Brain Communication and Plasticity

Question 1

the synapse

Answer 1

• Synapse from the Greek ‘syn’ (together) and ‘haptein’ (to clasp)
  
  • Introduced by Charles Sherrington (1857-1952) English neurophysiologist and histologist, Nobel Laureate 1932
    He identified the join or connection between different synapses in the nervous system

Question 2

postsynaptic potentials- generation

Answer 2

• The postsynaptic cell membrane is polarised- resting potential of approx -70mv electrostatic pressure
  
  • Neurotransmitters in the synaptic cleft bind to receptors on the postsynaptic membrane and open channels
    This allows sodium (+), chloride (-) or calcium (+) ions to enter the cell changing the degree of positive or negative charge inside of the cell
  • Internal composition of the neurons in the brain is different in terms of charge to the extra cellular state
  • Creates electrostatic pressure
  • Neurons are then held by pumps of negative voltage
    When they bind to postsynaptic receptor cell they allow changes to occur in terms of membrane potential- open channels to allow ions to flow inside the cell along the electrostatic gradienta

Question 3

adding positive or negative ions has one of two effects

Answer 3

1. Positive ions increase the likelihood that a signal will be sent by the neurone
   
   • By making the charge on the postsynaptic membrane more positive e.g. -70mv to 67mV
   • Therefore they depolarise the neurone (EPSPs)
   • Called excitatory postsynaptic potentials
     2. Negative ions make it less likely that a signal will be sent
   • By making the charge on the postsynaptic membrane more negative e.g. -70mV to 72mV
   • Therefore hyperpolarising the neurone
     Called inhibitory postsynaptic potentials (IPSPs)

Question 4

the change in post synaptic potential is graded

Answer 4

• The change in the post synaptic potential is graded
  ○ Stronger signals from communicating neurones will result in greater depolarisation (excitation) or hyperpolarisation (inhibition)
  Postsynaptic potentials are spoken about as small nudges e.g. lots of incoming excitatory makes it a bigger nudge

Question 5

postsynaptic potentials- conduction

Answer 5

• The potential conducts passively from the site of origin
  
  • Conduction of PSPs has 2 important characteristics
    ○ Rapid- instantaneous
    ○ Decremental- they get smaller as they travel
    PSPs do not travel more than a couple of mm from their site of generation before they degrade

Question 6

PSPs- integration

Answer 6

• Typical postsynaptic neurone receive signals from many presynaptic neurones at the same time
  
  • The balance between excitatory and inhibitory PSPs (the net effect) determines whether an action potential fires
    ○ This means that all of the PSPs are balanced- if enough inhibitory or excitatory there will be an impact
  • Integration- combining a number of signals into one signal
  • Threshold of excitation- usually approximately -55mV. If the net sum of signals reaching the ‘axon initial segment’ just next to the axon hillock depolarises membrane to this level than an action potential will fire
  • PSP integration > generation of an action potential
    Spatial summation- integrating incoming signals over space

Question 7

generation of an action potential

Answer 7

If the integration of post-synaptic potentials conducts and surpasses the threshold of excitation at the axonal hillock then an action potential will fire
- Action potential
○ The membrane potential is reversed (from negative to positvely charged)
○ Very quick (~1msec)
Action potentials are all or none responses

Question 8

generation of an action potential- ionic basis

Answer 8

• Resting potential- voltage gated ion channels are closed
  
  • Depolarisation: Na+ (sodium) channels open, rapid influx of Na+ into cell
  • Peak: Na+ channels begin to close, K+ (potassium) channels open
  • Repolarisation: Na+ stops entering the cell, K+ ions move out
    Hyperpolarisation: K+ channels start to close but some K+ iona continue to move out of cell

Question 9

refractory period

Answer 9

• Represents the brief period in the cell after AP when the cell is hyperpolarised and is in an inhibited state
  
  • Absolute refractory period- brief period when it is impossible to generate an action potential
    Relative refractory period- higher than normal levels of stimulation required to generate an action potential- greater excitatory input
  • Responsible for:
    ○ Direction of travel- soma to axon. Prevents action potential from firing backwards. In our cellular communication, it can only occur in one direction- this means the signal cannot reverse and feedback information
    Rate of firing- indicates strength of stimulus. Strong stimulus will allow neurone to fire after absolute refractory period. Weak stimulus will not generate an action potential until relative refractory period has ended

