and supplementing with NAC, N-acetylcysteine, both of which can support glutathione production and detoxification." (said at 1:21:17)

The host's statement that supplementing with N-acetylcysteine (NAC) supports glutathione production and detoxification is well supported by established biochemistry and clinical literature. NAC serves as a bioavailable precursor of L-cysteine, the rate-limiting substrate for cellular glutathione (GSH) biosynthesis. In clinical pharmacology and toxicology, NAC administration is widely demonstrated to replenish intracellular glutathione pools and facilitate Phase II detoxification, most notably in the detoxification of toxic drug metabolites (such as N-acetyl-p-benzoquinone imine during acetaminophen exposure).

1:38:33Andrew Huberman (host)supportedhigh

The first phase of sleep provides deep sleep and a surge of growth hormone that supports bodily repair.

"The data would say that that first round of short sleep, you're grabbing your deep sleep. You're getting your growth hormone surge, which is great, bodily repair sufficient to keep you healthy enough." (said at 1:38:33)

Extensive physiological research confirms that slow-wave (deep) sleep predominates during the early sleep cycles, and sleep onset triggers a major pulsatile surge of growth hormone (GH). In healthy young men, approximately 70% of the 24-hour GH output occurs during early sleep in direct temporal association with the first period of slow-wave sleep. GH plays a primary role in cellular anabolism, protein synthesis, and tissue repair.

1:40:46Read Montaguesupportedhigh

In the ultimatum game, responders offered an 80/20 split are indifferent and reject the offer roughly 50% of the time.

"And at about 80/20, you're indifferent. In other words, 80% to me, 20% offered to you. 50% of the time, you're going to say, "I'll take it." 50% of the time, you're going to send me a signal and say, "You know, go home. I'm not taking that money."" (said at 1:40:46)

In classic experimental economics literature examining the Ultimatum Game (pioneered by Güth et al. and extensively replicated across cultures and laboratory settings), offers of 20% of the total stake (an 80/20 split) represent the standard empirical threshold where responders are roughly indifferent between accepting the money and punishing the proposer, leading to an approximate 50% rejection rate. Offers below 20% are rejected the vast majority of the time, whereas offers above 30% to 40% are almost always accepted.

1:57:15Andrew Huberman (host)supportedmoderate

Mild dehydration can impair both cognitive and physical performance.

"Even a slight degree of dehydration can diminish your cognitive and physical performance." (said at 1:57:15)

Evidence supports the claim that mild-to-moderate dehydration (hypohydration) can impair physical performance and certain aspects of cognitive function. A systematic review and meta-analysis on aerobic exercise performance found that pre-exercise hypohydration significantly reduced aerobic exercise performance by 2.4% and peak oxygen consumption by 2.4%. For cognitive performance, randomized crossover trials show that mild dehydration induced during daily activities impairs executive function and working memory, which reverses with rehydration; however, broader meta-analyses across active exercise contexts note that cognitive impairments may vary depending on the specific cognitive domain, task complexity, and whether dehydration is accompanied by heat stress.

2:02:18Read Montaguesupportedmoderate

Dopamine functions as a neural common currency by assigning a unified value metric to dissimilar options and outcomes.

"I refer to it as a currency mainly for the reason that a currency is used. It's a way to take dissimilar objects and assign a common value scheme to them." (said at 2:02:18)

Extensive neurobiological and neuroeconomic research supports the concept that dopamine and its target structures represent subjective value on a common scale or 'currency' across distinct reward types and attributes. Single-unit recordings in nonhuman primates demonstrated that midbrain dopamine prediction error responses integrate subjective value across multidimensional and vastly different rewards (such as food and liquid) into a unified value scale that predicts choice behavior. Similarly, rodent studies confirm that dopamine neurons can integrate appetitive and aversive outcomes into a value prediction error functioning as a common currency.

2:05:35Read Montaguesupportedmoderate

The entire human brain operates on approximately 23 watts of power.

"But we don't understand how it is that we get away to run our entire brain on 23 watts." (said at 2:05:35)

The human brain accounts for approximately 20% of the body's basal metabolic energy expenditure. Given a resting basal metabolic rate of roughly 100 W (corresponding to ~2,000 kcal/day), the total metabolic power required by the adult human brain is widely estimated in neuroscience and biocomputing literature to be around 20 watts (typically cited between 15 and 25 watts).

2:06:33Read Montaguesupportedmoderate

Echidnas experience REM sleep, contrary to earlier scientific belief.

