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Neurobiology of Disease > Exam III > Flashcards

Exam III Flashcards

1
Q

Alzheimer’s Disease is characterized by
a. Lewey bodies
b. Tau neurofibrillary tangles
c. Spongiform holes in the brain
d. Prion-induced protein misfolding

A

b. Tau neurofibrillary tangles

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2
Q

Successful pharmacological clearance of amyloid plaques in Alzheimer’s suffers resulted in
a. Clearance or resolution of symptoms
b. Acceleration of symptoms
c. Remission of symptoms
d. No effect on symptoms

A

d. No effect on symptoms

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3
Q

Amyloid plaques are highly correlated with Alzheimer’s disease. What is the problem with other proteins correlated with Alzheimer’s disease?
a. Tau
b. Alpha-synuclein
c. Poly Q DNA binding motifs
d. CAG expansion

A

a. Tau

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4
Q

Amyloid Beta plaque formation is associated with Alzheimer’s disease. What is the problem with the other protein correlated with Alzheimer’s disease?
a. It is also misfolded in a prionic mechanism
b. It forms plaques
c. It is hyperphosphorylated
d. It is degraded and recycled in the lysosome

A

c. It is hyperphosphorylated

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5
Q

The length of the CAG expansion is associated with what disease feature?
a. Disease severity
b. Onset of disease
c. Variations in symptom presentation
d. A shift from negative to positive symptoms in Parkinson’s disease

A

b. Onset of disease

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6
Q

What makes Kuru unique as a human prion disease?
a. It doesn’t involve the prion protein
b. It was primarily transmitted through cannibalism
c. It is genetically transmitted
d. It only affects cows

A

b. It was primarily transmitted through cannibalism

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7
Q

Protein folding occurs as a progressive process. Which are proteins that aid in this process as the folding protein is produced
a. Telomerase
b. Chaperone proteins
c. Bell hop proteins
d. Valet proteins
e. Tau

A

b. Chaperone proteins

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8
Q

Ubiquitin is a common protein that may play a role in a couple of the neurodegenerative disorders. The basic role of ubiquitin is
a. To activate gene transcription
b. To target proteins for degradation
c. To target proteins to the nucleus
d. To block gene transcription

A

b. To target proteins for degradation

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9
Q

Which of the following organelles is most disrupted by problems with alpha-synuclein in Parkinson’s Disease?
a. Nucleus
b. Peroxisome
c. Mitochondria
d. Endoplasmic reticulum

A

c. Mitochondria

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10
Q

Mutations of which of the following genes is associated with Fatal Familial Insomnia (FFI)
a. APP
b. HTT
c. CAG
d. PRNP

A

d. PRNP

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11
Q

Disruption of the above organelle by alpha-synuclein results in a build-up of
a. Proteinaceous plaques
b. Tau fibrils
c. Cytochrome C
d. Oxidative stress or free radicals

A

d. Oxidative stress or free radicals

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12
Q

Post-mortem diagnosis of Parkinson’s requires the identification of
a. Amyloid plaques
b. Necrosis
c. Lewy bodies
d. Huntingtin mutations

A

c. Lewy bodies

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13
Q

Huntington’s disease results from a mutation of which gene?
a. APP
b. HTT
c. Ubiquitin
d. CAG

A

b. HTT

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14
Q

Which is a protein secondary structure?
a. Beta loop
b. Alpha helix
c. Pore lop motif
d. None of the above

A

b. Alpha helix

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15
Q

Using the connection diagram above, activation of the cortex in the direct pathway does what to the activation of the globus pallidus?
a. Decreases it
b. Increases I t
c. Does nothing
d. Reclassifies it as inhibitory

A

a. Decreases it

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16
Q

Using the connection diagram shown above, activation of the cortex does what to the activation of the thalamus?
a. Decreases it
b. Increases it
c. Does nothing
d. Reclassifies it as inhibitory

A

b. Increases it

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17
Q

Using the connection diagram shown above, which cell is inhibited as a result of activation of the cortex?
a. A. Cortex
b. B. Caudate putamen
c. C. Globus pallidus
d. D.Thalamus

A

c. C. Globus pallidus

18
Q

Using the connection diagram shown above, which cell is disinhibited as a result of the activation of the cortex?
a. Cortex
b. Caudate putamen
c. Globus pallidus
d. Thalamus

A

c. Globus pallidus

19
Q

Using the connection diagram shown above, which cell(s) are tonic active in the system?
a. Thalamus and caudate putamen
b. Caudate putamen and globus pallidus
c. Caudate putamen and thalamus
d. Globus pallidus and thalamus

A

d. Globus pallidus and thalamus

20
Q

Using the diagram shown above, which structure is the thalamus?
a. A
b. B
c. F
d. G
e. H

A

d. G

21
Q

Using the diagram shown above, which structure is the caudate?
a. A
b. B
c. F
d. G
e. H

A

b. B

22
Q

Using the diagram shown above, which structure is the globus pallidus internal segment?
a.A
b.B
c.C
d.D
e. E

A

d. C

23
Q

What brain region is most associated with negative symptoms of schizophrenia?
a. Substantia nigra
b. Dorsolateral prefrontal cortex
c. Temporal lobe
d. Dorsal anterior midcingulate cortex

A

b. Dorsolateral prefrontal cortex

24
Q

Which of the following is consistent with the dopamine hypothesis of Schizophrenia?
a. Too m uch dopamine activity in the amygdala
b. Too much dopamine in the hippocampus
c. Too much dopamine activity in the nucleus accumbens
d. Too little dopamine activity in the nucleus accumbens

A

c. Too much dopamine activity in the nucleus accumbens

25
Q

An example of a positive symptom in schizophrenia is
a. Depression
b. Catania
c. Delusions
d. Anhedonia

