WEEK 1 - GAME TRAINING 1. nutrition 2. Health-related behaviour 3. Biochemistry. Val/Val (warriors) → low baseline DA, fast DA loss → flexibility
Reward, Learning & Games - Howard et al. Nutrition: use epidemiological studies, as intervention studies (high striatal DA). Met/Met (worriers)→ high baseline DA, slow
Reinforcement learning: relies upon midbrain dopaminergic have limitations. → Good for longevity usually good for the brain. loss → stability. Val worse sustained attention, improve with
response to reward (enhanced attention): ventral tegmental Dendrate gyrus: only BA that generates new neurons. Varies amp. while Met shows decline. Dual-state theory: high DA PFC
area (VTA) → DA to PFC, NA, amygdala, hippo. Otherwise with stress, glucose level, growth factors, aerobic fitness, good for stabilization but bad for flexibility, vice-versa for high
neutral stimuli become valuable. Influences declarative nutrition. Nutrition child hood: B12(myelin formation, red striatum DA. Conclusion: 1. Distinct optimum levels of DA exist
memory. Long-term potentiation (LTP): learning and blood cells, growth factors) D (nerve growth factors, glia cells, for different cognitive functions 2. Cognitive control is a multi-
memory. Two fases: 1. early phase, considered to comprise brain size). Mineral depletion: Iodine during pregnancy factorial phenomenon, requiring a dynamic balance between
changes in synaptic strength, associated retention, over a scale (retardation brain growth), Iron childhood (learning & memory cognitive stability and cognitive flexibility 3. Manipulation of DA
of minutes and perhaps hours. DA less involved. 2. later phase, deficiencies), Zinc (memory, ADHD, aggression, adult cog. will have paradoxical cognitive consequences depending on the
considered responsible for making memories permanent, decline). Blue zones: highest longevity; Sicily, Öland, Okinawa, type of task component under study, the brain region that is
through processes of synaptic plasticity involving protein Costa Rica, Greece → combines diet, climate & life style. French implicated, & baseline DA levels in that brain region within that
synthesis. Rewards closely linked to achievement can be paradox: how Mediterranean diet low cv-disease? → omega 3, individual.
assumed to reflect more strongly on self-esteem and social- anti oxidants, polyphenols. COMT in response to AMP - Mattay et al.
esteem. Amphetamine enhanced efficiency of prefrontal cortex function
Brain training - Simons et al. during a WM-task in val/val genotype subjects (lower PFC DA)
Disagreement effectiveness of brain training (BT) →different at all levels of task difficulty → Subjects met/met genotype
standards. Review finds evidence BT improves performance on (superior baseline prefrontal function), drug had no effect on
trained tasks, less on closely related tasks, little on distantly cortical efficiency at low-to-moderate WM-load, caused
related tasks, no everyday CE. → Major shortcomings in design/ deterioration at high WM-load → inverted-U functional-response
analysis, no study conformed all best practices. Formal curve.
discipline theory: mental capacities can be improved through Cogn dysf in recr/dep cocaine users – Vonmoos
exercise. Near, far, horizontal & vertical transfer. BT logic Dependent CU display broad cognitive impairments in attention,
VT & FT → train skills that can be applied in substantive content WM declarative memory, executive functions. The performance
domains and in different contexts. Mixed results: comparable of recreational CU in all four domains was intermediate between
expectations CG & IG (placebo)? Publication bias: weaker that of controls and dependent users, they displayed significant
effects. Moderating effects. Improvements: preregistration, deficits foremost in attention & WM. ADHD symptoms, craving
randomisation & sampling, dosing, blinding, control conditions, + age at onset important modulators of cognitive function in CU.
report reliability, provide data & statistics. → changes frontostriatal network.