Question 10

action potential: conducting along the axon (propagation)

Answer 10

• Action potentials- travel along the axon of the neurone depolarizing the axon as it goes
  
  • In grey matter- active process (non-decremental)
    As with AP generation, the conduction of AP along the axon occurs due to the influx of sodium

Question 11

action potential conduction- myelinated axon

Answer 11

Action potentials trave; faster when the axon is myelinated e.g. in the brains white matter
- Saltatory conduction- within the myelinated sections of the axon the signal is conducted passively (therefore decrementally) without requiring opening of channels
This has an augmenting effect on efficiency and speed of transmission

Question 12

summary of PSPs and APs

Answer 12

• Neurons are polarised due to an imbalance of ions on either side of the membrane]
  
  • Binding of a neurotransmitter at its receptor contributes to wither and an excitatory or inhibitory post synaptic potential and changes the degree of polarisation
  • Summation (temporal or spatial) determines the overall response of the postsynaptic neurone
  • If membrane potential exceeds the threshold of excitation an action potential fires which is propagated along the neuron
  • Saltatory conduction increases speed of signalling in myelinated axons
    A refractory period follows an action potential which dictates the direction of travel and restricts how often the cell can fire

Question 13

different types of neurotransmitters

Answer 13

• 2 categories based on size (number of constituent parts): small and large
  
  • Small molecule neurotransmitters have few components e.g. single amine components or short chains (amino acids)
  • Large molecule neurotransmitters contain between 3-36 amino acid molecules
    ○ Often structurally in the form of peptides (strings of amino acids)- ‘neuropeptides’
    +100 identified, categorised into functional groups e.g. pituitary peptides, opioids or brain gut peptides

Question 14

amino acids

Answer 14

• Amino acids are short chain molecules which come together to build peptides
  
  • GABA, the brain principle inhibitory NT
    ○ Dampens down brain activity e.g. GABAergic medicines in epilepsy treatment for anti-convulsing
  • Glutamate, the most prevalent excitatory transmitter
    Increases the likelihood of firing e.g. ADHD medication

Question 15

monoamines

Answer 15

• Monoamines are made up of singular components (not short chains)
  
  • Catecholamines- dopamine, norepinephrine, epinephrine
    Indolamines- serotonin

Question 16

dopamine and serotonin

Answer 16

• Modulatory NTs- they can have both excitatory and inhibitory effects (varies by receptor)
  ○ At least 5 dopamine subtype receptors
  ○ At least 14 serotonin receptor types
  The prevalence of receptors governing various function can form patterns in the brain known as pathways
  Dopamine mapping- chemical that bonds to a specific receptor in the brain we can discover and map pathways of dopamine (green)

Question 17

major dopaminergic pathways

Answer 17

• Dopamine present throughout the whole brain but some pathways are more relevant
  
  • Nigrostriatal: substantia nigra -> striatum (motor control)
    ○ Parkinson’s disease is related to dopamine deficiency
    and specific receptor subtypes which are dying in the brain
    ○ For Parkinson’s patients this is the effected pathway
  • Mesolimbic: VTA -> limbic system (reward/reinforcement- addiction)
    ○ Important for rewarding properties- reward base system blind to the type of reward so is activated whenever we have a reward
  • Mesocortical: VTA -> prefrontal cortex (working memory and planning)
    Tuberoinfundibular tract: hypothalamus -> pituitary (neuroendocrine regulation)

Question 18

major serotonergic pathways

Answer 18

• Less well defined than dopamine
  
  • Underpin a miriad of behaviours- this is why when we talk about serotonergic medicines e.g. SSRIs have lots of potential side effects this is because of how much serotonin effects the brain
  • Dorsal Raphe Nuclei -> cortex, striatum
  • Medial Raphe Nuclei -> cortex, hippocampus
  • Roles in:
    ○ Mood
    ○ Eating
    ○ Sleeping and dreaming
    ○ Arousal
    ○ Pain
    Aggression

Question 19

production of a neurotransmitter

Answer 19

• Synthesised in the cell body or terminals
  
  • Packaged into vesicles
  • Released into the synaptic cleft
  • Release ready pool vesicles
    Docked against the inside of the pre synaptic membrane less than 1% of the total stored in cell

Question 20

neurotransmitter release- exocytosis

Answer 20

• Action potential reaches the terminal of the neurone
  
  • Calcium ions enter the terminal
  • Vesicles nearest to membrane (release ready pool) fuse with membrane
  • Vesicles release neurotransmitters
    Large neurotransmitters are released more slowly than small

