Pharmacology of Neurodegenerative Disease Flashcards by Some One

Drugs acting on CNS are two types

1 Work on presynaptic neurons:

Affect the synthesis of neurotransmitter
Affect the storage of neurotransmitter
Affect the release of neurotransmitter
Affect the termination of action of
neurotransmitter

2 Work on post synaptic receptors:
Activate the receptors
Blocks the receptors

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What is the shared basic function of neurons in both the CNS and ANS?
a) Sensory perception
b) Transmission of information
c) Muscle contraction
d) Hormone secretion

b) Transmission of information

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How do neurons in both the CNS and ANS primarily communicate?
a) Electrical impulses only
b) Chemical signals only
c) Both electrical impulses and chemical signals
d) Hormonal signals

c) Both electrical impulses and chemical signals

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Differences between CNS and ANS

ANS
1) There are two neurotransmitters
2)less complex
3)Much lesser number of synapsis
4)No inhibitory neurons

CNS
1) There are numerous.
neurotransmitters
2) More complex circuits
3) Much greater number of
synapsis
4)There are networks of
inhibitory neurons constantly
active modulating the rate of
neuronal transmission

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Types of neurodegenerative Disease

Dementia type:
Alzheimer’s disease
Demyelinating disease:
Multiple Sclerosis (MS)
Parkinson Type
Parkinson disease
Other forms of parkinsonism
Motor neuron disease
Amyotrophic lateral Sclerosis
(ALS)
5.Prion disease لم ندرسه

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Neurodegenerative disorders those
respond to drug therapy

Parkinson’s disease
Alzhiemer’s Disease
Multiple Sclerosis (MS)
Amyotrophic Lateral Sclerosis (ALS)

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Which of the following statements correctly describes the neurotransmitter characteristics of the Central Nervous System (CNS)?
a) The CNS utilizes only two neurotransmitters.
b) The CNS exhibits numerous neurotransmitters.
c) The CNS does not utilize neurotransmitters.
d) The CNS primarily relies on electrical impulses for communication.

b) The CNS exhibits numerous neurotransmitters.

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In terms of circuit complexity, which nervous system component displays more intricate circuits?
a) Central Nervous System (CNS)
b) Autonomic Nervous System (ANS)
c) Both CNS and ANS exhibit similar circuit complexity.
d) Neither CNS nor ANS exhibits circuit complexity.

a) Central Nervous System (CNS)

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Which nervous system component is characterized by a significantly higher number of synapses?
a) Central Nervous System (CNS)
b) Autonomic Nervous System (ANS)
c) Both CNS and ANS have a similar number of synapses.
d) Neither CNS nor ANS have synapses.

a) Central Nervous System (CNS)

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What distinguishes the Central Nervous System (CNS) from the Autonomic Nervous System (ANS) regarding the presence of inhibitory neurons?
a) The CNS has inhibitory neurons, while the ANS does not.
b) The ANS has inhibitory neurons, while the CNS does not.
c) Both CNS and ANS lack inhibitory neurons.
d) Both CNS and ANS have inhibitory neurons, but they function differently.

a) The CNS has inhibitory neurons, while the ANS does not.

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Excitatory Postsynaptic Potentials (EPSP) are initiated by the release of neurotransmitters such as:
a) Dopamine and serotonin
b) Glutamate and GABA
c) Acetylcholine and dopamine
d) Glutamate and acetylcholine

d) Glutamate and acetylcholine

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During an EPSP, neurotransmitters bind to:
a) Presynaptic receptors
b) Dendritic spines
c) Axon terminals
d) Postsynaptic receptors

d) Postsynaptic receptors

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What is the primary effect of an EPSP on the postsynaptic neuron?
a) Hyperpolarization
b) Inhibition of neurotransmitter release
c) Depolarization due to an influx of sodium ions
d) No change in membrane potential

c) Depolarization due to an influx of sodium ions

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How does an EPSP affect the membrane potential of the postsynaptic neuron?
a) The membrane potential becomes more negative
b) The membrane potential remains unchanged
c) The membrane potential becomes more positive, moving closer to its firing threshold
d) The membrane potential becomes more positive, moving further away from its firing threshold

c) The membrane potential becomes more positive, moving closer to its firing threshold

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Inhibitory Postsynaptic Potentials (IPSP) are initiated by the release of neurotransmitters, such as:
a) Glutamate and acetylcholine
b) Serotonin and dopamine
c) Gamma-aminobutyric acid (GABA) and glycine
d) Norepinephrine and histamine

c) Gamma-aminobutyric acid (GABA) and glycine

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During an IPSP, neurotransmitters bind to:
a) Presynaptic receptors
b) Dendritic spines
c) Axon terminals
d) Postsynaptic receptors

d) Postsynaptic receptors

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What is the primary effect of an IPSP on the postsynaptic neuron?
a) Depolarization due to an influx of sodium ions
b) Hyperpolarization due to an influx of potassium ions
c) Hyperpolarization due to an efflux of potassium ions and influx of chloride ions
d) No change in membrane potential

c) Hyperpolarization due to an efflux of potassium ions and influx of chloride ions