WEEK 3 - PLASTICITY
Lecture notes Acute cocaine effects 2models inhibitory control- Fillmore
Plasticity of visual cortex/amblyopia – Sengpiel
Paper vs screen: 1 navigation: location helps memorise, Both tasks showed cocaine-induced facilitation of inhibitory
Amblyopia: not simply a monocular deficit, new non-invasive
turning pages. 2 mental resources: paper, wall of text, less control, but dose-response functions differed depending on
approaches force eyes to cooperate, instead punish good eye.
distractions, easier lost; internet, shorter articles, more measures. Stop-signal measure revealed a quadratic dose-
Ocular dominance (OD) is probed by monocular deprivation
distractions. 3 attitude: digital media for relaxation → response function, cued go-no-go measure showed more
(MD)(patching). NMDA receptor key role mediating functional
associative learning. Flynn effect: gain mean IQ. orderly, linear improvement as function of dose → suggests
plasticity → blocking NMDA receptor function abolished OD shift
Multitasking: heavy vs light → shapes in blue & red, memorise two-phasic dose-response: facilitating effects of stimulant
towards open eye during the critical period. NMDA receptor
orientation, blue are distractors. Result: LMMT performed drugs on inhibitory control limited to a range of intermediate
mediated plasticity is bidirectional → changes to synaptic
consistently, HMMT sensitive to distractors! Diff in accuracy. No doses, above which improvement is no longer evident &
transmission caused 1form visual experience (complete
proof task switching HMMT. → chicken/egg problem. Video impairing effects emerge. Limitations: mis-labelling
darkness) reversed by other experience (normal day–night
games: skills, knowledge, behaviour, enhance cog. Hype dependent/recreational, sample bias (high end).
cycle).Threshold level GABA required to open critical period +
cycle: 1. Peak inflated exp. Effect of tyrosine stress/cogn demand – Jongkees
balance of excitation and inhibition (E/I) controls time course of
(overhyped), 2. Trough of TYR: precursor DA & NE → cover L-dopa, limited to
critical period. Amblyopia treatable appropriate sensory
disillusionment (not as great) concentration TH enzyme (no overdose) effects DA U-curve can
stimulation alone. Caveat: humans may not want to sit in
3. Slope of enlightenment be maintained! Preferred > L-dopa, since L-dopa can be
prolonged periods of total darkness. Other strategy: aimed at
(what is possible) 4. Plateau of overdosed & have severe side-effects. Seems to enhance
reducing intracortical inhibition or altering the E/I balance;
productivity. Game training: cognitive performance in short-term stressful/ cognitively
involves repetitive rTMS or tDCS applied to the visual cortex.
Gozli: track dot → gamers demanding situations (+stress, + DA/NE activity). Clinical
Most successful: ‘training’ vision through amblyopic eye.
steeper improvement & smaller effect less promising. Effect depend heavily on weather a
Alternative approach: video games for training by engaging
deviation (learning effects). shortage of TYR directly contributes to the pathology & if DA
attentional mechanisms.
Why? Fun, rewards (operant conditioning, uncertainty, reward synthesis is affected by the disorder (park. Reduced TH).
Brain machine interfaces - Lebedev et al.
scheduling (%), anticipation, adaptivity (difficulty/progress))→ Increased pos vs neg affective perception following serotonin &
Non-invasive: severely and partially paralyzed patients
50% most effective, DA level. Flow: match difficulty & skill. NE reuptake inhibition - Harmer et al.
reacquire basic communication & motor control using EEG-based
Social factors, engagement/identity. BT-programs: little Can antidepressant drugs modulate neural processing of
BMIs, motor recovery limited → would require high-resolution
evidence (learning effects & near transfer) shortcomings affective information? Results: citalopram + reboxetine
signals which can be done using invasive approaches (EcoGs,
publication bias, null-findings also findings, transfer (N-back: reduced identification of negative facial expressions (anger,
fMRI). Invasive: 1. extract motor signals from firing patterns of
visual WM/ auditory WM), no control groups (passive fear). Citalopram abolished increased startle response found in
neuronal populations 2. use these to reproduce motor
(hawthorne effect: engaging leads to improvement), active context negative affective images. Both increased relative recall
behaviours in actuators → BMI devices need to act and feel
(motivation?), experimental), expectation/motivation, of positive (versus negative) emotional material. Reboxetine
consistent to patients own limbs. Bottlenecks: 1. Stable, long-
multi/single tasking. decreased subjective ratings hostility & elevated energy → Such
term recordings of large pops of neurons from multiple brain
WEEK 2 - BODILY INFLUENCES effects ameliorate negative biases in information processing
areas 2. Computationally efficient algos that incorporate BMI
Aerobic fitness - Talukdar et al. that characterise mood & anxiety disorders. Antidepressants
software for translating neuronal activity into high-accuracy
Aerobic fitness enhances structural brain plasticity → Study modulate perception & memory for negative/ positive emotional
command signals capable of limb control 3. Learning how to use
investigated effects of aerobic fitness (measured by VO2max) material.
