Cognitive enhancers Flashcards

1
Q

What are some of the cognitive enhancers?

A
  1. Psycho-stimulants like Ritalin, amphetamines
  2. Atomoxetine
  3. Galanatamine
  4. Rivastigmine
  5. Tacrine
  6. Mermantine
  7. Modafinil
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2
Q

What is ADHD?

A

Overactivity and limited attnetion span which can disrupt educational and social dev.

  • impulsivity and hyperacitivty
  • thought to be involved NE and DA pathways of FC and BG
  • estimated that occurs in 10% of children
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3
Q

What does the acadamy of pediatric guidelines state about the DX of ADHD?

A

Children need to have a least 6 attn symptoms or 6 hyperactivity/impulsivity symptoms

  • must happen before the age of 7
  • the symptoms must be present in multiple settings
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4
Q

What are ADHD first-line treatment?

A

Psycho-stimulants

- have a calming effect and tolerance develops at slower rate in pts with ADHD

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5
Q

what are the areas involved with focusing and attn?

A

Prefrontal and limbic systems- which are also involvedin prioritizing behaviors

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6
Q

What is the MOA of strattera and what is it used for?

A

Highly selectively NET inhibitor!

Used to treat adult ADHD

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7
Q

Is there abuse potential involved with someone taking Strattera?

A

No, its not involved with DA pathways of the nucleus accumbens or striatum but its does elevated DA levels in the prefrontal cortex

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8
Q

What is the mechanism of action of modafinil?

A

DA increased in striatum and NucA
NE increase release in hypothalamus
5ht increased in amygdala and frontal cortex
-also elevates hypothalamic Histamine, activated glutamanergic channels and inhibits GABA NT

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9
Q

What are the main pathological features of AD?

A
  • Amyloid plaques
  • neurofibillary tangles
  • loss of neurons (especially in cholinergic neuron of basal forebrain)
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10
Q

What is APP?

A

Amyloid precursor protein, which is a normal neuronal protein

  • not well understood what it does but
    1. synaptic repair
    2. Anterograde neuronal transport
    3. iron export
    4. hormonal regulation
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11
Q

How is APP made?

A

It is cleaved at 2 sites of the APP gene

  • one by beta secretases
  • another by gamma secretases
  • mutations in the gene or cleaving sites can lead to defective proteins and later accumulation of amyloid aggregates
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12
Q

What are neurofibrillary tangles?

A

They are intracellular aggregates of highly phosphorylated form of normal neuronal protein TAU

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13
Q

What can account for loss of memory and learning in a pt with AD?

A

Loss of cholinergic neurons

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14
Q

What are some potential treatment mechanisms for AD?

A
  1. Beta-secretase inhibitors
  2. Gamma secretase inhibitors and modulators
  3. Ab (amyloids) vaccines and monoclonal antibodies
  4. Ab Aggregation inhibitors
  5. Tau lowering and anti-aggregation compounds
  6. Regulators of abnormal inflammatory mechanisms
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15
Q

What is ApoE4 protein and its connection with AD?

A

It is a protein that decreases clearance of extracellular AB

- thus too much of it would be bad or some varients of the protein are better at decreasing clearance

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16
Q

What was the first drug approved for AD? Is it still used?

A

Tacrine which was highly hepatotoxic and is no longer used

17
Q

What is the MOA of Tacrine?

A

It inhibits AChe

  • many drug interactiosn
  • short half life and trouble with complicance
18
Q

What are some other drugs that act like Tacrine? A cholinesterase inhibitor?

A

Donepezil, Rivastigmine and galantamine

  • which all have only slight improvement of cognitive function
  • but may be to small to be effective
19
Q

What are some of the side effects of Cholinesterase inhibitors?

A

GI symptoms of N, D, and cramps
Altered sleep and unpleasant dreams
Bradycardia
and muscle cramps

20
Q

What is the MOA of Memantine?

A

It is a weak antagonist of NMDA receptors

  • which is used for moderate to severe AD
  • produces modest cognitive improvement
  • typically used with conjunction with AChe or by itself
21
Q

Adverse effects of Memantine?

A

Ha, SOB, HTN, Constipation, confusion, dizziness and drowsiness