Lecture 8: Cognitive Enhancers Flashcards
What are nootropic drugs?
enhance cognition in healthy brain
How is sleep produced?
when neurons are fired they consume ATP which convert to adenosine
accumulation of adenosine
adenosine bind to adenosine receptor to promote sleepiness
accumulate when brain is awake
cleared when brain in asleep
2 MOA of caffeine
- antagonist of adenosine receptor
- inhibitor of phosphodiesterase (PDE-inhibitor)
How does caffeine prevent sleep through PDE inhibition?
prevent degradation of cAMP leads to amplification of NE signalling
NE promotes alertness and attention
similar effect as adrenaline (dry mouth, increase heartbeat)
Cocaine
DAT and NET blocker
prevent reuptake and recycling of dopamine
lead to accumulation of dopamine at synaptic cleft
Neurotransmitter level in Alzheimer disease
reduced acetylcholine, serotonin and norepinephrine
elevated glutamate
What areas of brain atrophy is observed in alzheimer disease
temporal lobe and parietal lobe
frontal cortex and cingulate gyrus
Donepezil, Galantamine, Rivastigmine
reversible cholinesterase inhibitor
prevent breakdown of ACh, increase cortical ACh level
Adverse effect of donepezil
cholinergic crisis
nausea, GI upset, vomiting, diarrhea
bradycardia, anorexia, vivid dreams
Long term potentiation
repeated stimulation of NMDA receptor (glutamate)
calcium influx to trigger cascade that lead to increase AMPA receptors at synapse
What is NMDA receptor
Ca and Na channel
What blocks NMDA receptor?
magnesium ion at pore prevent opening
only removed when membrane is depolarized
Memantine
low affinity, non-competitive NMDA receptor antagonist
How does memantine reduce decline in cognition?
excessive activation of NMDA receptors are known to cause EXCITOTOXICITY
when neurons die they release glutamate that can trigger excitotoxicity
has neuroprotective effects
Adverse effect of memantine
headache, body ache, fatigue, dizziness
can be used in combination of cholinesterase inhibitor
