Answer the following “cause-effect” true/false questions using the answer key: A: Only statement A is true. B: Only statement B is true. C: Both statements A and B are true, but B is not the exclusive cause of A.. D: Both statements A and B are true, and B is the exclusive cause of A. E: Neither statement A nor B is true. Question 2: A. Parkinson Disease (PD) is a neurodegenerative disease that can be effectively managed for decades after disease onset because B. There are highly efficacious, curative treatments for the disease.
Answer the following “cause-effect” true/false questions using the answer key:
A: Only statement A is true.
B: Only statement B is true.
C: Both statements A and B are true, but B is not the exclusive cause of A..
D: Both statements A and B are true, and B is the exclusive cause of A.
E: Neither statement A nor B is true.
Question 2:
A. Parkinson Disease (PD) is a neurodegenerative disease that can be effectively managed for decades after disease onset because
B. There are highly efficacious, curative treatments for the disease.
Question 3:
A. L-DOPA formulations include inhibitors of
B. AADC inhibitors prevent the conversion of L-DOPA to dopamine in the periphery.
Question 4:
A. PD is characterized by more localized neuronal loss compared to global neuronal loss because
B. Alpha-synuclein aggregates in PD accumulate intracellularly rather than extracellularly.
Question 5:
A. The ubiquitin-proteasome system and the lysosomal autophagy system (LAS) play opposing roles in the formation and degradation of alpha-synuclein oligomers because
B. Age-related decline in the function of the lysosomal autophagy system (LAS) is associated with greater accumulation of alpha-synuclein in dopaminergic neurons.
Question 6:
A. Nonmotor symptoms of PD may occur prior to the onset of motor symptoms because
B. Symptomatic PD involves 70-80% loss of dopaminergic neurons.
Question 7:
A. Controlling motor symptoms is one of the goals of PD treatment because
B. Non-motor symptoms are relatively rare until the advanced stages of PD.
Question 8:
A. Changes within the brain are rarely present in the preclinical or prodromal stage of PD because
B. Early changes associated with the prodromal stage of PD might stem from changes in the gut enteric nerves.
Question 9:
A. Dopaminergic neurons in the ventral tegmental area may be particularly vulnerable to oxidative stress because
B. Dopaminergic neurons in the ventral tegmental area undergo autonomous cytosolic calcium oscillations.
Question 10:
A. Use of L-DOPA over time can lead to drug-induced side effects such as involuntary muscle movements because
B. L-DOPA dosing is complicated by its long half-life.
Question 11:
A. PD may cause increased activity of the ubiquitin-proteasome system because
B. Accumulation of alpha-synuclein oligomers increases the activity of the ubiquitin-proteasome system to increase degradation.
Question 12:
A. Monoamine Oxidase Type B (MAOB) inhibitors increase the amount of L-DOPA reaching the central nervous system because
B. MAOB inhibitors prevent the conversion of L-DOPA to dopamine in peripheral tissues.
Question 13:
A. Loss of dopaminergic input to the striatum leads to bradykinesia because
B. The striatum directly innervates the efferent motor neurons of the spinal cord.
Question 14:
A. PD is usually more common in men than in women because
B. Most cases of PD are caused by a monogenetic, sex-linked recessive allele.
Question 15:
A. Treatment with dopamine agonists may cause altered impulse control because
B. Dopamine agonists acting on D3 receptors may stimulate the brain’s rewards centers.
Question 16:
A. Deep brain stimulation (DBS) has become a viable treatment option for patients who are resistant to treatment with L-DOPA because
B. Treatment with DBS is associated with fewer motor fluctuations and a decreased daily off time.
Question 17:
A. Clinical diagnosis of PD requires the presence of bradykinesia because
B. Motor symptoms are generally unilateral at the onset of the disease.
Question 18:
A. Dopaminergic neuron loss in PD leads to decreased excitatory input to the cerebral cortex because
B. In PD, the direct neural pathway becomes less active, and the indirect neural pathway becomes more active.
Question 19:
A. Increased expression of PGC1-alpha contributes to mitochondrial dysfunction in PD because
B. PGC1-alpha leads to increased alpha-synuclein oligomerization and more toxicity.
Question 20:
A. “Seeding” of misfolded alpha-synuclein proteins from one brain region to another is one mechanism of disease spread because
B. As alpha-synuclein aggregates become larger, they become insoluble.
Question 21:
A. Striatal dopamine content is reduced by 80% or more in symptomatic PD because
B. PD is characterized by a loss of dopaminergic neurons in the substantia nigra.
Question 22:
A. Mutations in LRRK2 are most likely associated with a classic PD
B. Disease causing mutations in LRRK2 are considered autosomal dominant
Question 23:
A. Diagnosis of PD requires either loss of dopaminergic neurons in the substantia nigra OR neuronal deposition of alpha-synuclein because
B. PD is not characterized by gross macroscopic atrophy of the brain.
Question 24:
A. Administration of tyrosine has shown efficacy in the treatment of PD because
B. Dopamine is synthesized enzymatically from tyrosine within nerve terminals by VMAT2.
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