Neuroethics exam

Neurocognitive enhancements

enhancement of normal neurocognitive function by pharmacological means, intended to bring users to above

What can be considered neurocognitive enhancements

drugs, supplements, non-medical use of prescription drugs

soft enhancers

energy drinks and non-prescription drugs 

What are the targets for pharmacological enhancements?

attention, sleep, focus, memory, executive function and sleep

what’s the prevalence of neuroenhancement?

Very difficult to get reliable data because most studies are conducted on volunteers (selection bias) and rarely double ling and placebo controlled.

what are characteristics of those who use neuroenhancers?

lower levels of self-efficacy, score higher on neuroticism scales, more likely to misuse other legal and illegal substances for self-medication

Why are they used among college students?

many university students see them as an acceptable means to cope with stress related to academic demands (Wolff)

Xanax and Valium

these benzodiazepines are neuroenhancers

Methylphenidate, modafinil, dextroamphetamine

prescribed stimulants

donepezil, galantamine, rivastigmine

acetylcholinesterase inhibitors

What are Benzodiazepines used for?

emotional enhancer that is a relaxant and anti-anxiety effects. has sedating properties that can help with sleep, this is associated with improved cognitive performances

How do benzodiazepines work?

enhance activity of GABA. binds to GABA receptors and hyperpolarize the neuron with results in CNS depression

What are some risks of benzodiazepines?

respiratory depression, drowsiness, headache, diarrhea, interactions with alcohol that can result in increased respiratory depression via synergistic effect

what are prescribed stimulants used for?

may increase vigilance, arousal and motivation.

what systems are involved with prescribes stimulants?

Effects on norepinephrine and dopamine systems that may improve attention, concentration and other functions associated with working memory

what is working memory?

capacity to hold and use information for brief periods and is critical for decision making

Methylphenidate

CNS stimulant typically used to treat ADD, ADHD, and narcolepsy

dextroamphetamine

CNS stimulant typically used for the treatment of narcolepsy and ADHD

Methylphenidate and dextroamphetamine

moderate enhancing effects on these functions by increasing levels of dopamine.

Who benefits from the use of methylphenidate and dextroamphetamine?

People with a lower baseline of working memory. In some instances people with a higher baseline of wkm experience impairments in cognitive functions.

Does taking methylphenidate have any effects?

children with ADHD seem to do better academically when taking methyl and other stimulants than those iwth the same disorder who do not. But there is no evidence that these drugs improve performance of those that dont have adhd

What are some risk of methylphenidate and dextroamphetamine?

Chronic use could be problematic this is because both meds inhibit excessive reuptake of dopamine with could disrupt the reward system and make one susceptible to addictive behavior

what are more potential risk of chronic use of prescription stimulants?

hypertension, increased risk of stroke and myocardial infarction, insomnia a dn psychosis

what does modafinil do?

activates dopamine, which then activates NE and histamine blocking the hypothalamus from promoting sleep enabling people to be more alert and focused

why is modafinil used?

prescribed for sleep disorders, used by airplane pilots, students, and researchers

What are the risk of modafinil

Chronic use could be problematic as sleep deprivation could be a risk factor for metabolic and endocrine disorders (obesity and diabetes) and cardiovascular disease.

what systems could be impacted?

being constantly awake could cause hyperactivation of the HPA and SAM systems

What should be kept in mind for these psychostimulants?

the effects are limited to certain cognitive functions, can vary among individuals, and may not always be beneficial.

What would be some trade off for the psychstims?

trade-off to be more focused on a specific task. Some studies have shown that a broad attention span and less focus on a specific task may facilitate creative thinking and effective problem solving

What do acetylcholinesterase inhibitors do

improve the chronic transmission by reducing ACh degradation, commonly used in treating AD and PD

What about enhancement of enhancing the capacity to store and retrieve more episodic and

semantic memories?

protein synthesis in hippocamp and structures in the MTL is necessary for encoding and consolidation of these memories, drugs that increase the rates could in theory increase capacity to recall more

What is the distinction between using a drug for therapeutic purposes and using for enhancing purposes?

if used for therapeutic reasons then it aims to restore a person to a healthy baseline while enhancements aim to improve upon normal functioning

is this a coherent distinction?

Its a bit breaky because many interventions can be both therapeutic and enhancing depending on the context used and the individual. the normal baseline is also vague. Basically everything depends on context and the individuals condition

is this an ethically or socially important decision?

Can include fairness and equality, authenticity of human nature. Socially would be regulation and policy

is it permissible for artists to use performance enhancing drugs to stimulate their creativity or to enhance their craft?

use the 4 main principles. 

Farah 2.5

Drugs like Adderall, Ritalin, and modafinil aren’t just for patients anymore; they’re also used by students and professionals to sharpen focus, memory, and alertness.