Question 21

post synaptic receptor binding

Answer 21

• Fischer’s Lock and Key Hypothesis (1890)
  
  • Receptors on postsynaptic membrane will only accept particular neurotransmitters (like a lock and key)
  • Therefore neurotransmitters can only affect specific neurones
  • Anything that binds to a receptor is called a ligand
    Therefore any neurotransmitter is a ligand of its receptor

Question 22

postsynaptic signal- receptor subtypes

Answer 22

• Receptor subtypes vary in location and response e.g. dopaminergic receptors- D1, D2, D3, D4, D5
  
  • Dopamine can bind with several of these different dopamine receptors
    ○ Like a key that unlocks several different locks
    ○ Different effect depending on the receptor/location
  • Certain areas of the brain may have more subtypes than others e.g. parts of the brain will have a lot of D1, others D5
    The same exists for the other receptor types e.g. at least 14 for serotonin

Question 23

postsynaptic signal- ionotropic receptor (direct method)

Answer 23

• Associated with Ligand-gated ion channel
  
  • Impact refers to the likelihood of open ion channels
    Ionotropic methods where neurotransmitters bind directly to an ion channel and ions flow in and out of the cell

Question 24

postsynaptic signal- meoabotrobic receptor (indirect method)

Answer 24

• More common than ionotropic
  
  • Slower response
  • More varied (different types)
  • Indirect method where neurotransmitters bind to a receptor that brings about a chain reaction effect that brings about the opening of the ion channel
    More convoluted process but happens more often than ionotropic because although it is slower it allows for more variation and flexibility of potential outcomes

Question 25

postsynaptic signal

Answer 25

• Receptor binding opens up a channel in the cell (directly or indirectly) leading to the flow of ions which
  ○ Makes it more positive (excitatory)
  ○ More negative (inhibitory)
  Integration surpassing the threshold of excitation will lead to an action potential generation in the next cell beginning a new cycle

Question 26

autoreceptors

Answer 26

• Autoreceptors are located on the presynaptic neurone
  ○ They bind to their neurones own neurotransmitter
  ○ They are located in the presynaptic membrane
  
  • Autoreceptors DO NOT control ion channels
  • Always metabotropic
    Autoreceptors control internal processes including the synthesis and releasing of neurotransmitters

Question 27

neurotransmitters summary

Answer 27

• We categorise neurotransmitter according to size of molecules: 2 basic types (small and large)
  ○ Monoamines (dopamine and serotonin)
  ○ Short chain amino acids (glutamate and GABA)
  ○ Peptides (large chains of amino acids)
  
  • Neurotransmitters are released by exocytosis
  • Neurotransmitters are ligands and bind specifically to postsynaptic receptors
  • Neurotransmitters generate a postsynaptic signal via either direct (ionotropic) or indirect (metabotropic) methods
    Synaptic signalling is terminated via reuptake or degradation of neurotransmitter

Question 28

brain plasticity

Answer 28

• Brain plasticity (sometimes called neuro plasticity) refers to changes in the micro (cellular) and macro (global) structures of the brain
  
  • Changes result from alterations in neural pathways and synapses
  • Brain plasticity changes are a natural part of our growth and development
  • But they also occur in:
    ○ Response to learning
    ○ Changes in our behaviour or the environment
    May arise following brain or bodily injury

Question 29

mechanisms of brain plasticity

Answer 29

• There are a variety of reason which necessitate brain plasticity changes throughout the lifespan
  ○ Brain development
  ○ Degeneration
  
  • But others may be dependent on environmental factors or external changes
    ○ Brain or body injury
    ○ Learning (change in structure as a result of changing functional demand)
    Brain plasticity likely utilises some distinct and overlapping mechanisms to elicit these various changes in brain structure

Question 30

hebbian theory

Answer 30

• Hypothesising potentially theoretical mechanisms for plasticity- adapting because of functional demand
  ○ ‘two cells or systems of cells that are repeatedly active at the same time will tend to become associated, so that activity in one facilitates activity in the other’
  
  • Cells or systems which are functionally demanded together regularly form enhanced connections or structural abilities that enhance their ability to work together
    This refers to systems as well as cells

