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Pharmacology Test #6 > Alzheimer's > Flashcards

Alzheimer's Flashcards

1
Q

AD symptoms

A
  1. memory loss (especially recent memories)
  2. impaired ability to learn, reason
  3. impaired ability to carry out daily activities; confusion, untidiness
  4. anxiety, suspicion, hallucinations
  5. motor dysfunction can also occur in late-stage disease
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2
Q

Environmental risk factors of AD

A
  1. Age
  2. Low educational level
  3. Reduced mental activity in late life
  4. Reduced physical activity in late life
  5. Risks for vascular disease
  6. Hear injury
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3
Q

AD neuropathology

A
  1. loss of brain volume
  2. amyloid plaques and neurofibrillary tangles
  3. synapse loss
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4
Q

Amyloid plaques

A

extracellular; consist of amyloid-beta peptide (Abeta)

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5
Q

Neurofibrillary tangles

A

intracellular; consist of hyperphosphorylated tau

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6
Q

Neuropathology primarily affects which areas of high cognitive function?

A
  1. Entorhinal cortex
  2. Hippocampus
  3. Basal forebrain cholinergic systems
  4. Neocortex
  5. Nucleus basalis
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7
Q

A striking feature of neurons with neurofibrillary tangles and neurons in the vicinity of amyloid plaques is

A

destruction of synapses

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8
Q

Synapse loss results in

A
  1. reduced levels of neurotransmitters - especially acetylcholine, but also serotonin, norepinephrine, and dopamine
  2. dysregulated glutamate -> excess excitotoxicity and neurotoxicity
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9
Q

Genetic evidence that suggests a key role for Abeta?

A
  1. Mutations in the gene encoding the Abeta precursor protein, APP, are linked to early onset AD
  2. Trisomy 21 is associated with an AD-like phenotype, and the APP gene is located on chr 21
  3. Mutations in the gene encoding presenilin proteins involved in cleaving Abeta from APP are linked to early onset AD
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10
Q

Abeta peptide is released from

A

the transmembrane amyloid precursor protein (APP) by the activity of beta-secretase (BACE1) and gamma-secretase

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11
Q

Cleavage of APP by alpha-secretase in the middle of the Abeta segment releases

A

a non-amyloidogenic (non-toxic) fragment

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12
Q

Mutations in the APP gene favor

A

cleavage by beta- or gamma-secretase, resulting in the production of more Abeta or more Abeta42

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13
Q

What do mutations in the gene encoding presenilin-1 or presenilin-2 (PSEN1 or PSEN2) do?

A

alter APP cleavage by gamma-secretase, resulting in the production of more Abeta or more Abeta42

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14
Q

Abeta aggregation is thought to promote

A

tau hyperphosphorylation, leading to neurofibrillary tangle formation, cytoskeletal anomalies, and disruption of axonal trafficking

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15
Q

What is Entresto?

A

Valsartan + Sacubitril: new CHF drug

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16
Q

What is the concern about Entresto?

A

It is a Neprilysin inhibitor and there’s concern that inhibitors of Neprilysin could contribute to AD

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17
Q

Neurofibrillary tangle formation results in

A

cytoskeletal defects

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18
Q

What happens in unhealthy areas of the brain where tangles have accumulated?

A

the cytoskeletal tracks are disrupted and disorganized, resulting in trafficking defects and synaptic dysfunction

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19
Q

Abeta is thought to induce neurotoxicity indirectly by

A

triggering microglial activation, a process that is probably aimed at clearing amyloid from the brain

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20
Q

Activated microglia release

A
  1. pro-inflammatory cytokines (PGs, interleukins, TNF-alpha) that cause neuroinflammation
  2. reactive nitrogen species and reactive oxygen species that cause oxidative stress
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21
Q

CV risk factors in AD

A
  1. elevated LDL and decreased HDL increase AD risk
  2. vascular disease may accelerate AD pathogenesis (decreased nutrient delivery to the brain, decreased Abeta clearance, increased Abeta accumulation)
22
Q

How does diabetes increase the risk of AD?

