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Neuropharmacology > Dementia > Flashcards

Dementia Flashcards

1
Q

What is dementia caused by?

A

abnormal changes in the brain that damage brain cells and disrupts communication which affects thinking, behaviour and emotions

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2
Q

Why is memory loss the first symptom of dementia?

A

cells in the hippocampus are often the first to be damaged

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3
Q

What are the 2 main risk factors of dementia?

A

age (over 65) and family history

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4
Q

What are the main causes of dementia?

A
  • protein deposition
  • infections and immune disorders
  • metabolic or endocrine problems
  • low levels of certain nutrients e.g. vitamin B1, B6, B12, copper or vitamin E
  • medicine side effects (withdrawing some drugs may improve dementia)
  • normal-pressure hydrocephalus (abnormal buildup of CSF in the brain)
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5
Q

What are the most important dementing disorders?

A
  • AD (most common)
  • dementia with Lewy bodies (second most common and includes dementia associated with PD)
  • frontotemporal dementia
  • progressive supranuclear palsy
  • vascular cognitive impairment
  • normal pressure hydrocephalus
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6
Q

What is AD?

A

a progressive neurodegenerative disease

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7
Q

What are the 4 stages of AD?

A
  1. preclinical
  2. early-stage (mild cognitive impairment)
  3. mid-stage
  4. late-stage
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8
Q

Aside from memory, what else is affected over the course of AD?

A

visuospatial, executive and language skills

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9
Q

What are the pathological hallmarks of AD?

A
  • neuritic amyloid plaques
  • neurofibrillary tangles
  • synaptic and neuronal loss
  • oxidative stress
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10
Q

What are the causes of AD pathology?

A
  • misfolded proteins (plaques) → Aβ-amyloid protein
  • disintegrated MTs in neurons → collapse into twisted neurofibrillary tangles due to Tau
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11
Q

By which mechanisms do Aβ and tau induce neuronal dysfunction and death?

A
  • direct impairment of synaptic transmission and plasticity
  • excitotoxicity
  • oxidative stress
  • neuroinflammation
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12
Q

What happens to APP in AD?

A

it is abnormally processed, leading to the formation of A β peptides that aggregate into plaques

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13
Q

How do ApoE mutations increase the risk of developing AD?

A

they interfere with clearance Aβ and tau-mediated neurodegeneration

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14
Q

What are the 3 steps of AD pathology?

A
  1. Aβ -amyloid plaques
  2. tau-neurofibrillary triangles
  3. loss of cholinergic neurons
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15
Q

Give examples of conventional AD drugs

A
  • cholinesterase inhibitors e.g. donepezil, rivastigmine and galantamine
  • NMDA antagonists e.g. memantine
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16
Q

What drugs are used to treat AD cognitive symptoms?

A
  • cholinesterase inhibitors
  • NMDA antagonists
  • amyloid immunotherapy
17
Q

What drugs are used to treat AD non-cognitive symptoms?

A
  • antipsychotics
  • SSRIs
  • BZDs
18
Q

What are the first line treatment of AD?

A

cholinesterase inhibitors

19
Q

What is the MOA of cholinesterase inhibitors?

A

they inhibit ACh esterase enzymes which prevents breakdown of ACh and increases ACh synaptic availability; they boost cholinergic neurotransmission and enhance memory and learning

20
Q

What are disadvantages of cholinesterase inhibitors?

A

they have no effect on disease progression and no improvement in psychological and behavioural symptoms

21
Q

Which cholinesterase inhibitor is competitive?

A

galantamine

22
Q

What are side effects of cholinesterase inhibitors?

A
  • GI symptoms
  • bradycardia
23
Q

What do NMDA antagonists do?

A

block NMDA receptors and inhibit excitotoxicity

24
Q

What are NMDA antagonists used for?

A

moderate and severe AD dementia for modest cognitive improvement

25
Q

What are side effects of NMDA antagonists?

A
  • headache
  • dizziness
  • constipation
  • shortness of breath
  • hypertension
26
Q

Give examples of disease modifying drugs

A

anti-amyloid immunotherapy drugs e.g. lecanemab and donanemab

27
Q

What is the MOA of anti-amyloid immunotherapy drugs?

A

they drugs bind to Aβ aggregates and cause phagocytosis and therefore reduction of the amyloid plaques

28
Q

How are anti-amyloid immunotherapy drugs administered?

A

monthly by intravenous infusion for mild cognitive impairment (require MRI monitoring for ARIAs at 6 months interval)

29
Q

What are ARIAs?

A

side effects of aducanumab drugs

30
Q

Give examples of ARIAs

A
  • localised areas of cerebral oedema (ARIA-E)
  • microhaemorrhages (ARIA-H)
31
Q

What are symptoms of ARIAs?

A

dizziness, nausea and other neurological symptoms

32
Q

Why are amyloid immunotherapies more effective in earlier stages of AD?

A

amyloid plaques begin depositing approximately 15 years before symptom onset

33
Q

Give examples of newer therapeutic approaches for AD

A
  • neurotransmitter regulation
  • gut microbiota regulators
  • anti-inflammatory drugs
  • lipid metabolism regulators
  • autophagic modifiers
  • circadian rhythm regulators
  • natural compounds
  • gene and cell therapies
  • nonpharmacological interventions
34
Q

Give examples of behavioural and psychiatric symptoms of dementia

A
  • irritability
  • agitation
  • paranoia and delusional thinking
  • wandering
  • anxiety and depression
35
Q

Why are atypical antipsychotics not commonly used for agitation and psychosis in AD?

A
  • their use is often limited by adverse effects including parkinsonism, sedation and falls
  • use has been associated with a higher risk of stroke and overall mortality
36
Q

Describe benzodiazepine treatment of AD

A

can be used for occasional control of acute agitation but are not recommended for long-term management because of their adverse effects on cognition and other risks in the elderly population

37
Q

How may the typical antipsychotic haloperidol be useful for AD?

A

treatment of aggression in acute episodes only

Neuropharmacology (12 decks)

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