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How does an IPSP affect the membrane potential of the postsynaptic neuron?
a) The membrane potential becomes more positive, moving closer to its firing threshold
b) The membrane potential remains unchanged
c) The membrane potential becomes more negative, moving further away from its firing threshold
d) The membrane potential becomes more negative, moving closer to its firing threshold

c) The membrane potential becomes more negative, moving further away from its firing threshold

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What neurotransmitter is primarily released by neurons in the substantia nigra?
a) Serotonin
b) Dopamine
c) Acetylcholine
d) GABA

b) Dopamine

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Which term best describes the firing pattern of dopaminergic neurons from the substantia nigra?
a) Phasic
b) Sporadic
c) Tonic
d) Oscillatory

c) Tonic

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What is the primary function of the mutual inhibitory pathway between the substantia nigra and neostriatum?
a) Excitation of both areas
b) Inhibition of both areas
c) Excitation of substantia nigra and inhibition of neostriatum
d) Inhibition of substantia nigra and excitation of neostriatum

b) Inhibition of both areas

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Which system does the substantia nigra belong to?
a) Limbic system
b) Autonomic nervous system
c) Central nervous system
d) Extrapyramidal system

d) Extrapyramidal system

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What role does the nigrostriatal pathway play in motor activity?
a) Excitatory
b) Inhibitory
c) Both excitatory and inhibitory
d) No role in motor activity

b) Inhibitory

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What neurotransmitter is primarily released by neostriatum neurons to the substantia nigra?
a) Dopamine
b) Glutamate
c) GABA
d) Serotonin

c) GABA

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Dysfunction of the nigrostriatal pathway is associated with which neurological disorder? a) Alzheimer's disease b) Parkinson's disease c) Huntington's disease d) Multiple sclerosis

b) Parkinson's disease

Which neurotransmitter deficiency is characteristic of Parkinson's disease? a) Dopamine b) Serotonin c) Acetylcholine d) Glutamate

a) Dopamine

What type of neurons originate from the substantia nigra and terminate in the neostriatum? a) Glutamatergic b) GABAergic c) Dopaminergic d) Serotonergic

c) Dopaminergic

What is the primary cause of Parkinson's disease? a) Overproduction of dopamine b) Destruction of cells in the neostriatum c) Degeneration of nerve terminals secreting dopamine in the neostriatum d) Excessive activity of cholinergic neurons in the substantia nigra

c) Degeneration of nerve terminals secreting dopamine in the neostriatum Destruction of cells in the substantia nigra results in the degeneration of the nerve terminals that secrete dopamine in the neostriatum.

How does the diminished inhibitory influence of dopamine in the neostriatum contribute to Parkinson's disease? a) It leads to overproduction of acetylcholine b) It increases the production of dopamine c) It decreases the production of acetylcholine d) It has no effect on neurotransmitter levels

a) It leads to overproduction of acetylcholine the normal inhibitory influence of dopamine on cholinergic neurons in the neostriatum is significantly diminished That results in overproduction, or a relative overactivity, of acetylcholine by the stimulatory neurons.

What is the primary pharmacological action of antipsychotic drugs that can lead to secondary parkinsonism? a) Stimulation of dopamine receptors b) Inhibition of cholinergic receptors c) Blockade of dopamine receptors d) Blockade of acetylcholine receptors

c) Blockade of dopamine receptors

What is the term used to describe parkinsonian symptoms induced by antipsychotic drugs such as phenothiazines and haloperidol? a) Primary parkinsonism b)c&d c) Pseudoparkinsonism d) Drug-induced parkinsonism

b)c&d

Parkinson's disease primarily affects which aspect of neurological function? a) Sensory perception b) Memory formation c) Muscle movement d) Language comprehension

c) Muscle movement

What is the typical age group that Parkinson's disease mostly affects? a) Under 30 years b) Between 30 and 45 years c) Between 45 and 65 years d) Over 65 years

d) Over 65 years

What is the estimated incidence of Parkinson's disease in the general population? a) 1 in 1,000 individuals b) 1 in 500 individuals c) 1 in 100 individuals d) 1 in 50 individuals

c) 1 in 100 individuals

Manifestations of Parkinson's Disease “ 4 Ds “

1) Motor Manifistations Dyskinesia 2) Non Motor Manifistations Depression Dementia Disturbance of Sleep

Dyskinesia of Parkinson Disease 6”