"It used to be thought the echidna didn't have REM sleep, but that's no longer—that's false." (said at 2:06:33)

Early sleep studies (such as by Allison et al. in the 1970s) concluded that the short-beaked echidna (Tachyglossus aculeatus) lacked REM sleep because cortical EEG remained synchronized during sleep. Subsequent electrophysiological investigations by Siegel and colleagues demonstrated that echidnas exhibit brainstem neuronal activation and discharge variability characteristic of REM sleep concurrent with synchronized cortical EEG, disproving the earlier belief that monotremes lack REM sleep.

2:07:25Read Montaguesupportedhigh

Every cell in the human body contains internal circadian clocks.

"Now what we know is every cell in your body has clocks in it, and many multiple clocks." (said at 2:07:25)

Extensive molecular and cellular evidence confirms that cell-autonomous circadian clocks are present throughout the human body. In nucleated cells across peripheral tissues, this is driven by autonomous transcriptional-translational feedback loops (TTFL) involving core clock genes (e.g., CLOCK, BMAL1, PER, CRY). Furthermore, even enucleated cells lacking genomic transcription, such as mature red blood cells, maintain cell-autonomous ~24-hour circadian rhythms driven by non-transcriptional redox oscillations (e.g., peroxiredoxins) and rhythmic ion transport.

2:08:57Read Montaguesupportedmoderate

Cannabis consumption causes people to perceive that a long period of time has passed when only a short period has elapsed.

"What we do know is that people who smoke cannabis oftentimes think a long period of time went by and they find out that a very short period of time." (said at 2:08:57)

Acute cannabis and THC administration commonly alters interval timing and temporal estimation. In laboratory studies, acute THC exposure reliably produces time overestimation (estimating that more time has elapsed than the actual objective duration) and time underproduction in infrequent or non-tolerant cannabis users, an effect often attributed to an acceleration of the internal biological clock.

2:10:34Read Montaguesupportedmoderate

Approximately 5% of the population is stereoblind.

"He goes, "Oh, you're stereoblind. It's about, I don't know, 5% or something."" (said at 2:10:34)

A 2019 best-evidence synthesis review on the prevalence and diagnosis of stereoblindness in adults under 60 years of age found that multiple diagnostic approaches converged on a stereoblindness prevalence of approximately 7% (with higher rates observed in older populations). The estimate of ~5% closely matches the established epidemiological and psychophysical literature.

2:11:40Read Montaguesupportedhigh

In clinical trials of psychotropic medications with good outcome variables, 50% to 80% of the observed response is attributable to the placebo effect.

"Psychotropic meds, when you have a good outcome variable, 50 to 80% is a placebo effect, meaning not explained by any—you can't explain the variance by anything, but that doesn't mean it's a fake effect." (said at 2:11:40)

Extensive meta-analyses of clinical trials for psychotropic medications (most notably antidepressants) show that the placebo response accounts for approximately 65% to over 80% of the total symptom improvement observed in the active drug arm. An individual participant data analysis of 232 randomized placebo-controlled trials submitted to the FDA (n = 73,388; Stone et al., 2022, BMJ) demonstrated that the average difference between active antidepressant and placebo was only 1.75 points on the 17-item Hamilton Depression Rating Scale (HAMD-17), indicating that the vast majority of symptom reduction observed in clinical trials is shared with or accounted for by the placebo response, with only about 15% of participants experiencing a substantial benefit specific to the drug beyond the placebo effect.

2:27:14Read Montaguesupportedhigh

Blocking dopamine receptors reduces positive symptoms of schizophrenia, including auditory hallucinations.

"the most conspicuous feature of schizophrenia is the fact that blocking dopamine receptors turns the symptoms down a little bit. We discovered that a long time ago. It was very early on seen as a hyperdopaminergic state. And it is that. I mean, it is that if you block dopamine receptors, you don't hear voices anymore." (said at 2:27:14)

The dopamine hypothesis of schizophrenia and the clinical efficacy of dopamine D2 receptor antagonists in reducing positive symptoms (such as auditory hallucinations and delusions) represent standard psychiatric pharmacology. Extensive randomized trials and systematic reviews establish that blocking dopamine D2 receptors reduces positive psychotic symptoms in schizophrenia.

2:16:40Read Montaguesupportedhigh

John Jumper and Demis Hassabis were awarded the Nobel Prize for developing AlphaFold to predict protein structure from sequence data.

"AlphaFold is the program that takes DNA sequences and predicts protein structure, and this is what Jumper and Hassabis got the Nobel Prize for." (said at 2:16:40)

Demis Hassabis and John M. Jumper were awarded the 2024 Nobel Prize in Chemistry (jointly with David Baker) specifically for developing AlphaFold, an artificial intelligence system that predicts the 3D structures of proteins from their sequence data, solving a long-standing challenge in structural biology.

Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.