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SL22044 Neuroscience > Neurodegeneration 3 > Flashcards

Neurodegeneration 3 Flashcards

1
Q

Main issue with current ND treatment?

A

Most ND have on cure, treatment only alleviates/delays symptoms

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2
Q

Main target of ND treatment?

A

Aggregates

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3
Q

Time course for an ND patient?

A

Usually over 50 with no evidence–> develop minor psychological/behaviour/motor issues–> develop memory loss, or issues with navigation–> begin differential diagnosis–> begin QOL treatments–>delay symptoms treatment–> alleviate symptoms–> palliative care–> death from another casue

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4
Q

Do ND kill people?

A

No, usually smthn like pneumonia

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5
Q

What is special about Wilsons Disease?

A

It can be treated

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6
Q

How does someone get Wilsons Disease?

A

Inherited–> genetic mutation

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7
Q

Main cause of Wilsons Disease?

A

Copper metabolism disease

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8
Q

Which protein is mutated in Wilsons disease?

A

Copper ion transporting P type ATPase (ATP7B)

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9
Q

Role of Copper ion transporting P type ATPase (ATP7B)?

A

Movement of copper scross the membrane

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10
Q

Symptoms of Wilsons disease?

A

Abdominal pain, dark urine, jaundice, mood changes, rings around edge of cornea, tremor and stiff muscles

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11
Q

How is wilsons disease treated?

A

A copper chelator–> helps remove copper from the body

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12
Q

What are two copper chelators used to treat wilsons disease?

A

Penicillamine and trientine

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13
Q

What are the two ways that aggregates are targeted in ND?

A

Preventing their formation or causing their breakdown

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14
Q

What are causes other than aggregates that can cause ND?

A

Oxidative stress (toxic radicals–> e.g. superoxide)
Mitochondrial damage–> could produce cytochrome C

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15
Q

How is aggregate formation prevented?

A

Target parent protein, stimulate breakdown enzymes, prevent misfolding

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16
Q

How are aggregate parent proteins targeted?

A

Antisense RNA, genetic knockout (CRISPR-Cas9)

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17
Q

How is breakdown of aggregates increased?

A

Increases the action of the proteasome on that specific protein, use antibody treatments

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18
Q

Which disease could be treated with antisense RNA?

A

Huntingtons

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19
Q

Which protein is targeted by antisense RNA in huntingtons?

A

Huntingtin (HTT)

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20
Q

Which (failed) treatment of Alzheimers involved gamma secretase inhibitors?

A

Brought in a gamma secretase to reduce the amount of beta amyloid being produced

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21
Q

How effective have antibodies against aBeta been in alzheimers?

A

Reduced cognitive decline by 20-40%

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22
Q

How are the antibodies for Azheimers treatment delivered?

A

Cannula infusion

23
Q

How are alzheimers antibodies believed to work?

A

Recruitment of microglia

24
Q

Main cause of PD?

A

Loss of dopaminergic neurons in substantia nigra in pathway to striatum

25
Q

What are parkinsons treatments aimed at?

A

Restoring dopamine for the normal function of the striatum

26
Q

What are the two kinds of receptor in the striatum?

A

D1 and D2

27
Q

What are the two pathways running between the striatum and the motor cortex?

A

Facilitatory, direct pathway, and the inhibitory, indirect pathway

28
Q

Effect of dopamine on the facilitatory pathway between the striatum and the motor cortex?

A

It enhances it

29
Q

Effect of dopamine on inhibitory pathway between the striatum and the motor cortex?

A

It inhibits it

30
Q

Which dopamine receptor is targeted by dopamine for the facilitatory pathway?

A

D1

31
Q

Which dopamine receptor is targeted by dopamine for the inhibitory pathway?

A

D2

32
Q

Effect of dopamine loss in PD?

A

Reduced motor cortex activity

33
Q

How can dopamine be increased?

A

Provide more dopamine or more dopamine precursor, decrease its reuptake, inhibit its breakdown, provide a dopamine agonist

34
Q

Most common parkinsons treatment?

A

Provide L-Dopa

35
Q

Why is L-Dopa provided instead of dopamine?

A

L-Dopa can cross the blood brain barrier

36
Q

Main issues with L-Dopa?

A

It can be converted to dopamine (which cant cross BBB) in the blood

37
Q

Which drug is given alongside L-Dopa to prevent dopamine formation in the blood?

A

Cabidopa (dopa decarbodylase inhibitor)

38
Q

Side effect of L-Dopa?

A

Dyskinesia–> severe involuntary movement

39
Q

How is the dyskinesia of L-Dopa treatment managed?

A

Patients have an “off” time where they dont take any L-Dopa in order to reduce the prevalence of side effects

40
Q

Second treatment aim at PD after L-Dopa?

A

Inhibit breakdown of dopamine

41
Q

How is dopamine breakdown inhibited?

A

Monoamime oxidase B (MAOB) inhibitors

42
Q

What is the main MAOB inhibitor?

A

Selegeline

43
Q

PD treatment after L-Dopa and MAOB inhibitor?

A

Catechol O-Methyl Transferase (COMT) inhibitor

44
Q

Side effects of L-Dopa?

A

Nausea and dizziness

45
Q

Side effects of COMT?

A

Toxicity to liver cells, diarrhoea and sleep disturbances

46
Q

Main COMT used for PD?

A

Tolcapone

47
Q

How do dopamine agonists work?

A

Acts directly on dopamine receptors

48
Q

Side effects of dopamine agonists?

A

Nausea, dizziness, hallucinations, sleep attacks, hypotension

49
Q

Examples of dopamine agonists?

A

Pramipexole, Ropinirole, Bromocriptine

50
Q

What is deep brain stimulation?

A

Implanting an electrode into the striatum–> can stimulate it directly and thus stimulate the activity

51
Q

Benefits of deep brain stimulation?

A

Doesnt have the same side effects of L-Dopa

52
Q

Complications of deep brain stimulation?

A

Brain hemorrhage, seizures, death

53
Q

Issues with stem cell treatment for ND?

A

Cost and time

54
Q
A

SL22044 Neuroscience (34 decks)

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