Farah 2.5 main ethical concerns

Safety: known and unknown short and long term side effects of drug use. Freedom: escaping social or workplace pressure for enhancement. Fairness: distribution of drugs may further disadvantage

Farah 2.5 policy suggestions

Invest in solid research, set professional guidelines, increase public awareness, and pass limited legislation for responsible use⟶ Bottom line: Cognitive enhancement isn’t going away; our job is to regulate wisely to maximize benefits (beneficence) and minimize risk (nonmaleficence), not ban them outright. ⟶ Motivations: Boost focus, study longer, perform better on tests.
○ Secondary: Partying, staying up, weight
loss
⟶ Placebo & perception: Much of the “boost” may
come from staying awake, feeling more motivated, or
believing performance has improved, rather than big
objective gains.
⟶ Takeaway: Prescription stimulants are seen as “smart
pills,” but evidence shows modest and mixed effects
○ Helpful for alertness and memory, not a
shortcut to intelligence

TES  stimulation: give and take 

This study compared automaticity and numerical learning.

what is automaticity?

Automaticity is the increased mindless task performance though the dorsolateral prefrontal cortex (DLPFC).

what is numerical learning?

increased learning skills though the posterior parietal cortex (PPC)

What were the results for TES stimulation?

when one skill was improved, the other was hindered and vise versa, showing a mental cost of cognitive enhancement

AMPAkines: breaking species limits

Positive AMPA modulators (ampakines) allow cortical networks to expand past their normal species limits. these changes persist beyong drug exposure, having long lasting learning effects

what are some tradeoffs of enhancements?

We dont know the long-term effects, we could be sacrificing much later on for current gains. Are we meant to push ourselves beyond what’s natural?

What is a direct impact injury?

you get hit on one spot of the head

what is acceleration-deceleration injury

when the brain moves back and forth typical after car accidents

blast injury?

from bombs and stuff

what can a mTBI do?

stretch and bruise nerves and blood vessels, cause neural and glial chemical changes

can an mTBI cause permanent damage?

no, but it does bring up the growing importance of subconcussions

how is TBI diagnosed?

there’s no single test for TBI. there are many guidelines that are left open to interpretation

what are sone symptoms of TBI?

somatic like headaches, sleep disruptions, slow processing speed, problems with attention/memories. increased irritability, anxiety, depression

what is the Eyebox diagnostic device used for ? 

test, saccades (rapid eye movement), smooth persuit, fixation, convergence and the vestibular-ocular reflex

what is the Glasgow comma scale used for?

scores how conscious is through measuring eye response, motor response, verbal response and pupil response

what are some characteristics for a mTBI

normal structural imaging, loss of consciousness <30min, alteration of consciousness from a moment to 24 hrs, post traumatic amnesia 0-1 day. 13-15 on glasgow

what are symptoms for moderate tbi?

normal/abnormal structural imaging, 30 min-24hrs loss of consciousness, >24hrs of alteration of mental state, >1 and <7 days post traumatic amnesia. 9.12

severe symptoms of TBI

normal or abnormal. >24hrs, >24hrs, >7 days. 3-8

how many individuals sustain a TBI?

2.8 million americans sustain one every year.

why are young children, teenagers, and seniors most likely to sustain TBI?

fall risks, more rigorous activities like skateboarding for teenagers

what is CTE?

Chronic traumatic encephalopathy, linked to repeated head trauma like those who play contact sports, serve in the military, IPV

what does gyrencephalic mean?

describes brain that has convoluted surface with folds called gyri

what does perivascular mean?

enlarged blood vessels within the brain

WHAT is CTE?

its a progressive degenerative disease, formally known as dementia pugilistica

what are the symptoms of CTE

It takes a while usually 8-10yrs after experiencing repetitive mTBI. Changes in behavior, cognition and mood. alongside impulsivity, anxiety, apathy, need to have documented decline and delayed onset

What is the tau protein?

its a microtubule associated protein that stabilized microtubules. microtubules are essential for neurotransmission

what causes tau to dissociate from microtubules?

Calcium influx and glutamate hyperexcitotoxicity. hyperphosphorylation causes the misfolding and aggregation of tau that can eventually form neurofibrillary tangles and glial tangles

what is TDP-43

plays a crucial role in regulation of RNA processes, the accumulation of it aggregates in the CNS (a common feature of neurodegenerative diseases?

what is TDP associated with?

correlated with brain regions of atrophy and the stage of dementia, its considered to reflect a common downstream mechanism of neurodegeneration

What is amyloid-beta deposition?

found in 40-45% of individuals with CTE, typically less dense, and contrasted with AD where nearly all cases have extensive deposition

immuno-excitotoxicity what is it?

when microglia fail to return to reparative phenotype and instead are pro-inflammatory. contribute to the continued glutamate excitotoxicity.