A

defects in insulin signaling may lead to accumulation of toxic glucose metabolites in the brain, decreased Abeta clearance

23
Q

ApoE responsible for

A

transporting cholesterol in brain (LDL); defects in cholesterol metabolism may alter membrane structure and function, which in turn affects Abeta deposition

24
Q

Three ApoE isoforms

A

ApoE2, ApoE3, and ApoE4

25
Q

Significance of individuals with one or two ApoE4 alleles?

A

One or two ApoE4 alleles increase the risk of AD

26
Q

Significance of individuals with an ApoE2 allele

A

decreases the risk of AD

27
Q

Cholinesterase inhibitors block

A

The conversion of acetylcholine to acetic acid and choline; thereby compensating for the loss of acetylcholine that results from the degenration of cholinergic nerve terminals in AD

28
Q

Cholinesterase inhibitors

A
  1. Donepezil (Aricept)
  2. Rivastigmine
  3. Galantamine
29
Q

Donepezil (Aricept)

A

specific, reversible inhibitor of acetylcholinesterase

30
Q

Rivastigmine

A

inhibits acetylcholinesterase and butyrylcholinesterase

31
Q

Galantamine

A

selective, reversible inhibitor of acetylcholinesterase and enhances the action of acetylcholine on nicotinic receptors (increases acetylcholine release from cholinergic neurons)

32
Q

Memantine

A

NMDA antagonist that blocks glutamatergic neurotransmission via a noncompetitive mechanism

33
Q

Glutamate is an

A

excitatory neurotransmitter that is involved in long-term potentiation, a neuronal mechanism required for learning and memory

34
Q

Excess glutamate signaling leads to

A

excitotoxicity, a mechanism that can result in neuronal death

35
Q

Candidate agents that target Abeta generation

A

beta and gamma-secretase inhibitors

36
Q

Molecules that modulate Abeta generation or aggregation, including cholesterol or ApoE

A

statins and bexarotene

37
Q

Candidate agents that target Abeta aggregation

A

inositol, polyphenols [resveratrol], peptides

38
Q

Candidate agents that target Abeta clearance

A

vaccines, Abeta antibodies

39
Q

Candidate tau kinase inhibitors

A

lithium, valproate

40
Q

Candidate agents that reduce inflammation or oxidative stress

A

NSAIDs, dietary antioxidants [Vitamin E, polyphenols]

41
Q

Florbetapir

A

radiolabeled agent that binds beta-amyloid, visualized by PET scanning

42
Q

Limitation of florbetapir/PET scan

A

does not establish AD diagnosis (amyloid in other diseases could also be detected)

43
Q

Non-AD dementias

A
  1. Vascular dementia
  2. Dementia with Lewy bodies (DLB)
  3. Frontotemporal demena - Pick’s disease
44
Q

Common initial presentation of vascular dementia

A

impaired judgment or executive function

45
Q

Vascular dementia occurs as a result of

A

brain injury, associated with vascular disease or stroke

46
Q

The nature of deficit in thinking or physical function in vascular dementia is determined by

A

location of the brain injury

47
Q

Dementia with Lewy bodies

A

combination of cognitive decline and parkinsonian symptoms; cognitive decline more prevalent at disease onset than for PD

48
Q

Core diagnositic feature of dementia with Lewy bodies

A

visual hallucinations

49
Q

Neuropathology of dementia with Lewy bodies is characterized by

A

the presence of cortical Lewy bodies

50
Q

Frontotemporal dementia (Pick’s disease)

A

disinhibited behavior, poor impulse control, antisocial behavior, disturbances in executive functioning

51
Q

Neuropathology of Pick’s disease is characterized by

A

presence of tau accumulations (Pick’s bodies)

Pharmacology Test #6 (12 decks)

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