1 Akinesia 2 Bradykinesia 3 Muscular rigidity 4 Tremors 5 Postural abnormalities 6 Gait abnormalities

What is the primary goal of therapy for Parkinson's disease? a) Increasing the number of cholinergic neurons in the neostriatum b) Inhibiting the release of dopamine in the basal ganglia c) Antagonizing the excitatory effect of acetylcholine d) Reducing the number of inhibitory dopaminergic neurons

c) Antagonizing the excitatory effect of acetylcholine

Which neurotransmitter is primarily targeted for restoration in the basal ganglia during Parkinson's disease therapy? a) Serotonin b) Glutamate c) Dopamine d) GABA

c) Dopamine

What is the main aim of antagonizing the excitatory effect of acetylcholine in Parkinson's disease therapy? a) To increase cholinergic activity b) To reduce dopamine levels c) To restore the balance between dopamine and acetylcholine d) To enhance inhibitory dopaminergic neurons

c) To restore the balance between dopamine and acetylcholine

What neurotransmitter imbalance characterizes Parkinsonism? A) GABAergic and glutamatergic imbalance B) Serotonergic and noradrenergic imbalance C) Cholinergic and dopaminergic imbalance D) Adrenergic and histaminergic imbalance

C) Cholinergic and dopaminergic imbalance

Strategy of Parkinson Disease Therapy is aimed at:

1.Restoring dopamine in the basal ganglia. 2. Antagonizing the Cholinergic excitatory effect. (reestablishing the correct dopamine/acetylcholine balance)

Antiparkinson's Disease

A) Drugs enhance Dopaminergic pathway 1) Central Dopamine release enhancers a) Dopamin Precursors L.dopa b)Peripheral decarboxylase inhibitors Carbidopa c) COMT inhibitors Entacapone , Tolcapone 2)Central Dopamine degradation inhibitors “MAOB inhibitors” Selegiline , Rasagiline 3) Dopamine Agonist Bromocriptine 4) Dopamine facilitators **Amantadine , Apomorphine B) Centrally Acting Anticholinergics Trihexiphenidyl Benztropine

Which of the following drugs inhibits the peripheral decarboxylation of levodopa? A) Selegiline B) Rasagiline C) Carbidopa D) Tolcapone

C) Carbidopa

Trihexyphenidyl and benztropine are examples of: A) Dopamine precursors B) Peripheral decarboxylase inhibitors C) MAOB inhibitors D) Centrally acting anticholinergics

D) Centrally acting anticholinergics

Levodopa enhances dopamine synthesis in the CNS by: A) Crossing the blood-brain barrier as dopamine B) Inhibiting the decarboxylase enzyme C) Acting as a direct precursor to dopamine D) Inducing dopamine release from synaptic vesicles

C) Acting as a direct precursor to dopamine

How does levodopa cross the blood-brain barrier? A) Through passive diffusion B) Via specific dopamine transporter proteins C) Using large neutral amino acid transporter (LAT1) D) By undergoing active transport mediated by COMT

C) Using large neutral amino acid transporter (LAT1)

Which enzyme converts levodopa to dopamine in the CNS? A) Catechol-O-methyl transferase (COMT) B) Monoamine oxidase B (MAOB) C) Dopamine beta-hydroxylase D)L-amino acid decarboxylase

D)L-amino acid decarboxylase

The main purpose of administering levodopa in Parkinson's disease is to: A) Inhibit the breakdown of dopamine B) Increase the synthesis of serotonin C) increase the activity of cholinergic neurons D) Compensate for the deficiency of dopamine in the brain

D) Compensate for the deficiency of dopamine in the brain

Which peripheral enzyme is responsible for the metabolism of levodopa into dopamine? A) Catechol-O-methyl transferase (COMT) B) Monoamine oxidase B (MAOB) C) Dopamine beta-hydroxylase D) L-amino acid decarboxylase

D) L-amino acid decarboxylase

What is the primary function of levodopa in the treatment of Parkinson's disease? A) Inhibition of dopamine degradation B) Enhancement of dopamine synthesis C) Blockade of dopamine receptors D) Inhibition of acetylcholine release

B) Enhancement of dopamine synthesis

Chat gpt Why can't dopamine itself effectively cross the blood-brain barrier? A) It is too large to pass through B) It is rapidly metabolized in the bloodstream C) It is actively transported out of the brain D) It is degraded by enzymes in the blood

A) It is too large to pass through

What is the primary location in the brain where levodopa is converted to dopamine? A) Substantia nigra B) Striatum C) Hippocampus D) Thalamus

A) Substantia nigra

What is the primary reason for the short half-life of levodopa? A) Rapid metabolism by catechol-O-methyl transferase (COMT) B) Inhibition of absorption in the gastrointestinal tract (GIT) C) High protein binding in the bloodstream D) Limited ability to cross the blood-brain barrier

A) Rapid metabolism by catechol-O-methyl transferase (COMT)

How does levodopa primarily cross the blood-brain barrier? A) Passive diffusion B) Active transport via dopamine transporter proteins C) Utilization of specific amino acid transporters (LAT1) D) Conversion to dopamine prior to crossing the barrier

C) Utilization of specific amino acid transporters (LAT1)