brain plasticity to incorporate prosthetic devices into body's
on individual differences in whole-brain functional connectivity Lecture notes
representation 4. Implementing prosthetics capable of accepting
assessed from resting state fMRI data. Stimulate: 1. Production Val: no diff accuracy with AMP, but better PFC efficiency at all
brain-derived control signals to perform movements (visual
of neurotrophic proteins 2. Development new vascular structure levels of load compared to placebo. Met: no diff accuracy or
feedback).
3. Increased connections 4. Increased volume of brain efficiency with amp at low load → low accuracy & PFC efficiency
Constraint-induced movement therapy - Kwakkel et al.
structures underlying executive function (prefrontal cortex) at high load compared to placebo. Tyrosine: can reverse mental
CIMT: overcome upper limb impairments after stroke (not the
attention + learning (basal ganglia),memory (hippocampus). decline & improve ST cognition (reverse DA depletion, ADHD).
lesion causes limitation in movement but disuse of limb that
Results: aerobic fitness associated with individual differences in 1-back task: no effect tyrosine compared to control. 2-back
reinforces non-movement) 1. graded practice restricted limb for
functional connectivity within core ICNs that are known to task: sig. effect → way harder, more stress! NLS:
task-specific improvement 2. constrained or forced use therapy
mediate beneficial effects of physical activity on executive Propranolol→drug used to reduce anxiety→ when administered
for non effected limb 3. transfer packages gained movements
function (frontoparietal network), attention + learning (dorsal before presentation, helps anxious people. beta-blocker / dep-
from lab to real-world→ Improved motor function, arm-hand
and ventral attention network), memory (default mode ressant that has anxiolytic effects by blocking the action of
activities, self-reported arm-hand functioning. No evidence
network). Sensitive regions displayed strong functional adrenaline and noradrenaline; 4 methods blocking neurotrans-
intensity of practice or timing affected outcome. mCIMT:
connections to nodes that fell outside their core functional mitters: 1 blocking release, 2 reuptake by axon terminals, 3
repetitive task-specific training of the restricted arm. Not well
network topology. Predictive of FI. deactivation by enzymes 4 blood diffusion; DA→reward, goal
understood→ enhanced cortical neuroplasticity might be
Exercise training - Erickson et al. proximity, motivation. ADHD = high DA transporter density, DA
associated with learned non-use and compensatory skill learning
Shrinking hippo leads to impaired memory + risk dementia. AET = reuptaken→inattention, reduced inhibition. DA antagonist
rather than neurological repair or recovery of impairment.
increases hippo volume (anterior hippo but not posterior, due to →reduced hallucinations in schizos. Assess perf in drug usage:
Critical period 5-14 days post stroke.
serum BDNF level changes) by 2% effectively reversing age- (based on exec funct) 1 WM: involved in updating / manipula-
Lecture notes
related loss in volume by 1 -2y. Hippo mediator neurogenesis ting, 2 Shifting 3 inhib: ability to ‘resist’ (stop signal, stroop);
visual cortex=several layers w distinct function/ocular
dentate gyrus. → Caudate nucleus and thalamus volumes were WM→stability; shifting→flexibility, competitive. Nigrostriatal
dominance columns. Cortisol pathway vision after blindness →
unaffected by the intervention (exercise does not influence all pathway→flexibility. Mesolimbic/mesocortical pathway→stab
rewired (=plasticity); vis cortex deprived. From sensory input →
brain regions uniformly). AET: +learning & retention, + grey & Effect caffeine on switching task perf→When interval between
axons grow less dense/branch less; critical period→neurons
white matter. > change fitness, > change volume, +baseline stimuli=high→more time to prepare for switching. Caffeine
extremely prone to plasticity; cortical areas of monkeys post
fitness – volume loss RH. →reduced switching cost for 1.5 s delays (time to prepare).