When can CTE be diagnosed?

only post-mortem through the gross examination: regional atrophy (frontal lobe), ventriculomegaly, wasting of the corpus callosum and the fenestration of the septum pellucidum.

What are the microscopic  findings of CTE?

NFTs= fibrillar intracytoplasmic inclusions and neuropil threads= swollen filament containing dendrites (also a characteristic of AD, likely to play a major role in cog impairment)

Who is Dr omalu

he coined the term CTE, his findings were the first official diagnosis of CTE.

how did the NFL react to Dr Omalu

in 2007- head dr of the nfl mtbi committe resigns, 2009-nfl changes policy for concussions, 2013- spend 100 mil on the health problems of players. later on the nfl class-action concussion litigation finalized

what are some of the issues the the litigation

its very difficult for the families of these players to get the money because of the different definitions of AD. physicians are also employed by the NFL may not want to say that players were injured.

How prevalent is CTE among professional football players?

Its pretty prevalent as seen with the brain bank samples of deceased nfl players, but this is subject to selection bias as many family members have an incentive to donate the brains. also it does not represent estimated prevalence of CTE in all current players, would need a sample from general pop

Stamm et all study

age at first exposure to football is associated with altered CC white matter microstrucure in former professional football players.

what is fractional anisotropy

a measure of the directional movement of water molecules in the body, ranging from 0 to 1. Former nfl players that had 1st exposure <12 years had significantly lower FA in the anterior CC regions than those older

Increased risk evidence

several studies report that playing before 12 is associated with greater risk of later life cognitive impairments, may alter neurodevelopmental tragectories

evidence of no significant risks

large scale and long term studies have found no link between youth particpation and later cognitive impairments, 4year cohort study found no sig association as well. Other study mentions that head impacts are common and factors such as an individual susceptibility, duration, and intensity of play may be more influental than age alone

What remains unknown?

the severity and number of injuries for triggering brain changes that lead to CTE.

IPV

eve was the first neural mechanistic studies of IPV-related TBI through neuroimaging and cognitive assessments. theres a link between brain injury severity and rediced functional connectivity in key networks like the right anterior insula and the posterior cingulate cortex/prenucleus 

what about children?

repeated abuse that involves head trauma can lead to CTE. its very challenging to identiy and very rare

can repeated physical abuse lead to CTE

challenging to identify since many abusers wouldn’t want to give any evidence of the abuse

case suggestive of CTE in 19yr old

suffered daily DV through repeated hits to the head for 15 years until the age of 16. the child presented with depressive syndrome, progressive failure in professional and daily activities and subjectively reported progressive cog dysfunction for 3 yrs

tau-pet for the 19 year old

it increased binding at frontal and parietal white/grey matter border, isolating cortical areas had moderately focally increased binding though there is limited agreement of this tau-pet isotope to post-mortem findings in CTE

MRI 19 yr old

showed a cavum septum pellucidum, reduced left-side hippocampal volume, and left midbrain lesion. isolated cortical areas had moderately focally increased binding

CSF

elevated total-tau and p-tau (biomarkers of neurodegeneration), this individual diagnosed with TES (traumatic encephalopathy syndrome)

How can we balance respect for an athlete’s career aspirations with the need

to preserve their long -term brain health?

By promoting better safety equipment, rule changes, and proper coaching techniques, sports can reduce repetitive head trauma. This allows athletes to pursue their career aspirations within a system that also prioritizes their long-term brain health.

What ethical obligations do sports organizations have to protect athletes from

repeated head injuries?

ethical obligation to protect athletes from repeated head injuries, which includes ensuring their safety, disclosing risks, and upholding a "duty of care". This duty extends to both preventing injuries and providing appropriate care when injuries occur. Remove from play: Any athlete suspected of a concussion must be immediately removed from practice or competition.

No same-day return: The "when in doubt, sit them out" approach is a critical part of this obligation. No athlete should return to play on the same day they suffered a suspected concussion.

Independent medical clearance: Organizations should mandate that an athlete receive written medical clearance from a qualified healthcare professional before returning to play. To avoid conflicts of interest, this clearance should ideally come from an independent medical expert.

chris

Factor Description

Athlete Autonomy Borland's decision highlights an individual athlete's right to prioritize their long-term health over their career. He researched the risks of head trauma in football and concluded that the risks were not worth it for him. His actions demonstrated a player's ability to make personal choices about their physical well-being, even when facing significant financial implications.

Systematic Failure (NFL Safety) Borland's retirement, coupled with numerous other players who have retired early citing similar concerns, suggests a potential systemic issue with player safety within the NFL. The league's initial reluctance to acknowledge the link between head trauma and long-term cognitive problems like CTE, as revealed by studies showing a high prevalence of CTE in former NFL players, raises questions about the league's commitment to player well-being. Borland's advocacy post-retirement has further fueled discussions about potential shortcomings in how the NFL addresses player safety and the impact on athlete health.