Which enzyme metabolizes levodopa into 3-O-Methyldopa in the circulation? A) Aromatic L-amino acid decarboxylase (AADC) B) Monoamine oxidase (MAO) C) Catechol-O-methyl transferase (COMT) D) Dopamine beta-hydroxylase

C) Catechol-O-methyl transferase (COMT)

Why does the amount of levodopa that reaches the CNS remain limited? A) Rapid degradation by MAO in the bloodstream B) Competition at LAT1 by 3-O-Methyldopa C) Inhibition of absorption in the small intestine D) High affinity for binding to plasma proteins

B) Competition at LAT1 by 3-O-Methyldopa

How does the extensive metabolism of levodopa in the gastrointestinal tract (GIT) affect its bioavailability? A) Increases bioavailability due to enhanced absorption B) Decreases bioavailability due to decreased absorption C) Does not affect bioavailability as levodopa is not absorbed in the GIT D) Converts levodopa into dopamine, increasing its bioavailability

B) Decreases bioavailability due to decreased absorption

Which enzyme is primarily responsible for the metabolism of levodopa in the gastrointestinal tract (GIT)? A) Monoamine oxidase (MAO) B) Catechol-O-methyl transferase (COMT) C) decarboxylase D) Dopamine beta-hydroxylase

C) decarboxylase

Why is levodopa preferably administered on an empty stomach? A) To minimize gastrointestinal side effects B) To enhance its absorption from the small intestine C) To reduce the risk of drug interactions D) To prevent rapid metabolism by COMT

B) To enhance its absorption from the small intestine

What is the primary metabolic pathway of levodopa in the circulation? A) Conversion to dopamine by monoamine oxidase (MAO) B) Metabolism into 3-O-Methyldopa by catechol-O-methyl transferase (COMT) C) Breakdown into inactive metabolites by aromatic L-amino acid decarboxylase (AADC) D) Direct excretion unchanged through the kidneys

B) Metabolism into 3-O-Methyldopa by catechol-O-methyl transferase (COMT)

G.R The amount of levodopa that reaches the CNS is too small?

due to peripheral decarboxylation and competition at LAT1 by 3-O-Methyldopa.

Which of the following side effects is primarily caused by the peripheral metabolism of levodopa leading to an increase in dopamine? A) Muscle rigidity B) Dyskinesias C) Nausea and/or vomiting D) Depression

C) Nausea and/or vomiting

Stimulation of dopaminergic receptors by dopamine produced from the decarboxylation of levodopa can lead to: A) Hypertension B)Hypoglycemia C) Cardiac arrhythmias D) Hyperglycemia

C) Cardiac arrhythmias The peripheral metabolism of levodopa will cause the increase in dopamine that will cause the following side effects: Nausea and/or vomiting Cardiac arrhythmias Hypotension

The peripheral metabolism of levodopa can contribute to which of the following cardiovascular side effects? A) Hypertension B) Bradycardia C) Hypotension D) Peripheral edema

C) Hypotension

Which receptor type is primarily involved in mediating the side effects such as nausea, vomiting, and cardiac arrhythmias caused by the peripheral metabolism of levodopa? A) Alpha-adrenergic receptors B) Beta-adrenergic receptors C) Dopaminergic receptors D) Serotonergic receptors

C) Dopaminergic receptors

What is the underlying mechanism of the side effects induced by the peripheral metabolism of levodopa? A) Stimulation of adrenergic receptors B) Inhibition of acetylcholine release C) Stimulation of dopaminergic receptors D) Blockade of glutamatergic neurotransmission

C) Stimulation of dopaminergic receptors

How Can be done to increase the amount of Levodopa that reaches the CNS and reduce the side effects related to overproduction of Dopamine in peripheral tissues???

That can be done by preventing decarboxylation of levodopa by adding decarboxylase enzyme inhibitor. (Carbidopa)

Which of the following drugs can be co-administered with levodopa to increase the amount of levodopa that reaches the CNS and reduce the side effects related to the overproduction of dopamine in peripheral tissues? A) Bromocriptine B) Selegiline C) Tolcapone D) Carbidopa

D) Carbidopa

G.R Levodopa should always be giving combined with carbidopa?

The addition of carbidopa lowers the dose of levodopa needed by four- to five-fold and, consequently, decreases the severity of adverse effects arising from peripherally formed dopamine.

Cautions when taking levodopa:

1) To be given on empty stomach (at least 30 minutes before food) (because proteins interferes with its absorption). On - Off phenomenon: (when given with food it cause fluctuation in the effect >> sudden onset tremors, cramps and loss of ability to move). 2) Should not be stopped suddenly.