stroke→no rehab=total cortical area of contralateral hand
Nutrition impacts cognition/emotion - Spencer et al. Tryptophan→supplement useful in reducing anxiety/depression,
shrinks significantly, with constrain induced therapy→cortical
Understanding relationship diet, cognition, emotion is necessary while promoting sleep.
area almost back original size; critical period: after stroke brain
to uncover mechanisms involved in/ strategies to prevent WEEK 5 - PSYCHEDELICS AND MEDITATION
releases growth factors to promote repair→release of inhibiting
neurological conditions in obese individuals. Early-life diet and Pharmacological, neural & psychological mechanisms underlying
molecules→critical period when GF at peak, inh not there yet→5-
exposure to stress can lead to cognitive dysfunction throughout psychedelics - Elk & Yaden
14 days; Phantom pain→feel non present limb (cortical
life → nutritional interventions. High-fat diet Hippo 1. Biochemical level: serotonergic hallucinogens bind to 5-
pathways haven’t rewired yet), mirror-box therapy → little
neuroinflammatory response to mild immune challenge, causing HT2A serotonin receptors because of resemblance with
clinical evidence. Plasticity in senso- ry-substitution technology:
memory deficits. Low mega-3 contribute depression serotonin molecule. Psychoplastogen model: psy +
1 Tongue display unit (TDU) →ma- chine convert visual input to
Hormonal contra use predicts performance – Bradshaw neuroplasticity. Oxytocin critical period social reward learning,
stimulation on tongue w camera, activating sensory brain areas,
HC use associated lower self-control, brain differences. 2 anti-inflammatory properties. 2. Neural level: CSTC model:
applied to blind ppl → activation of visual areas
studies: HC use woman show less perseverance on simple and Psy release inhibitory control > gating (PFC) > overload sensory
brain(=plasticity); 2 brain-machine interfaces: people learn how
challenging tasks, performing worse (only on GRE problems) bc processing > increased stimulation serotonin, DA, GABA.
to control machine w brain 3 deep brain stim (DBS) →
they spent less time on the tasks. Perseverance predictive of: REBUS: Psy suppress bottom-up prediction & priors. CCC
restructures network’s structure through electrical stim
job performance, well-being, academic achievement. model: Psy destabilise cortical network & decouples claustrum
(=plasticity at very specific network lvl); pill for plasticity=focus
Nutrition/Prevention of cognitive impairment – Scarmeas from frontal areas → loss cognitive control.
on understanding growth inhib factors, goal = create antibody
Association between nutrition & cognitive outcomes stronger for 3. Psychological level: Altered & affective states (mystical
that binds to receptors, allowing cells to grow
healthy dietary patterns than for individual nutrients/ food experience, feeling of awe, ego dissolution) → increased global
WEEK 4 - DRUGS & NEUROTRANSMITTERS
groups → cumulative beneficial effects of many ingredients in connectivity high-level association areas & thalamus +
Between persistence and flexibility – Hommel
these diets. Nutrition=important lifestyle factor, can modify risk decreased default mode network activity.
2 DA pathways: 1. mesofrontal pathway (PFC +D1) 2.
of future cognitive impairment and dementia. Certain nutrients Meditation & plasticity of predictive mind – Laukkonen
nigrostriatal pathway (striatum+D2) → PFC and Striatum hold
or food ingredients: some B vitamins (particularly folate), Many-to-(n)one: meditation techniques bring subject closer to
opposite roles of controlling, PFC propagates stability, the
flavonoids, vitamin D, and n-3 fatty acids, have the potential to present moment & thereby progressively abating hierarchically
striatum flexibility. DA as mediator. Metacontrol state model
benefit cognitive function; Food groups: fish (possibly other deep predictive processing. Predictive processing: brain
(MSM): changes of control styles affect goal impact and
seafood), veggies, to lesser extent fruit, moderate alcohol & makes predictions based on past experience (hierarchy of
competitiveness between alternatives (+impact goal, +
coffee protect vs cognitive decline. Dash diet: low NA, high Ka, expectation, perceptual & active inference, attention, inferred
stability).
Ca, Mag → lower blood pressure. hierarchical self, fact free learning & insight). Meditation:
Inverted-U-shape DA on WM & Cogn control - Cools et al.
