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Y2 Pharm (LCRS1) > Alzheimers > Flashcards

Alzheimers Flashcards

1
Q

What are the main risk factors for alzheimers?

A
  • Main risk = age
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2
Q

What are the genetic risk factors for alzheimers?

A

Genetic risks

  1. Early onset Alzheimers
  • APP gene (amyloid precursor protein)
  • PSEN gene (Presenilin) - part of the gamma-secretase complex
  1. Late-onset Alzheimers
    * ApoE (apo lipoprotein E)
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3
Q

What are the clinical symptoms of Alzheimer’s?

A

Deterioration of the higher functions

  • Memory loss – especially recently acquired information
  • Disorientation/ confusion – forgetting where they are
  • Language problems – stopping in the middle of a conversation
  • Personality changes – becoming confused, fearful, anxious
  • Poor judgement – such as when dealing with money
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4
Q

How does amyloid processing occur in normal physiology?

A
  • APP (amyloid precursor protein) found in neuronal membranes in the CNS
  • APP is cleaved by alpha-secretase
  • sAPPalpha (secreted APP alpha) released leaving C83 fragment in the membrane
  • C83 is then digested by gamma-secretase
  • Products are then removed
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5
Q

What are the hypotheses for Alzheimer’s?

A
  1. Amyloid hypothesis
  2. Tau hypothesis
  3. Inflammatory hypothesis
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6
Q

How does amyloid processing happen in Alzheimer’s pathology?

A
  1. APP cleaved by ß-secretase
  2. sAPPß (secreted APP ß) released leaving the C99 fragment in the membrane
  3. C99 is digested by gamma-secretase
  4. Releases ß-amyloid protein (Aß)
  5. Aß is a monomer that can form multimers
  6. Multimers associate with other elements to form toxic ß-amyloid plaques
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7
Q

What is the tau hypothesis in Alzheimer’s?

A
  • Tau becomes hyper-phosphorylated
  • Phosphorylated tau is insoluble and dissociates from microtubules
  • This causes microtubule instability
  • Phosphorylated Tau forms self-aggregates called neurofibrillary tangles
  • These are neurotoxic
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8
Q

What is tau protein in normal physiology?

A
  • Soluble protein present in axons
  • Very important for assembly and stability of microtubules
  • Microtubules are very important for stability of axon and axonal transport
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9
Q

What is the inflammatory hypothesis for Alzheimer’s?

A
  1. Microglia are macrophage-like cells of the CNS
  2. In Alzheimer’s they become dysfunctional:
  • increased release of inflammatory mediators & cytotoxic proteins
  • increased phagocytosis
  • decreased levels of neuroprotective proteins
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10
Q

What effect does taking ibuprofen have on Alzheimer’s?

A

Decreases likelihood of developing Alzheimer’s as the NSAI effect reduced the neurotoxic effects of microglial cells in Alzheimer’s

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11
Q

What are the classes and names of drugs effective at treating Alzheimer’s?

A
  1. Anticholinesterases
  • Donepezil
  • Rivastigmine
  • Galantamine
  1. NMDA receptor blockers
    * Memantine
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12
Q
A
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13
Q

What are the feature of Donepezil treatment?

A
  1. Gold standard for Alzheimer’s treatment
  2. Only needs 1 tablet per day - long plasma half life
  3. Treatment benefits only last for 1 year
  4. Inhibitor of AChE
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14
Q
A
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15
Q

What kind of drug is Rivastigmine?

A

‘Pseudo-reversible’ AChE and BChE inhibitor

Pseudo because it can’t be agreed whether it is reversible or not

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16
Q

Why does rivastigmine have more side effects than donepezil?

A

Rivastigmine inhibits both isoforms of the cholinesterase enzyme

BChE is found primarily in the liver

Inhibiting this causes many nasty side effects

17
Q

What are the half lives of the Anticholinesterases used to treat Alzheimer’s?

A
  1. Donepezil = 70 hours
  2. Rivastigmine = 8 hours
  3. Galantamine = 7-8 hours
18
Q

What is significant about the action of galantamine?

A
  • Directly activates NEURONAL nicotinic ACh receptors (alpha 7 nAChR agonist)
  • Doesn’t activate muscle type ACh receptors
19
Q

How is the NMDA receptor linked to Alzheimer’s?

A
  • NMDA receptor is activated by glutamate
  • It is activated excessively in neurodegenerative disorders like Alzheimer’s
  • There is less GABA inhibition in neurodegeneration so more glutamate activity
  • This, in turn, leads to more neurodegeneration because of increased NMDA activity - vicious cycle
20
Q

What is memantine?

A
  • Use-dependent non-competitive NMDA receptor blocker with low channel affinity
  • Only licensed for moderate-severe AD
  • Long plasma half-life

Y2 Pharm (LCRS1) (34 decks)

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