Cognitive Enhancers Flashcards
e) Main drugs used to enhance cognitive performance (often in the absence of medical advice)
i) Caffeine
ii) Amphetamines
iii) Methylphenidate
iv) Modafinil
i) improve mental performance in fatigued subjects (simple, tedious tasks)
ii) increase ability to focus and maintain self control. In addition to reducing fatigue,
g) Amphetamines
reduces fatigue and has a positive effect on long-term memory consolidation
h) Methylphenidate
improves attention in rested individuals, while improving wakefulness, memory and executive functions in sleep-deprived individuals
i) Modafinil
ii) Overactivity and limited attention span disrupt their education and social development
iii) Thought to be disorder of NE and DA pathways in the frontal cortex and basal ganglia
2) ADHA
2) ADHA
b) Characterized by co-existence of what three things?
i) Inattentive
ii) Hyperactivity
iii) Impulsive
g) Brain Pathways and ADHD
i) Thought to be disorder of NE and DA pathways in the _____________ and _________
frontal cortex and basal ganglia
3) Neurotransmitters and ADHD
a) _________ (NE) and __________(DA) pathways are involved in maintaining and focusing attention
Prefrontal and mesocortical
4) Drugs Used to Treat ADHD
a) CNS stimulants
i) Examples
___________ and ________
ii) 80% to 90% effective in children
iii) First-line treatments
(1) Amphetamines
(2) Methylphenidate
5) CNS stimulants
b) Methylphenidate
a) Amphetamines
5) CNS stimulants
a) Amphetamines
i) Immediate-release (Dexedrine)
ii) Sustained-release (Dexedrine Spansules, and Adderall XR) formulations
5) CNS stimulants
b) Methylphenidate
i) Immediate-release (Ritalin)
ii) Sustained-release (Concerta and Metadate CD)
a) Areas of the prefrontal and limbic cortex involved with focusing and maintaining attention and prioritizing behaviors are activated by psychostimulants at ___________ doses
low (therapeutic)
b) Areas of the brain involved in motor activity and arousal get activated at ___________ doses
higher (euphoric or toxic)
c) People who abuse amphetamine may develop reverse tolerance
i) Become psychotic with chronic use of the drug, even without dose escalation
sensitization
a) Highly selective NE reuptake inhibitor
b) also elevates DA levels in the prefrontal cortex but not in the nucleus accumbens or the striatum
9) Atomoxetine (Strattera)
c) Only ADHD medication that has no abuse potential
i) Not a controlled substance
9) Atomoxetine (Strattera)
mediates the euphoric properties (i.e., abuse liability) of the psychostimulant
ii) Nucleus accumbens
9) Atomoxetine (Strattera) Adverse effects
e) Adverse effects
i) nausea, vomiting, weight loss
ii) sleep problems
iii) liver damage
10) Alzheimer Disease
Main pathological features
i) amyloid plaques
ii) neurofibrillary tangles
iii) loss of neurons (particularly cholinergic neurons of the basal forebrain)
aggregates of the Aβ fragment of amyloid precursor protein (APP), a normal neuronal membrane protein, produced by the action of β- and γ-secretases
c) Amyloid plaques
h) Loss of _____________is believed to account for much of the learning and memory deficit in AD
cholinergic neurons
epidemiological studies suggested that some ______ reduce the likelihood of developing AD
NSAIDs
a) Cholinesterase Inhibitors
b) _______ - first drug approved for treating AD
i) Enhancement of cholinergic transmission
ii) Slight improvements in tests of memory/cognition in ~40% of AD patients
iii) No improvement in other functional measures that affect quality of life
Tacrine
a) Cholinesterase Inhibitors - Tacrine side effects
(1) Nausea, abdominal cramps, etc.
v) Hepatotoxicity, so no longer used
i) Cholinesterase Inhibitors - Same basis as tacrine, also limited efficacy
ii) Produce a measurable, but slight, improvement of cognitive function in AD patients
iii) Less toxicity than tacrine
c) Donepezil, rivastigmine, galantamine
d) Overall, small improvement in cognitive function, with no effect on disease progression.
e) Cholinesterase Inhibitors
b) Weak antagonist at NMDA receptors
c) Orally active
d) Produces a modest cognitive improvement in moderate or severe AD
e) Not neuroprotective
a) Memantine
f) Possible mechanism
i) Selective inhibition of excessive, pathological NMDA receptor activation
ii) Preserves more physiological NMDA receptor activation
Memantine
g) Long plasma half-life
h) Used in conjunction with cholinesterase inhibitors or by itself
i) Slows cognitive deterioration and decreases caregiver burden for patients with moderate to severe AD
Memantine