Lecture notes focussed attention. Open monitoring: natural state of the
COMT-gene influence: inactivate DA release PFC.
Reward, Learning & Games - Howard et al. Nutrition: use epidemiological studies, as intervention studies (high striatal DA). Met/Met (worriers)→ high baseline DA, slow
Reinforcement learning: relies upon midbrain dopaminergic have limitations. → Good for longevity usually good for the brain. loss → stability. Val worse sustained attention, improve with
response to reward (enhanced attention): ventral tegmental Dendrate gyrus: only BA that generates new neurons. Varies amp. while Met shows decline. Dual-state theory: high DA PFC
area (VTA) → DA to PFC, NA, amygdala, hippo. Otherwise with stress, glucose level, growth factors, aerobic fitness, good for stabilization but bad for flexibility, vice-versa for high
neutral stimuli become valuable. Influences declarative nutrition. Nutrition child hood: B12(myelin formation, red striatum DA. Conclusion: 1. Distinct optimum levels of DA exist
memory. Long-term potentiation (LTP): learning and blood cells, growth factors) D (nerve growth factors, glia cells, for different cognitive functions 2. Cognitive control is a multi-
memory. Two fases: 1. early phase, considered to comprise brain size). Mineral depletion: Iodine during pregnancy factorial phenomenon, requiring a dynamic balance between
changes in synaptic strength, associated retention, over a scale (retardation brain growth), Iron childhood (learning & memory cognitive stability and cognitive flexibility 3. Manipulation of DA
of minutes and perhaps hours. DA less involved. 2. later phase, deficiencies), Zinc (memory, ADHD, aggression, adult cog. will have paradoxical cognitive consequences depending on the
considered responsible for making memories permanent, decline). Blue zones: highest longevity; Sicily, Öland, Okinawa, type of task component under study, the brain region that is
through processes of synaptic plasticity involving protein Costa Rica, Greece → combines diet, climate & life style. French implicated, & baseline DA levels in that brain region within that
synthesis. Rewards closely linked to achievement can be paradox: how Mediterranean diet low cv-disease? → omega 3, individual.
assumed to reflect more strongly on self-esteem and social- anti oxidants, polyphenols. COMT in response to AMP - Mattay et al.
esteem. Amphetamine enhanced efficiency of prefrontal cortex function
Brain training - Simons et al. during a WM-task in val/val genotype subjects (lower PFC DA)
Disagreement effectiveness of brain training (BT) →different at all levels of task difficulty → Subjects met/met genotype
standards. Review finds evidence BT improves performance on (superior baseline prefrontal function), drug had no effect on
trained tasks, less on closely related tasks, little on distantly cortical efficiency at low-to-moderate WM-load, caused
related tasks, no everyday CE. → Major shortcomings in design/ deterioration at high WM-load → inverted-U functional-response
analysis, no study conformed all best practices. Formal curve.
discipline theory: mental capacities can be improved through Cogn dysf in recr/dep cocaine users – Vonmoos
exercise. Near, far, horizontal & vertical transfer. BT logic Dependent CU display broad cognitive impairments in attention,
VT & FT → train skills that can be applied in substantive content WM declarative memory, executive functions. The performance
domains and in different contexts. Mixed results: comparable of recreational CU in all four domains was intermediate between
expectations CG & IG (placebo)? Publication bias: weaker that of controls and dependent users, they displayed significant
effects. Moderating effects. Improvements: preregistration, deficits foremost in attention & WM. ADHD symptoms, craving
randomisation & sampling, dosing, blinding, control conditions, + age at onset important modulators of cognitive function in CU.
report reliability, provide data & statistics. → changes frontostriatal network.