Which medication should always be combined with levodopa to enhance its efficacy and reduce the severity of adverse effects arising from peripherally formed dopamine? A) Bromocriptine B) Selegiline C) Tolcapone D) Carbidopa

D) Carbidopa

What is the primary reason for combining carbidopa with levodopa? A) To inhibit the peripheral metabolism of levodopa B) To enhance the central metabolism of levodopa C) To potentiate the effects of levodopa on dopamine receptors D) To reduce the risk of gastrointestinal side effects

A) To inhibit the peripheral metabolism of levodopa

What phenomenon may occur when levodopa is taken with food? A) Tolerance development B) On-off phenomenon C) Placebo effect D) Drug-induced psychosis

B) On-off phenomenon

GPT Why is it cautioned against stopping levodopa suddenly? A) Due to the risk of rebound hypertension B) To prevent the development of drug resistance C) To avoid exacerbation of Parkinson's symptoms D) Because of the potential for serotonin syndrome

C) To avoid exacerbation of Parkinson's symptoms

Adverse Effects of Levodopa

1)GIT Side Effects: Anorexia, nausea, and vomiting (chemoreceptor trigger zone). 2)Cardiac Side Effects: -Tachycardia and ventricular extra-systole. -Hypotension (postural /orthostatic) 3)Mixed Side Effects: -Blood dyscrasias -Sweat, saliva and urine may turn brownish color. -Visual and auditory hallucinations 4)Motor Side Effects: -Dyskinesia (repetitive involuntary abnormal movements affecting the face, trunk, and limbs) (Akinesia paradoxia is a sudden freezing of movement).= mask face 5)CNS Side efects: Mood changes Depression Psychosis (exacerbation of pre-existing psychotic symptoms) Dream alterations

Anorexia, nausea, and vomiting associated with levodopa primarily result from stimulation of receptors in which area? A) Substantia nigra B) Striatum C) Chemoreceptor trigger zone D) Hypothalamus

C) Chemoreceptor trigger zone

Which of the following cardiac side effects is commonly associated with levodopa therapy? A) Bradycardia B) Hypertension C) Tachycardia

C) Tachycardia

Which of the following is considered a mixed side effect of levodopa? A) Hyperthermia B) Respiratory depression C) Blood dyscrasias D) Peripheral neuropathy

C) Blood dyscrasias

The discoloration of sweat, saliva, and urine to a brownish color is a result of the metabolism of levodopa into which compound? A) Dopamine B) Serotonin C) Epinephrine D) Melanin

A) Dopamine

Visual and auditory hallucinations are among the adverse effects of levodopa due to its actions on which neurotransmitter system? A) Dopaminergic B) Serotonergic C) GABAergic

A) Dopaminergic

Levodopa can cause tachycardia and ventricular extrasystoles as part of its: A) Gastrointestinal side effects B) Cardiac side effects C) Mixed side effects D) Central nervous system effects

B) Cardiac side effects

Levodopa can cause discoloration of sweat, saliva, and urine, which may turn a: A) Yellowish color B) Greenish color C) Bluish color D) Brownish color

D) Brownish color

What sensory disturbances are commonly associated with levodopa use? A) Gustatory hallucinations B) Tactile hallucinations C) Visual and auditory hallucinations D) Olfactory hallucinations

C) Visual and auditory hallucinations

Which of the following motor side effects is characterized by repetitive involuntary abnormal movements affecting the face, trunk, and limbs? A) Akathisia B) Bradykinesia C) Dyskinesia D) Dystonia

C) Dyskinesia

What is akinesia paradoxia? A) Sudden onset of rapid movements B) Inability to initiate voluntary movements despite the intention to move C) Sudden freezing of movement D) Repetitive involuntary abnormal movements

C) Sudden freezing of movement

Which of the following central nervous system side effects is associated with levodopa therapy? A) Memory loss B) Euphoria C) Dysarthria D) Dream alterations

D) Dream alterations

Levodopa therapy may lead to exacerbation of pre-existing psychotic symptoms, known as: A) Dystonia B) Akathisia C) Psychosis D) Dyskinesia

C) Psychosis

Which vitamin is known to increase the peripheral breakdown of levodopa? A) Vitamin C (ascorbic acid) B) Vitamin B6 (pyridoxine) C) Vitamin B12 (cobalamin) D) Vitamin D

B) Vitamin B6 (pyridoxine)

Nonselective monoamine oxidase inhibitors (MAOIs), such as phenelzine, when used together with the levodopa can lead to: A) Bradycardia B) Hypertensive crisis C) Hypotension D) Hyperthermia

B) Hypertensive crisis

How do antipsychotic drugs typically affect dopamine receptors? A) Enhance dopamine release B) Inhibit dopamine reuptake C) Potently block dopamine receptors D) Increase dopamine synthesis

C) Potently block dopamine receptors

Which class of antipsychotic drugs is commonly used to treat levodopa-induced psychotic symptoms? A) Typical antipsychotics B) Benzodiazepines C) Selective serotonin reuptake inhibitors (SSRIs) D) Atypical antipsychotics

D) Atypical antipsychotics Antipsychotic drugs potently block dopamine receptors. Low doses of atypical antipsychotics, such as quetiapine or clozapine, are used to treat levodopa-induced psychotic symptoms.