Question 31

structural changes in the growing brain

Answer 31

• Neuroplasticity is any change in neuronal form or function
  
  • Foetal brains contain 30-60% more axons than adult brains
  • Change in brain development gave rise to the first neuronal mechanism of brain plasticity that was postulated- synaptic pruning

Question 32

synaptic pruning

Answer 32

• At birth each neuron in the babies cerebral cortex has approximately 2500 synapses per neuron
  
  • This number rapidly expands in a periodof post-natal development as babies brain is flooded with sensory information. Peaking in young children at up to 15,000 synapses per neuron.
  • As we progress towards adulthood the number of synaptic connections are steadily reduced.
  • The resulting synaptic connections are more efficient.
  • Pruning may represent the learning process
  • Pruning can occur (to a lesser extent than childhood) throughout the lifespan
  • Follow Hebb’s theory: Synapses that are frequently used have strong connections whereas those that are rarely used are eliminated.

Question 33

synaptic sprouting

Answer 33

• The creation of new synapses requires growth of new pathways.
  
  • In this example, after the death of cell A, cell B generates new dendrites to foster a connection with the isolated neuron in place of cell A.
  • This particular example is known as dendritic sprouting.
    This is useful when we need to forge new brain pathways, e.g., following a lesion in the brain caused by stroke.

Question 34

glial cells

Answer 34

• Glial cells play an important role in neuroplasticity.
  
  • Research compared activity of neurones
  • Yellow dots signify synapses
  • Glial cells provide the ‘scaffolding’ to promote formation of new synapses.
    Glial cells also play a similar role in synaptic pruning.

Question 35

synaptic plasticity- long term potentiation

Answer 35

• Synaptic plasticity refers to changes in the strength of connections between synapses.
  
  • Long-term potentiation (LTP)
  • Long-term depression (LTD)
• Increased or decreased activity leads to changes in synaptic transmission to potentiate (upregulate, LTP) or depress (down-regulate, LTD) the synapse
• Alter number of receptors in membranes and number of vesicles active
• Changes in which proteins are expressed inside the cell
  Affected by autoreceptors

Question 36

reorganisation of the brain

Answer 36

• Synaptic plasticity, sprouting and pruning occur at the cellular level of the neurone.
• However, cellular changes can have far reaching consequences.
• The brain is also organised into functional systems
  
  • E.g., Sensory information from certain parts of the body projects to specific regions of the cerebral cortex.
• This leads to a cortical representation of the body resembling a map (or homunculus).
  Drastic functional changes (e.g., post amputation) causes re-organization of homunculi.

Question 37

evidence of reorganisation- learning and memory

Answer 37

• Maguire et al (~2000)
• Experienced taxi drivers found to have larger hippocampi than novices and controls.
• Area associated with memory
• Grew as they spent more time in the job
  Shrunk when they retired

Question 38

learning modulates brain plasticity changes

Answer 38

• Musicianship requires motor learning and improved brain communication, e.g., somatomotor + auditory processing.
• Piano expertise requires:
  
  • Bimanual coordination (left and right hand working in unison)
  • Integration of information from separate brain networks (integration of auditory and motor networks)
• Research to compare experts and novices, or to evaluate people as they learn a skill.
  Expert pianists have increased grey matter density in somatomotor and auditory cortices (Gaser & Schlaug 2003)
  piano playing requires bimanual coordination
• Expert pianists demonstrate increased corpus callosum (CC) volume.
• CC represents the white matter bundles that support fast transmission of information between hemispheres.
  
  • Fine-tuned transfer between hemispheres
  • Faster conduction speed
• This has been replicated many times (Since Schlaug 1995)
  Interestingly, musicians who begin learning before the age of 7 have greatest volumes.

Question 39

evidence of reorganisation- functional development

Answer 39

• Pascual-Leone et al’s (1993) Braille readers
• Mapped motor cortex representations of reading finger using EEG and electrical stimulation.
  
  • Braille readers and controls
• Cortical representation of reading finger is significantly enlarged at the expense of representation of other fingers in Braille readers
  Can even observe changes within a day when Braille is practiced for 4-6 hours (Pascual-Leone et al., 1995)

Question 40

phantom limbs

Answer 40

• Phantom limb - a phenomena experienced by people who have undergone limb amputations.
  Cortical reorganisation appears to play an important role in phantom limb sensation.

