Lecture 3 Flashcards

1
Q

What is PD commonly misdiagnosed as

A

Multiple systems atrophy and progressive supranuclear palsy

Or drug induced symptoms can be similar

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2
Q

Drug induced PD symptoms

A

Neuroleptic

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3
Q

Neuroleptic

A

Antipsychotic agents, gastric motility inhibitors like metocloperamide, and catecholamines release modulators like reserpine and tetrabenazine

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4
Q

What is the difference between PD and drug induced symptoms similar to PD

A

Tremor is less with drug induced symptoms

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5
Q

Will drug induced PD symptoms go away

A

Yes eventually

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6
Q

Difference between PD and MSA and PSP

A

They progress faster than PD and PD meds will only work for a short period of time on them

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7
Q

What hormone do PD patients have low levels of

A

Dopamine

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8
Q

Why do PD patients have low dopamine

A

SN that produces dopamine is destroyed

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9
Q

Can dopamine levels be tested to check for PD

A

No because it is hard to test for

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10
Q

DATscan

A

Visualizes dopamine transporter (DAT) in the putamen. Measuring DAT in neurons is an indirect way of quantifying the amount of dopamine in the neurons

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11
Q

More DAT =

A

More dopamine

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12
Q

Is there a lab test for PD

A

No

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13
Q

What percent of PD is misdiagnosed

A

10-20%

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14
Q

__ cases of PD per 100,000 individuals

A

100-300

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15
Q

More than ___ cases of PD globally

A

6 million

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16
Q

Twin studies showed high/low concordance rates for PD in monozygotic and dizygotic twins

A

Low

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17
Q

What does it show that both twins don’t get PD

A

Strong non-genetic factors in causation of PD

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18
Q

Environmental toxins that cause PD

A

MPTP (mitochondrial toxin) with structure similar to herbicide paraquat (insecticide)

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19
Q

What areas is PD incidence highest in

A

Agricultural

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20
Q

Do more men or women have PD

A

Men

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21
Q

What continents is PD less prevalent in

A

Asian and African

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22
Q

Smoking and PD

A

40-70% less likely in smokers

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23
Q

Coffee and PD

A

Protective effect

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24
Q

Early onset PD age

A

less than 40 years old

25
Q

Prevalance of early onset PD

26
Q

What causes early onset PD

A

Genetic mutations

27
Q

Late onset PD age

A

Over 60 years

28
Q

Prevalance of late onset PD

29
Q

a-synuclein mutation

A

(aSYN) single base pair mutation from alanine to threonine at position 53

30
Q

What is aSYN the main constitute of

31
Q

How is neuronal cell death caused by aSYN

A

Mutated aSYN forms fibrils

32
Q

How is PD risk increased genetically

A

Duplication and triplication of normal aSYN

33
Q

___ of aSYN is pathogenic

A

Overproduction

34
Q

Other genes besides aSYN that are involved in PD

A

Leucine-rich repeat kinase-2 (LRRK2), Parkin, and PINK1

35
Q

How do Leucine-rich repeat kinase-2 (LRRK2), Parkin, and PINK1 cause PD

A

They are involved in ubiquitination

36
Q

Ubitiquination

A

Marks old proteins and damaged organelles for destruction

37
Q

What happens if old proteins and damaged organelles are not marked for destruction

A

Accumulation of junk

38
Q

What does junk buildup in cells lead to

A

Damaged mitochondria

39
Q

What is caused when mitochondria are damaged

A

Decrease pH, ROS produced and cell death

40
Q

What does the gold standard treatment for PD do

A

Increase dopamine levels in the brain

41
Q

Can we inject dopamine to increase the levels

A

No, it does not cross the BBB

42
Q

Levodopa action

A

Levodopa crosses the BBB and once it is in the neurons it is converted to dopamine

43
Q

How can enzymes be used to increase dopamine

A

Preventing the destruction of dopamine in the synapse

44
Q

How many enzymes destroy dopamine in our body

45
Q

Enzymes that destroy dopamine in our body

A

Monoamine oxidase type B (MAO-B) inhibitors

Catecholamine ortho-methyltransferase (COMT) inhibitors

46
Q

MAO-B inhibitors

A

Prevent breakdown of dopamine in the brain

47
Q

COMT inhibitors

A

Block the breakdown of dopamine in the periphery

48
Q

Ablation

A

Cutting or destroying a part of the body

49
Q

What is ablation used for in PD

A

Destroy GPi

50
Q

What is used to destroy the GPi in ablation

A

Surgical or chemicals like MPTP

51
Q

What symptoms does ablation help

A

Bradykinesia, akinesia, and rigidity

52
Q

Deep brain stimulation

A

Stimulate the subthalamic nuclei by electrical wires

53
Q

What will be the result of deep brain stimulation of the subthalamic nuclei

A

Increased GPi inhibition of the thalamus (will not stimulate movement –> reduces the tremor)

54
Q

How many electrical impulses are sent to the brain in deep brain stimulation

A

More than 100

55
Q

Future treatments for PD

A
  1. Cell transplantation
  2. Gene transfer
  3. Trophic factors
56
Q

Cell transplantation

A

Dopamine producing cells are transplanted into the substantia nigra

57
Q

How is gene transfer done

A

Via virus, chemical mediated

58
Q

Trophic factors

A

Make neurons grow and divide (injected into the substantia nigra)