Contraindications of levodopa:

1)Psychotic patients >> levodopa exacerbates symptoms. 2)Cardiac patients >> possible development of arrhythmias. 3)Patients with narrow-angle glaucoma.! 4)Patients with peptic ulcer disease.!

Which patient population should avoid levodopa due to the possible development of arrhythmias? A) Patients with Parkinson's disease B) Patients with congestive heart failure C) Patients with rheumatoid arthritis D) Patients with depression

B) Patients with congestive heart failure

GPT Levodopa is contraindicated in patients with narrow-angle glaucoma due to its potential to: A) Worsen visual acuity B) Increase intraocular pressure C) Cause retinal detachment D) Induce cataract formation

B) Increase intraocular pressure

GPT Patients with peptic ulcer disease should avoid levodopa due to the risk of: A) Gastrointestinal bleeding B) Gastric perforation C) Esophageal stricture D) Intestinal obstruction

A) Gastrointestinal bleeding

Carbidopa protects levodopa from peripheral decarboxylation, but, what can increase levodopa transport through blood brain barrier??

Adding COMT inhibitor will reduce formation of 3 - 0 - Methyldopa that compete with Ldopa at LAT1 >> more levodopa can be transported to the CNS Tolcapone Entacapone

What is the primary function of carbidopa when administered with levodopa? A) Inhibiting peripheral decarboxylation B) Enhancing dopamine synthesis C) Blocking COMT activity D) Preventing levodopa metabolism in the liver

A) Inhibiting peripheral decarboxylation

Which of the following drugs increases levodopa transport through the blood-brain barrier by inhibiting COMT activity? A) Tolcapone B) Amantadine C) Pramipexole D) Benztropine

A) Tolcapone

Which statement accurately describes the absorption of entacapone and tolcapone? A) Tolcapone is better absorbed than entacapone from the gastrointestinal tract (GIT). B) Entacapone has a longer duration of action compared to tolcapone. C) Both entacapone and tolcapone are poorly absorbed from the GIT. D) Both entacapone and tolcapone are well absorbed from the GIT.

D) Both entacapone and tolcapone are well absorbed from the GIT.

Why is entacapone preferred over tolcapone in clinical practice despite both drugs improving response to levodopa-carbidopa therapy? A) Entacapone has fewer side effects compared to tolcapone. B) Entacapone has a shorter duration of action compared to tolcapone. C) Tolcapone induces fulminant hepatic necrosis, whereas entacapone does not. D) Tolcapone has a faster onset of action compared to entacapone.

C) Tolcapone induces fulminant hepatic necrosis, whereas entacapone does not.

Which statement accurately describes the pharmacokinetic properties of tolcapone and entacapone? A) Tolcapone has a shorter duration of action compared to entacapone. B) Both tolcapone and entacapone require dose adjustment in liver cirrhosis. C) Entacapone improves response to levodopa-carbidopa therapy, while tolcapone reduces the wearing-off phenomenon. D) Tolcapone has a faster onset of action compared to entacapone.

B) Both tolcapone and entacapone require dose adjustment in liver cirrhosis.

Which statement accurately describes the pharmacokinetic properties of tolcapone and entacapone? A) Tolcapone has a longer duration of action compared to entacapone. B) Entacapone improves response to levodopa-carbidopa therapy, while tolcapone reduces the wearing-off phenomenon. C) Tolcapone has a faster onset of action compared to entacapone.

A) Tolcapone has a longer duration of action compared to entacapone.

Which statement accurately describes the pharmacokinetic properties of tolcapone and entacapone? A) Tolcapone has a shorter duration of action compared to entacapone. B) Both tolcapone and entacapone does not require dose adjustment in liver cirrhosis. C) Both tolcapone and entacapone improve response to levodopa-carbidopa therapy and reduce the wearing-off phenomenon. D) Tolcapone has a faster onset of action compared to entacapone.

C) Both tolcapone and entacapone improve response to levodopa-carbidopa therapy and reduce the wearing-off phenomenon.

Which statement accurately describes the side effects of tolcapone and entacapone? A) Tolcapone and entacapone have distinct side effect profiles compared to levodopa. B) Both tolcapone and entacapone have similar side effects to levodopa. C) Tolcapone has fewer side effects compared to entacapone. D) Entacapone has a higher incidence of gastrointestinal side effects compared to tolcapone.

B) Both tolcapone and entacapone have similar side effects to levodopa.

What is the effect of selective MAO-B inhibitors on dopamine levels in the brain? A) Decrease dopamine levels B) Have no effect on dopamine levels C) Increase dopamine levels D) Convert dopamine into serotonin

C) Increase dopamine levels

In what capacity are selective MAO-B inhibitors typically used in relation to levodopa-carbidopa therapy? A) They replace levodopa-carbidopa B) They enhance the peripheral decarboxylation of levodopa C) They antagonize the effects of levodopa-carbidopa D) They are used as adjuvants to levodopa-carbidopa

D) They are used as adjuvants to levodopa-carbidopa

Which medications should be avoided when taking selective MAO-B inhibitors? A) Non-steroidal anti-inflammatory drugs (NSAIDs) B) Selective serotonin re-uptake inhibitors (SSRIs) C) Beta-blockers D) Calcium channel blockers

B) Selective serotonin re-uptake inhibitors (SSRIs) These drugs should be avoided in patients taking selective serotonin re-uptake inhibitors (SSRIs), tricyclic antidepressants, and meperidine.