A

c. Delusions

26
Q

In schizophrenia, the negative symptoms are likely to result from
a. Increased dopamine in the mesolimbic dopamine pathways
b. Decreased dopamine in the mesolimbic dopamine pathway
c. Increased dopamine in the mesocortical dopamine pathway
d. Decreased dopamine in the mesocortical dopamine pathway

A

d. Decreased dopamine in the mesocortical dopamine pathway

27
Q

Regarding the figure above IBZM is a radiotracer that labels what structure?
a. D1 receptors
b. D2 receptors
c. 5HT1A receptors
d. GABAa receptors

A

b. D2 receptors

28
Q

Regarding the figure above values on the y axis show
a. Amphetamine administration and impulsivity
b. Changes in dopamine concentration with amphetamine administration
c. Relationship between amphetamine administration and negative symptoms
d. Changes in positive symptoms from amphetamine administration

A

b. Changes in dopamine concentration with amphetamine administration

29
Q

Regarding the figure above: values on the x axis show
a. Amphetamine administration and impulsivity
b. Changes in dopamine concentration with amphetamine administration
c. Relationship between amphetamine administration and negative symptoms
d. Changes in positive symptoms from amphetamine administration

A

d. Changes in positive symptoms from amphetamine administration

30
Q

What is the relationship demonstrated by the above figure?
a. Increased dopamine release is associated with increased positive symptoms.
b. Decreased dopamine release is associated with decreased positive symptoms
c. Increased dopamine release is associated with deficits of working memory in individuals with schizophrenia
d. Increased dopamine release is associated with decreased impulsivity

A

a. Increased dopamine release is associated with increased positive symptoms.

31
Q

Describe the infectious agent in prion diseases and how it causes infection in acquired or transmitted cases.

A

The infectious agent in prion diseases is the structure of the diseased prion protein. It causes infection by coming into contact with native prion proteins and forces them into a misfolded state ( in a prion disease protein manner.)

32
Q

List and very briefly describe the phases of the onset of schizophrenia

A
  • Risk: no detectable changes ( etiology + epistatic influences)
  • Prodrome: onset of some detectable changes ( ex: changes in thoughts, social isolation, etc.)
  • Psychosis: onset of hallucinations and delusions
  • Chronic disability: no interventions help with revision ( cognitive and negative symptoms contribute most to chronic disability)
33
Q

Briefly describe the glutamate hypothesis of schizophrenia

A

This hypothesis suggests that reduced NMDA receptor function leads to impaired glutamate signaling, disrupting neural circuits and causing schizophrenia symptoms.

34
Q

Describe some evidence that the amyloid cascade hypothesis might not fully account for the etiology of Alzheimer’s disease. How might this evidence be addressed, or rebutted, by proponents of the hypothesis?

A

The amyloid cascade hypothesis describes that the misfolding and mis cleavage of B-amyloid leads to the lining up of B-sheets. This lining up causes it to stick to each other and leads to B-amyloid aggregations and the formation of fibrils. This evidence can be rebutted because the removal of B-amyloid plaques does not relieve symptoms or helps with the remission of AD.

35
Q

Briefly describe the nucleation condensation model of protein folding

A

This model proposes that local secondary structures form first, followed by a rapid collapse into a folded state, balancing local and global interactions.

36
Q

Briefly describe an experiment used to assess differences in autonomic activation of psychopaths compared to non-psychopaths

A

Psychopaths show lower skin conductance responses during fear-conditioning experiments, indicating reduced autonomic arousal compared to non-psychopaths.

37
Q

Briefly describe the role of serotonin and its interaction with testosterone In psychopaths

A

Low serotonin levels impair emotional regulation, while high testosterone enhances aggression, contributing to impulsive, antisocial behavior in psychopaths.

38
Q

Identify and label on the diagram the site affected by Parkinson’s disease

A

Substantia Nigra Pars Compacta

39
Q

What is the problem with the substantia nigra pars compacta structure that leads to symptoms?

A

Dopaminergic neuron degeneration in Substantia Nigra
* This leads to decreased dopamine in the striatum
* Disrupts balance between direct and indirect pathways
* Causes motor symptoms like tremor, rigidity, and bradykinesia

40
Q

Identify and label on the diagram the site affected by Huntington’s disease

A

Striatum

41
Q

What is the problem with the striatum structure that leads to those symptoms?

A
  • The genetic mutation causing neuronal death in the striatum
  • Disrupts medium spiny neurons
  • This leads to uncontrolled movement (chorea)
  • Progressively impairs motor control coordination**
42
Q

What is the role of Dopamine in the direct and indirect pathway? Be precise.

A

Direct Pathway (Facilitates Movement): Dopamine binds to D1 receptors on striatal neurons in the direct pathway, enhancing their activity. This strengthens the inhibition of the internal globus pallidus (GPi), reducing its inhibitory output to the thalamus. The result is increased thalamic excitation of the motor cortex, promoting movement.
Indirect Pathway (Suppresses Movement): Dopamine binds to D2 receptors on striatal neurons in the indirect pathway, reducing their activity. This weakens the inhibition of the external globus pallidus (GPe), leading to greater inhibition of the subthalamic nucleus (STN). Reduced STN activity decreases stimulation of the GPi, which further decreases the GPi’s inhibitory output to the thalamus. This also results in increased thalamic excitation, facilitating movement.

In summary, dopamine enhances movement by activating the direct pathway (via D1 receptors) and inhibiting the indirect pathway (via D2 receptors), creating a net effect of reduced inhibition on the motor cortex. A dopamine deficit, as seen in Parkinson’s disease, disrupts this balance, impairing movement.

Neurobiology of Disease (4 decks)

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