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PHRM 845 > (3.7) Patho and Pharmacology of Alzheimer's and other Dementias > Flashcards

(3.7) Patho and Pharmacology of Alzheimer's and other Dementias Flashcards

1
Q

What are the cardinal signs of Alzheimer’s?

A

Brain shrinkage, senile plaques, neurofibrillary tangles

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2
Q

What is the ratio of females to males that have AD?

A

2:1 female to male

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3
Q

What are the sxs of AD?

A
  • Memory loss (esp recent mem)
  • Impaired ability to learn, reason
  • Impaired ability to carry out ADLs
  • Confusion, untidiness
  • Anxiety, suspicion, hallucinations
  • Motor dysfunction in late stage disease
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4
Q

What are environmental risk factors for AD?

A
  • Age
  • Low educational level
  • Reduced mental activity in late life
  • Reduced physical activity in late life
  • Risks for vascular disease
  • Head injury
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5
Q

What is the neuropathology of AD in simplest terms?

A

Loss of brain volume

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6
Q

What is present in the brains of AD pts?

A

Amyloid plaques and neurofibrillary tangles

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7
Q

Where are amyloid plaques?

A

Extracellular

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8
Q

What do amyloid plaques consist of?

A

Amyloid-beta peptide (AB)

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9
Q

Where are neurofibrillary tangles?

A

Intracellular

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10
Q

What do neurofibrillary tangles consist of?

A

Hyper-phosphorylated tau

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11
Q

What parts of the brain does earlier stage AD start at?

A
  • Entorhinal complex (memory formation/consolidation)
  • Basal forebrain cholinergic systems (learning)
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12
Q

To what parts of the brain does AD spread to?

A
  • Hippocampus (memory formation/consolidation)
  • Neocortex (memory, learning, cognition)
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13
Q

What is a striking feature of neurons w NFT and/or in vicinity of plaques?

A

Destruction of synapses

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14
Q

What does synapse loss result in?

A

Reduced levels of neurotransmitters esp ACh, but also serotonin, NE, DA

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15
Q

What is another consequence of synapse loss?

A

Dysregulated glutamate which causes excess excitotoxicity and neurotoxicity

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16
Q

Regarding AB, what is linked to early onset AD?

A
  • Mutations in the gene encoding the AB precursor protein (APP)
  • Mutations in the gene encoding presenilin proteins involved in cleaving AB from APP
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17
Q

What is the connection between Down’s syndrome and AD?

A
  • Trisomy 21 is associated w an AD-like phenotype in 4th decade of life
  • APP gene is located on chromosome 21
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18
Q

What does NFT formations result in?

A

Cytoskeletal defects

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19
Q

What happens at unhealthy microtubules where tangles have accumulated?

A

Cytoskeletal tracks are disrupted and disorganized, resulting in defects in axonal transport that lead to synaptic dysfunction

20
Q

In addition to causing damage to the neurons directly, what else is AB thought to do?

A

Induce neurotoxicity indirectly by triggering microglial activation

21
Q

Why does AB induce microglial activation?

A

Process aimed at clearing the amyloid from the brain

22
Q

What do activated microglia release that causes damage?

A
  • Proinflammatory cytokines (e.g. prostaglandins, interleukins, tumor necrosis factor alpha) that cause neuroinflammation
  • Reactive nitrogen and oxygen species that cause oxidative stress
23
Q

What is ApoE?

A

Responsible for transporting cholesterol in brain

24
Q

What can altered ApoE function do?

A

Can affect AB aggregation or clearance

25
Q

Which individuals regarding ApoE genetics have an increased risk of AD?

A

Individuals w one or two ApoE4 alleles

26
Q

Which individuals regarding ApoE genetics have a decreased risk of AD?

A

Individuals w inheritance of ApoE2 allele

27
Q

What is MOA of cholinesterase inhibitors?

A

Block the enzymatic rxn of ACh to acetic acid + choline, thereby compensating for loss of ACh that results from degeneration of cholinergic nerve terminals in AD

28
Q

What drugs are in the cholinesterase inhibitors class?

A
  • Donepezil (Aricept)
  • Rivastigmine
  • Galantamine
29
Q

What is Donepezil?

A

A specific, reversible cholinesterase inhibitor of acetylcholinesterase

30
Q

What is Rivastigmine?

A

A cholinesterase inhibitor of acetylcholinesterase and butyrylcholinesterase

31
Q

What is Galantamine?

A

A selective, reversible cholinesterase inhibitor of acetylcholinesterase and enhances action of ACh on nicotinic receptors

32
Q

What drug is in the anti-glutamatergic therapy?

A

Memantine

33
Q

What is the MOA of memantine?

A

NMDA receptor antagonist that blocks glutamatergic neurotransmission via a noncompetitive mechanism

34
Q

What is the result of memantine’s MOA?

A

Reduced excitotoxicity

35
Q

What is Namzaric?

A

Combination drug of memantine ER + donepezil

36
Q

How is imaging of AB done?

A

A radiolabeled agent called Florbetapri (18F) binds to AB and is visualized by PET scan

37
Q

How is imaging of Tau done?

A

Using a tau specific radiolabeled agent called 18F-Flortaucipir

38
Q

What characterizes vascular dementia?

A
  • Impaired judgment or executive fxn
  • Less memory loss than AD
39
Q

How does vascular dementia occur?

A

Occurs as a result of brain injury associated w vascular disease or stroke

40
Q

How is the nature of vascular dementia’s sxs determined?

A

Location of brain injury

41
Q

What characterizes dementia w lewy bodies (DLB)?

A

Combination of cognitive decline and parkinsonian sxs

42
Q

What is a core diagnostic feature of DLB?

A

Visual hallucinations

43
Q

What is the neuropathology of DLB?

A

Presence of cortical lewy bodies

44
Q

What characterizes frontotemporal dementia (FTD) [e.g. Picks’ disease]?

A

Disinhibited behavior, poor impulse control, antisocial behavior

45
Q

What is the neuropathology of FTD?

A

Presence of tau accumulations (Picks’ bodies in case of Picks’ disease)

46
Q

What is mixed dementia?

A

Anomalies linked to more than one dementia can exist simultaneously in the brain

PHRM 845 (48 decks)

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