Question 41

phantom limb pain

Answer 41

• Phantom limbs are commonly associated with severe chronic pain which does not respond well to standard treatments.
• Occurs in at least 90% of limb amputees.
• Pain following amputation may have a central origin.
  
  • It stems from the within the CNS.
  • Maybe as a result of extreme plastic changes post-amputation.
    This is a form of maladaptive plasticity

Question 42

mirror box therapy

Answer 42

• The patient places good limb into one side of the box and the amputated limb is obscured in the other side.
• The patient sees a reflection of the good hand where the missing limb would be.
• The patient receives artificial visual feedback that the absent limb is now moving and obeying commands when they move the ‘good limb’ in synchrony.
  This renewed autonomy can reduce maladaptive neuroplastic changes and result in pain relief.

Question 43

neuroplasticity in brain syndromes

Answer 43

• Maladptive plasticity describes plastic changes in the brain that can have negative behavioural or clinical outcomes
• E.g., Chronic Pain
• Prolonged activation of pain pathways can lead to the system becoming overly sensitive and hyperactive.
• Eventually, this activity will maintain itself and prolong after the original source of pain has gone
  Termed ‘Central Sensitisation’.

Question 44

stroke

Answer 44

• Stroke - a blockage causes reduced blood supply which results in cell death in a part of the brain – ‘lesion’.
• A lesion will block neuronal pathways resulting in functional deficits.
• Symptoms depend on function relevant to the area.
  Muscle weakness, motor disorders (apraxia), speech (dysarthia), language (aphasia’s) or cognitive deficits are all common.

Question 45

stroke- secondary neural pathways

Answer 45

• After a lesion in the central nervous system, neuronal pathways are blocked or destroyed.
• We can develop secondary neuronal pathways to send neuronal signals around the blockage.
  
  • Sprouting
• Secondary neuronal pathways preexist the lesion, but become “unmasked” in the acute phase.
  
  • Synaptic plasticity - upregulation
• Accords with Hebb’s law, the desired changes in synaptic efficiency, new synapses and sprouting are dependent on activity.
  This is analogous to a bridge being demolished. Initially, we can take secondary roads and alternative routes which may take longer. Eventually, through necessity, more efficient paths may be developed.

Question 46

stroke- promoting good brain plasticity

Answer 46

• How can we promote the development of good secondary neural pathways post-stroke?
• Taub et al (1993). Studied patients with strokes leading to poor function of one upper limb.
• AIMS:
  
  • to foster adaptive plastic changes in line with recovery
  • to minimise maladaptive changes which could prevent recovery of function
• METHOD:
  
  • Discourage patients from using their good limb,
  • Therefore, encourage practiced use of dysfunctional limb
• RESULTS:
  Significant improvement in motor function after 2 weeks lasting up to two years

Question 47

constraint induced movement therapy

Answer 47

• This therapy builds on Taub’s theory.
• Restrain the unaffected limb and promote intensive use of the affected limb.
• Types of restraints: Sling, Triangular bandage, Splint, Mitt
• CIMT for 90% of patient waking hours.
• Receiving CIMT early (3-9 months post-stroke) results in greater functional gains than receiving delayed treatment (15-21 months post-stroke).
  CIMT brings about benefits by promoting adaptive plasticity in the affected brain hemisphere -more effective when adopted earlier in recovery process.

Question 48

summary: brain plasticity

Answer 48

• Until recently the brain was thought to be immutable from early childhood.
• Research into the effects of learning, environmental inputs, brain and bodily injury now suggest that the brain can change and alter throughout the lifespan.
• Mechanisms of brain plasticity include
  
  • Synaptogenesis: generation of new synapses e.g., sprouting
  • Removal of inefficient or unnecessary synapses e.g., pruning.
  • Strengthening or weakening of synaptic connections occurs in accordance with Hebb’s Law (‘fire together, wire together’).
  • Re-organisation of cortical maps
  • Uncovering secondary pathways following lesion (e.g., after-stroke).
• Some brain plasticity can be maladaptive with negative consequences, e.g., phantom limb pain, development of central sensitisation in chronic pain.
  We can utilise our knowledge of plasticity to improve clinical treatments, e.g., CIMT for stroke, Mirror box therapy for phantom limb

Question 49

MRI

Answer 49

• A strong magnetic field causes hydrogen atoms to align by orientation- lattice structure
  
