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Clinical Neuroscience > PD & ALS > Flashcards

PD & ALS Flashcards

1
Q

What are the characteristics of LMN disorders?

A

Atrophy, twitches, loss of muscle tone and less active tendon reflexes

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2
Q

What are the characteristics of UMN disorders?

A

Spasticity, overactive tendon reflexes

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3
Q

What causes myasthenia gravis? (MG) What are the effects?

A

Cause when antibodies block, alter, or destroy the nACh receptors at the neuromuscular junction. Decreasing effects in the muscle

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4
Q

What causes LEMS? What are the effects?

A

Ca2+ voltage channels are blocked on pre-synaptic neuron. EPPS are decreased

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5
Q

What happens in ALS?

A

Both the UMN and the LMN degenerate or die and stop innervating muscles.

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6
Q

What is the pathology of ALS?

A

As LMNs begin to die –> sprouting of other LMNs and aberrant activity (causes fasciculations & twitches)

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7
Q

What do you see in the cellular pathology of ALS patients?

A

Stress granules found in the cytoplasmic inclusion bodies of UMN. The granules contain TDP-43 aggregates and often become a target for ubiquitination. If a patient has SOD1 mutations then see aggregated SOD1 in stress granules.

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8
Q

What do aggregated proteins do?

A

The soluble alpha helix becomes an insoluble beta sheet and a change in 3D structure causes problems for functioning

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9
Q

What are the genes that cause an increased risk for ALS if mutated?

A

SOD1, FUS, TDP-43, C9orf72

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10
Q

What is cell autonomous?

A

A genetic trait in multicellular organisms in which only the genotypical mutant cells exhibit the mutant phenotype

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11
Q

What is cell non-autonomous?

A

A trait in which genotypical mutant cells can cause other cells to exhibit a mutant phenotype

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12
Q

What is the dying forward theory of ALS?

A

UMN –> LMN. Maybe glutamate excitotoxcity activates apoptosis via NMDA

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13
Q

What is the dying back theory of ALS?

A

Starts in muscles with loss of trophic factors

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14
Q

What does Riluzole do?

A

Inhibits Na+ channels, limits glu release

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15
Q

Label the parts of the Basal Ganglia

A
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16
Q

What is transient vs. tonic?

A

Transient: cell at rest doesn’t release anything
Tonic: At rest, cell dribbles a little bit out

17
Q

What happens when A is at rest in this disinhibitory circuit?

A
18
Q

What happens when A is excited in this disinhibitory circuit?

A
19
Q

What is the direct pathway of the basal ganglia?

A

Direct –> striatum (+), MSN (-), GPi (-), Thalamus (+)

20
Q

What are the enzymes required to synthesize DA?

A

Tyrosine hydroxylase and DOPA decarboxylase

21
Q

What kind of receptors do MSNs in the direct pathway have? What is the effect?

A

MSNs that project to GPi have D1 receptors with a Gs protein that activated adenylate cyclase

22
Q

What kind of receptors do MSNs in the indirect pathway have? What is the effect?

A

MSNs that project to GPe have D2 receptors with a Gi protein that inhibits adenylate cyclase

23
Q

What are the symptoms of Parkinson’s disease?

A

Motor: tremor at rest, slowness of movement, stiffness & rigidity
Non-motor: Change in executive function, apathy, depression, dementia

24
Q

What is the pathology of PD?

A

Loss of DA neurons in substantia nigra & over-expression of the alpha-synuclein protein leads to beta sheet confirmation and aggregates called Lewy bodies

25
Q

What is MPTP?

A

MPTP crosses the BBB and is taken up by glial cells and converted to MPP+. Dopaminergic cells specifically take up MPP+ via DAT and inhibits the electron transport chain in mitochondria

26
Q

What are the genetic risk factors for PD?

A

alpha-synuclein, Parkin, PINK1

27
Q

What are the 2 mechanisms for cells to get rid of misfolded proteins? How do they work?

A

The ubiquitin proteasome: misfolded proteins are recognized and ubiquitin is attached to them. These proteins are then recognized by the proteasome and degraded.
Autophagy: Misfolded proteins are enclosed by a double membrane structure and contents are degraded by lysosomal enzymes

28
Q

How is autophagy affected in PD?

A

Normal Parkin and PINK1 act together to remove failing mitochondria from cells

29
Q

Why are mitochondria vunerable?

A

Mitochondria produce ATP and there are many places along the way for electrons to escape and form ROS.

30
Q

What are the goals for treatment of PD?

A

Drugs that increase DA in striatum

31
Q

What do Levodopa and carbidopa do?

A

Dopamine doesn’t cross the BBB, so give L-DOPA as a precursor. Carbidopa is a peripheral DOPA decarboxylase inhibitor so more DOPA crosses the BBB

32
Q

Where would you put stem cells to treat PD?

A

Put them in the striatum not the SN because in PD the SN cells are already dead so they won’t move the new dopamine anywhere

Clinical Neuroscience (15 decks)

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