WEEK 3 - PLASTICITY
Lecture notes Acute cocaine effects 2models inhibitory control- Fillmore
Plasticity of visual cortex/amblyopia – Sengpiel
Paper vs screen: 1 navigation: location helps memorise, Both tasks showed cocaine-induced facilitation of inhibitory
Amblyopia: not simply a monocular deficit, new non-invasive
turning pages. 2 mental resources: paper, wall of text, less control, but dose-response functions differed depending on
approaches force eyes to cooperate, instead punish good eye.
distractions, easier lost; internet, shorter articles, more measures. Stop-signal measure revealed a quadratic dose-
Ocular dominance (OD) is probed by monocular deprivation
distractions. 3 attitude: digital media for relaxation → response function, cued go-no-go measure showed more
(MD)(patching). NMDA receptor key role mediating functional
associative learning. Flynn effect: gain mean IQ. orderly, linear improvement as function of dose → suggests
plasticity → blocking NMDA receptor function abolished OD shift
Multitasking: heavy vs light → shapes in blue & red, memorise two-phasic dose-response: facilitating effects of stimulant
towards open eye during the critical period. NMDA receptor
orientation, blue are distractors. Result: LMMT performed drugs on inhibitory control limited to a range of intermediate
mediated plasticity is bidirectional → changes to synaptic
consistently, HMMT sensitive to distractors! Diff in accuracy. No doses, above which improvement is no longer evident &
transmission caused 1form visual experience (complete
proof task switching HMMT. → chicken/egg problem. Video impairing effects emerge. Limitations: mis-labelling
darkness) reversed by other experience (normal day–night
games: skills, knowledge, behaviour, enhance cog. Hype dependent/recreational, sample bias (high end).
cycle).Threshold level GABA required to open critical period +
cycle: 1. Peak inflated exp. Effect of tyrosine stress/cogn demand – Jongkees
balance of excitation and inhibition (E/I) controls time course of
(overhyped), 2. Trough of TYR: precursor DA & NE → cover L-dopa, limited to
critical period. Amblyopia treatable appropriate sensory
disillusionment (not as great) concentration TH enzyme (no overdose) effects DA U-curve can
stimulation alone. Caveat: humans may not want to sit in
3. Slope of enlightenment be maintained! Preferred > L-dopa, since L-dopa can be
prolonged periods of total darkness. Other strategy: aimed at
(what is possible) 4. Plateau of overdosed & have severe side-effects. Seems to enhance
reducing intracortical inhibition or altering the E/I balance;
productivity. Game training: cognitive performance in short-term stressful/ cognitively
involves repetitive rTMS or tDCS applied to the visual cortex.
Gozli: track dot → gamers demanding situations (+stress, + DA/NE activity). Clinical
Most successful: ‘training’ vision through amblyopic eye.
steeper improvement & smaller effect less promising. Effect depend heavily on weather a
Alternative approach: video games for training by engaging
deviation (learning effects). shortage of TYR directly contributes to the pathology & if DA
attentional mechanisms.
Why? Fun, rewards (operant conditioning, uncertainty, reward synthesis is affected by the disorder (park. Reduced TH).
Brain machine interfaces - Lebedev et al.
scheduling (%), anticipation, adaptivity (difficulty/progress))→ Increased pos vs neg affective perception following serotonin &
Non-invasive: severely and partially paralyzed patients
50% most effective, DA level. Flow: match difficulty & skill. NE reuptake inhibition - Harmer et al.
reacquire basic communication & motor control using EEG-based
Social factors, engagement/identity. BT-programs: little Can antidepressant drugs modulate neural processing of
BMIs, motor recovery limited → would require high-resolution
evidence (learning effects & near transfer) shortcomings affective information? Results: citalopram + reboxetine
signals which can be done using invasive approaches (EcoGs,
publication bias, null-findings also findings, transfer (N-back: reduced identification of negative facial expressions (anger,
fMRI). Invasive: 1. extract motor signals from firing patterns of
visual WM/ auditory WM), no control groups (passive fear). Citalopram abolished increased startle response found in
neuronal populations 2. use these to reproduce motor
(hawthorne effect: engaging leads to improvement), active context negative affective images. Both increased relative recall
behaviours in actuators → BMI devices need to act and feel
(motivation?), experimental), expectation/motivation, of positive (versus negative) emotional material. Reboxetine
consistent to patients own limbs. Bottlenecks: 1. Stable, long-
multi/single tasking. decreased subjective ratings hostility & elevated energy → Such
term recordings of large pops of neurons from multiple brain
WEEK 2 - BODILY INFLUENCES effects ameliorate negative biases in information processing
areas 2. Computationally efficient algos that incorporate BMI
Aerobic fitness - Talukdar et al. that characterise mood & anxiety disorders. Antidepressants
software for translating neuronal activity into high-accuracy
Aerobic fitness enhances structural brain plasticity → Study modulate perception & memory for negative/ positive emotional
command signals capable of limb control 3. Learning how to use
investigated effects of aerobic fitness (measured by VO2max) material.