  • A radio frequency pulse is passed through the scanner
    ○ Atomic nuclei emit electromagnetic energy
  • The scanner detects energy radiated from each spatial location in the chamber
  • Computer reconstructs image a 3 dimensional; model
  • Advantages of MRI
    ○ No ionizing radiation exposure
    ○ Excellent spatial resolution
    ○ Horizontal, frontal or sagittal planes, explore the brain in 3D
  • Disadvantages
    ○ Cost
    No ferrous metal e.g. not allowed if you have a pacemaker

Question 50

structural MRI

Answer 50

• Structural MRI records a signal from each part of the brain by segmenting it into tiny chunks called voxels (~1mm^3)
  
  • The signal returned from each voxel differs depending on the water content of the regions imaged
  • Fatty tissues e.g. myelin sheath around white matter are lower in water content than grey matter, whereas the CSF has the greatest water content
    Structural imaging generates a single, high resolution depiction of the brains structure and usually takes around 7-10 minutes to record

Question 51

functional MRI

Answer 51

• Functional magnetic resonance imaging technique measures the amount of ‘activation’ in each voxel of the brain (~2-3^3mm)
  
  • Utilises same principle as structural MRI images but condition of magnet and radio pulse are adjusted
  • Oxyhaemoglobin and deoxyhaemoglobin in blood have differing paramagnetic qualities
  • fMRI targets a reading which differs according to the relative balance at each voxel throughout the brain
    Low resolution images are generated approximately every 2 seconds and we can passively monitor the brain or run an experimental manipulation

Question 52

BOLD signal

Answer 52

• In fMRI the measured variable is called the BOLD signal (Blood Oxugen Level Dependent)
  Neural activity is not measured directly but BOLD fluctuations during an fMRI scan can tell us that particular regions required more exogedn at certain times- therefore we can infer brain function

Question 53

structural MRI vs fMRI

Answer 53

• Structural MRI
  ○ Excellent contrast between tissue types and spatial resolution
  ○ Suitable for valuating structural abnormalities but one scan takes several minutes
  
  • fMRI
    ○ Indirect measure of neural activity
    ○ Low resolution image but can be updated frequently to evaluate activity changes associated with experimental conditions

Question 54

sMRI analysis- voxel based morphometry

Answer 54

• VBM is a structural analysis technique
  
  • Used to investigate differences in brain anatomy- grey matter density
    Results highlight regions of the brain which show significant differences in density e.g. between 2 groups

Question 55

how is MRI illustrated?

Answer 55

• MRI results, both structural and functional, are typically presented on top of a recognisable structural brain
  
  • Illustrated by overlaying on top of a sample structural image which provides spatial context for the audience
    In the case of fMRI, only the coloured ‘blob’ data actually comes from the study in question

Question 56

MRI- why do we need stats?

Answer 56

• fMRI studies give a ‘rich’ dataset
  
  • Typical resolution gives 6000 voxels per 2 second scam
  • 20 minute experiment gives 7.2 million data points
  • At P<.05 we can expect 360,000 false positive- greater risk of type 1 error
  • We need to perform many comparisons- good MRI methods compensate for this with statistical corrections

Question 57

stroke recovery (fMRI)

Answer 57

• fMRI can be used to observe or even quantify the amount of maladaptive plasticity in stroke patients
  
  • Rehme showed that patients recovery correlated with the ability of contralateral cortex to activate during movement of affected limb
  • Ipsilateral activation represents maladaptive plasticity
    (Rehme, Fink et al. 2011)
  • Neuroimaging research may help us to try and find ways to counter the maladaptive change and promote ‘good’ adaptive change
    For example we can also use fMRI as an objective measure to test new and novel treatment approaches

Question 58

plasticity and psychology

Answer 58

• CBT may impact on braun structure and function to bring about clinical benefits
  
  • Depressed patients demonstrate disrupted emotional regulation
    ○ Also show enhanced brain activity (fMRI) in amygdala during emotional stimuli
    ○ Those with the greates degree of amygdala dysfunction benefitted from greatest improvement post CBT
    Siegle, Carter et al. 2006)

Question 59

brain training

Answer 59

• Recently, meta analyses questioned the benefits of brain training
  
  • Likely to be specific to the trained task
    ○ Sudoku is unlikely to have clinical benefits against e.g. Alzheimers
    Brain imaging shows no reputable changes in brain function for wider cognitive tasks after training
    ○ Kauble, Caulfield et al 2017
    Much better evidence for brain benefits of physical exercise