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PT4024 > L2 Motor System Disorders > Flashcards

L2 Motor System Disorders Flashcards

1
Q

2 groups of neurodegenerative diseases

A
  1. Conditions affecting memory and conditions related to dementia
  2. Conditions causing problems with movements
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2
Q

Examples of NDDs

A

Alzheimer’s, vascular dementia, Parkinson’s, Huntington’s

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3
Q

What do NDDs have in common?

A
  • Role of aging
  • Glutamate excitotoxicity
  • Mitochondrial dysfunction → oxidative stress
  • Apoptosis
  • Protein misfolding & aggregation
  • Disruption of intracellular transport
  • Neuroinflammation
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4
Q

Average age of onset of PD

A

55

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5
Q

What percentage of PD cases are familial?

A

~10%

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6
Q

What genes are involved in autosomal dominant PD cases (rare)?

A

LRRK2
SNCA (encodes for α-synuclein production)

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7
Q

What genes are involved in autosomal recessive PD cases?

A

Parkin, PINK-1, DJ-1

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8
Q

Exposure to what toxin induces Parkinson’s-like symptoms?

A

MPTP

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9
Q

Neuronal pathways affected by PD

A

Selective loss of dopaminergic neurons (therefore less GABA inhibition), while cholinergic neurons remain intact

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10
Q

Main treatment for PD until L-DOPA was discovered

A

Atropine and related drugs

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11
Q

What reestablish the balance between DA and ACh?

A

Muscarinic receptor antagonists

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12
Q

What is the problem with anti-muscarinics?

A

Associated with troublesome side effects and are therefore now rarely used, except to treat Parkinsonian symptoms in patients on anti-psychotics (DA receptor antagonists → nullify effect of L-DOPA)

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13
Q

Treatment strategies for PD to increase DA signalling

A
  1. Increasing DA synthesis: L-DOPA (administered with DDC inhibitor)
  2. Inhibiting DA catabolism: Selegiline (MAOB inhibitor), COMT inhibitors (Tolcapone, Entacapone)
  3. Blocking uptake & enhancing release of DA: Amantadine
  4. DA receptor agonists: Bromocriptine & Pramipexole
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14
Q

Examples of DDC inhibitors

A
  • Carbidopa
  • Benserazide
  • Methyldopa
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15
Q

What type of disease is Huntington’s?

A

AD inherited NDD (no sporadic form)

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16
Q

What causes HD?

A

An insertion of multiple CAG repeats in the huntingtin (HTT) gene, resulting in an N-terminal polyglutamine expansion of HTT

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17
Q

What does disease severity in HD depend on?

A

the length of the polyQ stretch

18
Q

What suggests that HTT has a central role in cell functioning?

A
  • HTT is highly conserved from Drosophila to humans
  • HTT KO mice die at embryonic stage
19
Q

Neuronal pathways affected by HD

A

Some cholinergic neurons may be lost, but even more GABAergic neurons degenerate → more DA signalling

20
Q

Approved treatment for chorea (and hyperkinetic disorders similar to HD)

A

Tetrabenazine

21
Q

How does Tetrabenazine work?

A

Mainly as a VMAT-2 inhibitor, promoting the degradation of monoamines (in particular, DA)

22
Q

What was the first deuterated drug to have received FDA approval (in 2017)?

A

Deutetrabenazine (Austedo)

23
Q

All anti-psychotic drugs block __ receptors

A

D2

24
Q

200mg daily of what NMDA receptor antagonist likely moderately decreases HD chorea?

A

Riluzole

25
Q

Use of Amantadine in HD

A

Likely effective in decreasing chorea, but high doses can worsen cognitive function

26
Q

What is the most common motor neuron disease?

A

Amyotrophic lateral sclerosis

27
Q

What do most ALS patients die from?

A

Respiratory failure (usually within 3-5 yrs from onset of symptoms)

28
Q

True or False: Most ALS cases are sporadic.

A

True

29
Q

What is the only probable risk factor identified for ALS?

A

Smoking

30
Q

Most common causative gene mutation in ALS

A

SOD1

31
Q

Only approved drug for ALS in Europe

A

Riluzole

32
Q

How does Riluzole work?

A
  • blocks NMDA receptors (inhibits Glu release, stimulates reuptake)
  • blocks voltage-gated Na⁺ channels
33
Q

What is Edaravone?

A

A potent radical scavenger used to treat ALS in Japan & US

34
Q

What is Albrioza?

A

Sodium phenylbutyrate and taurursodiol combination used to treat ALS

35
Q

4 main types of multiple sclerosis

A
  • Progressive relapsing (PRMS)
  • Relapsing remitting (RRMS): ~80% of patients
  • Secondary progressive (SPMS)
  • Primary progressive (PPMS)
36
Q

What cells of MS patients are more reactive toward myelin components?

A

T cells (Th1, Th17)

37
Q

Examples of disease-modifying therapies for MS

A
  • Fingolimod (Gilenya)
  • IFN-β (Avonex, Betaferon)
  • Nataliuzumab (Tysabri): anti-VLA4 mAb
  • Alemtuzumab (Lemtrada): anti-CD52 mAb
38
Q

Only FDA-approved DMT for PPMS

A

Ocrelizumab (Ocrevus): anti-CD20 mAb

39
Q

Agents targeting nucleic acid metabolism

A
  • Mitoxantrone (Novantrone) infusion: topoisomerase II inhibitor
  • Oral Cladribine (Mavenclad): purine analog
  • Oral Teriflunomide (Aubagio): active metabolite of leflunomide, inhibits de novo pyrimidine synthesis
40
Q

Synthetic protein that mimics myelin basic protein

A

Glatiramer acetate (Copaxone) - induces switch from pro- to anti-inflammatory pathways

41
Q

What DMT for MS is based on a psoriasis treatment and induces a Th2 phenotype to cause immunosuppression?

A

Dimethyl fumarate (Tecfidera)

42
Q

__ are major targets for effective immunotherapy in relapsing MS

A

Memory B cells

PT4024 (12 decks)

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