brain plasticity to incorporate prosthetic devices into body's
on individual differences in whole-brain functional connectivity Lecture notes
representation 4. Implementing prosthetics capable of accepting
assessed from resting state fMRI data. Stimulate: 1. Production Val: no diff accuracy with AMP, but better PFC efficiency at all
brain-derived control signals to perform movements (visual
of neurotrophic proteins 2. Development new vascular structure levels of load compared to placebo. Met: no diff accuracy or
feedback).
3. Increased connections 4. Increased volume of brain efficiency with amp at low load → low accuracy & PFC efficiency
Constraint-induced movement therapy - Kwakkel et al.
structures underlying executive function (prefrontal cortex) at high load compared to placebo. Tyrosine: can reverse mental
CIMT: overcome upper limb impairments after stroke (not the
attention + learning (basal ganglia),memory (hippocampus). decline & improve ST cognition (reverse DA depletion, ADHD).
lesion causes limitation in movement but disuse of limb that
Results: aerobic fitness associated with individual differences in 1-back task: no effect tyrosine compared to control. 2-back
reinforces non-movement) 1. graded practice restricted limb for
functional connectivity within core ICNs that are known to task: sig. effect → way harder, more stress! NLS:
task-specific improvement 2. constrained or forced use therapy
mediate beneficial effects of physical activity on executive Propranolol→drug used to reduce anxiety→ when administered
for non effected limb 3. transfer packages gained movements
function (frontoparietal network), attention + learning (dorsal before presentation, helps anxious people. beta-blocker / dep-
from lab to real-world→ Improved motor function, arm-hand
and ventral attention network), memory (default mode ressant that has anxiolytic effects by blocking the action of
activities, self-reported arm-hand functioning. No evidence
network). Sensitive regions displayed strong functional adrenaline and noradrenaline; 4 methods blocking neurotrans-
intensity of practice or timing affected outcome. mCIMT:
connections to nodes that fell outside their core functional mitters: 1 blocking release, 2 reuptake by axon terminals, 3
repetitive task-specific training of the restricted arm. Not well
network topology. Predictive of FI. deactivation by enzymes 4 blood diffusion; DA→reward, goal
understood→ enhanced cortical neuroplasticity might be
Exercise training - Erickson et al. proximity, motivation. ADHD = high DA transporter density, DA
associated with learned non-use and compensatory skill learning
Shrinking hippo leads to impaired memory + risk dementia. AET = reuptaken→inattention, reduced inhibition. DA antagonist
rather than neurological repair or recovery of impairment.
increases hippo volume (anterior hippo but not posterior, due to →reduced hallucinations in schizos. Assess perf in drug usage:
Critical period 5-14 days post stroke.
serum BDNF level changes) by 2% effectively reversing age- (based on exec funct) 1 WM: involved in updating / manipula-
Lecture notes
related loss in volume by 1 -2y. Hippo mediator neurogenesis ting, 2 Shifting 3 inhib: ability to ‘resist’ (stop signal, stroop);
visual cortex=several layers w distinct function/ocular
dentate gyrus. → Caudate nucleus and thalamus volumes were WM→stability; shifting→flexibility, competitive. Nigrostriatal
dominance columns. Cortisol pathway vision after blindness →
unaffected by the intervention (exercise does not influence all pathway→flexibility. Mesolimbic/mesocortical pathway→stab
rewired (=plasticity); vis cortex deprived. From sensory input →
brain regions uniformly). AET: +learning & retention, + grey & Effect caffeine on switching task perf→When interval between
axons grow less dense/branch less; critical period→neurons
white matter. > change fitness, > change volume, +baseline stimuli=high→more time to prepare for switching. Caffeine
extremely prone to plasticity; cortical areas of monkeys post
fitness – volume loss RH. →reduced switching cost for 1.5 s delays (time to prepare).