What is the primary effect of selective monoamine oxidase B (MAO-B) inhibitors on dopamine levels in the brain? A) Decrease dopamine levels B) Have no effect on dopamine levels C) Increase dopamine levels D) Convert dopamine into serotonin

C) Increase dopamine levels

GPT Why are selective monoamine oxidase B (MAO-B) inhibitors well tolerated at recommended doses? A) Due to their high toxicity profile B) Because they have minimal effect on dopamine levels C) Because they selectively inhibit MAO-A D) Due to their minimal side effects

D) Due to their minimal side effects

MAOB inhibitors are primarily used in the treatment of: a) Hypertension b) Depression c) Parkinson's disease d) Schizophrenia

c) Parkinson's disease

MAOB inhibitors prevent the degradation of which neurotransmitter in the brain? a) Serotonin b) Dopamine c) Acetylcholine d) GABA

b) Dopamine

Which MAOB inhibitor is known to be metabolized into amphetamine and methamphetamine, potentially causing insomnia if administered later in the day? a) Selegiline b) Rasagiline c) Safinamide d) Entacapone

a) Selegiline

Among the listed MAOB inhibitors, which one is irreversible and possesses five times the potency of Selegiline? And it is not metabolized to an amphetamine-like substance. a) Selegiline b) Rasagiline c) Safinamide d) Entacapone

b) Rasagiline

Which MAOB inhibitor is not metabolized into amphetamine-like substances? a) Selegiline b) Rasagiline

b) Rasagiline Note Safinamide: Is also a selective inhibitor, of MAO-B

Dopamine agonists “Bromocriptine” are preferred in Parkinson's disease patients experiencing fluctuations in response to levodopa due to: a) Shorter duration of action compared to levodopa b) Longer duration of action compared to levodopa c) Greater risk of dyskinesias compared to levodopa d) Lower efficacy compared to levodopa

b) Longer duration of action compared to levodopa

Compared to initial therapy with levodopa, initial therapy with dopamine agonists “Bromocriptine” is associated with: a) Higher risk of dyskinesias b) Lower risk of dyskinesias and motor fluctuations c) Faster onset of action d) Greater efficacy in treatment-naive patients

b) Lower risk of dyskinesias and motor fluctuations

Dopamine agonists “Bromocriptine” are ineffective in patients who: a) Have not responded to levodopa b) Have never been treated with levodopa c) Are resistant to dopamine d) Are not experiencing motor fluctuations

a) Have not responded to levodopa

Bromocriptine's actions are similar to which other medication? a) Amantadine b) Selegiline c) Levodopa d) Benztropine

c) Levodopa

Which of the following best describes the mechanism of action of bromocriptine? a) Cholinergic agonism b) Dopaminergic agonism c) GABAergic antagonism d) Serotonergic agonism

b) Dopaminergic agonism

Compared to levodopa, bromocriptine is less likely to cause: a) Dyskinesia b) Psychiatric illness c) Peripheral vascular disease d) Myocardial infarction

a) Dyskinesia

Bromocriptine is contraindicated in patients with a history of the following except : a) Dyskinesia b) Myocardial infarction c) Peripheral vascular disease d) Psychiatric illness

a) Dyskinesia

Which of the following is a specific adverse effect of bromocriptine due to its ergot derivative nature? a) Dyskinesia b) Pulmonary and retroperitoneal fibrosis c) Peripheral vascular disease d) Myocardial infarction

b) Pulmonary and retroperitoneal fibrosis

Bromocriptine, an ergot derivative, shares similar actions to levodopa, with adverse effects that are also similar to levodopa, except for….

Dyskinesia

Bromocriptine Contraindications:

1 psychiatric illness. 2 Patients with a history of myocardial infarction or peripheral vascular disease due to the risk of vasospasm.

Bromocriptine (dopamine agonist)has the potential to cause pulmonary and retroperitoneal fibrosis?

Because it is an ergot derivative .

The antiparkinsonian action of amantadine was accidentally discovered while it was primarily used as a(n): a) Antibiotic b) Antiviral drug c) Antifungal agent d) Anticoagulant

b) Antiviral drug

Which of the following is NOT an adverse effect associated with amantadine use in Parkinson's disease? a) Restlessness b) Agitation c) Confusion d) Bradycardia

d) Bradycardia The drug may cause restlessness Agitation Confusion Hallucinations

Amantadine is believed to exert its antiparkinsonian effects by inhibiting which type of glutamate receptors? a) NMDA b) AMPA c) Kainate d) Metabotropic glutamate receptors

a) NMDA

Amantadine Mechanism of Action:

Not exactly known but it could be through 1 ) Increases the release of dopamine. 2) Blocking cholinergic receptors 3) Inhibiting NMDA type of glutamate receptors.