stroke→no rehab=total cortical area of contralateral hand
Nutrition impacts cognition/emotion - Spencer et al. Tryptophan→supplement useful in reducing anxiety/depression,
shrinks significantly, with constrain induced therapy→cortical
Understanding relationship diet, cognition, emotion is necessary while promoting sleep.
area almost back original size; critical period: after stroke brain
to uncover mechanisms involved in/ strategies to prevent WEEK 5 - PSYCHEDELICS AND MEDITATION
releases growth factors to promote repair→release of inhibiting
neurological conditions in obese individuals. Early-life diet and Pharmacological, neural & psychological mechanisms underlying
molecules→critical period when GF at peak, inh not there yet→5-
exposure to stress can lead to cognitive dysfunction throughout psychedelics - Elk & Yaden
14 days; Phantom pain→feel non present limb (cortical
life → nutritional interventions. High-fat diet Hippo 1. Biochemical level: serotonergic hallucinogens bind to 5-
pathways haven’t rewired yet), mirror-box therapy → little
neuroinflammatory response to mild immune challenge, causing HT2A serotonin receptors because of resemblance with
clinical evidence. Plasticity in senso- ry-substitution technology:
memory deficits. Low mega-3 contribute depression serotonin molecule. Psychoplastogen model: psy +
1 Tongue display unit (TDU) →ma- chine convert visual input to
Hormonal contra use predicts performance – Bradshaw neuroplasticity. Oxytocin critical period social reward learning,
stimulation on tongue w camera, activating sensory brain areas,
HC use associated lower self-control, brain differences. 2 anti-inflammatory properties. 2. Neural level: CSTC model:
applied to blind ppl → activation of visual areas
studies: HC use woman show less perseverance on simple and Psy release inhibitory control > gating (PFC) > overload sensory
brain(=plasticity); 2 brain-machine interfaces: people learn how
challenging tasks, performing worse (only on GRE problems) bc processing > increased stimulation serotonin, DA, GABA.
to control machine w brain 3 deep brain stim (DBS) →
they spent less time on the tasks. Perseverance predictive of: REBUS: Psy suppress bottom-up prediction & priors. CCC
restructures network’s structure through electrical stim
job performance, well-being, academic achievement. model: Psy destabilise cortical network & decouples claustrum
(=plasticity at very specific network lvl); pill for plasticity=focus
Nutrition/Prevention of cognitive impairment – Scarmeas from frontal areas → loss cognitive control.
on understanding growth inhib factors, goal = create antibody
Association between nutrition & cognitive outcomes stronger for 3. Psychological level: Altered & affective states (mystical
that binds to receptors, allowing cells to grow
healthy dietary patterns than for individual nutrients/ food experience, feeling of awe, ego dissolution) → increased global
WEEK 4 - DRUGS & NEUROTRANSMITTERS
groups → cumulative beneficial effects of many ingredients in connectivity high-level association areas & thalamus +
Between persistence and flexibility – Hommel
these diets. Nutrition=important lifestyle factor, can modify risk decreased default mode network activity.
2 DA pathways: 1. mesofrontal pathway (PFC +D1) 2.
of future cognitive impairment and dementia. Certain nutrients Meditation & plasticity of predictive mind – Laukkonen
nigrostriatal pathway (striatum+D2) → PFC and Striatum hold
or food ingredients: some B vitamins (particularly folate), Many-to-(n)one: meditation techniques bring subject closer to
opposite roles of controlling, PFC propagates stability, the
flavonoids, vitamin D, and n-3 fatty acids, have the potential to present moment & thereby progressively abating hierarchically
striatum flexibility. DA as mediator. Metacontrol state model
benefit cognitive function; Food groups: fish (possibly other deep predictive processing. Predictive processing: brain
(MSM): changes of control styles affect goal impact and
seafood), veggies, to lesser extent fruit, moderate alcohol & makes predictions based on past experience (hierarchy of
competitiveness between alternatives (+impact goal, +
coffee protect vs cognitive decline. Dash diet: low NA, high Ka, expectation, perceptual & active inference, attention, inferred
stability).
Ca, Mag → lower blood pressure. hierarchical self, fact free learning & insight). Meditation:
Inverted-U-shape DA on WM & Cogn control - Cools et al.
Lecture notes focussed attention. Open monitoring: natural state of the
COMT-gene influence: inactivate DA release PFC.