The main mechanism of action of benztropine and trihexyphenidyl in treatment of Parkinson's disease involves: a) Increasing dopamine release b) Decreasing acetylcholine activity c) Enhancing serotonin signaling d) Blocking glutamate receptors

b) Decreasing acetylcholine activity

Which symptom of Parkinson's disease do benztropine and trihexyphenidyl have a significant effect on? a) Bradykinesia b) Tremors and rigidity c) Postural reflexes d) Cognitive decline

b) Tremors and rigidity They have a significant effect on tremors and rigidity but little effect on bradykinesia and postural reflexes.

Which of the following is NOT a side effect commonly associated with benztropine and trihexyphenidyl? a) Mood change and confusion b) Xerostomia and constipation c) Visual problems d) Insomnia and nightmares

d) Insomnia and nightmares Side effects: Mood change and confusion (CNS) Xerostomia and Constipation (GIT) Visual problems (Eye)

Contraindications for the use of benztropine and trihexyphenidyl (centrally acting anticholenergics ) include: a) Glaucoma b) Hypertension c) Renal failure d) Osteoarthritis

a) Glaucoma Contraindications: 1. Glaucoma 2. Prostatic hyperplasia 3. Pyloric stenosis.

Benztropine and trihexyphenidyl, compared to levodopa, are characterized by: a) Greater efficacy in treating Parkinson's disease b) Lower efficacy in treating Parkinson's disease c) Comparable efficacy in treating Parkinson's disease d) Similar efficacy but different mechanism of action in treating Parkinson's disease

b) Lower efficacy in treating Parkinson's disease

Alzheimer disease has three distinguishing features:

1. Accumulation of senile plaques (beta-amyloid accumulations), 2. Formation of numerous neurofibrillary tangles 3. Loss of cortical neurons, particularly cholinergic neurons.

Alzheimer’s therapies aim either to: “2”

1)To Improve cholinergic transmission within the CNS 2)To prevent excitotoxic actions resulting from overstimulation of NMDA-glutamate receptors in selected areas of the brain.

What are the three distinguishing features of Alzheimer's disease? a) Accumulation of senile plaques, loss of cortical neurons, and formation of numerous neurofibrillary tangles b) Accumulation of tau proteins, loss of dopaminergic neurons, and formation of senile plaques c) Accumulation of amyloid-beta, loss of hippocampal neurons, and formation of neurofibrillary tangles d) Accumulation of neurofibrillary tangles, loss of cholinergic neurons, and formation of senile plaques

a) Accumulation of senile plaques, loss of cortical neurons, and formation of numerous neurofibrillary tangles

Which of the following is NOT a therapeutic target for Alzheimer's disease? a) Improving cholinergic transmission within the CNS b) Preventing excitotoxic actions resulting from overstimulation of NMDA-glutamate receptors c) Inhibiting the accumulation of tau proteins d) Alleviating symptoms through palliative care

c) Inhibiting the accumulation of tau proteins

True or False: Current pharmacologic interventions for Alzheimer's disease can alter the underlying neurodegenerative process. a) True b) False

b) False

Which protein accumulations are primarily associated with Alzheimer's disease? a) Tau proteins b) Amylin c) Beta-amyloid d) Alpha-synuclein

c) Beta-amyloid

What is the primary aim of therapies targeting cholinergic transmission in Alzheimer's disease? a) Enhancing memory formation b) Reducing neuroinflammation c) Improving motor function d) Alleviating behavioral symptoms

a) Enhancing memory formation

What is the mechanism of action of therapies aiming to prevent excitotoxic actions in Alzheimer's disease? a) Blocking acetylcholine receptors b) Inhibiting NMDA-glutamate receptors c) Enhancing serotonin reuptake d) Promoting dopamine release

b) Inhibiting NMDA-glutamate receptors

Which of the following is a characteristic feature of Alzheimer's disease pathology? a) Increased GABAergic neurotransmission b) Accumulation of Lewy bodies c) Loss of dopaminergic neurons in the substantia nigra d) Accumulation of beta-amyloid plaques and neurofibrillary tangles

d) Accumulation of beta-amyloid plaques and neurofibrillary tangles

Which of the following is NOT a reversible acetylcholinesterase inhibitor approved for the treatment of Alzheimer's disease? a) Donepezil b) Galantamine c) Rivastigmine d) Memantine

d) Memantine

Which acetylcholinesterase inhibitor is specifically approved for the management of dementia in Parkinson's disease? a) Donepezil b) Galantamine c) Rivastigmine d) Memantine

c) Rivastigmine

What is a common adverse effect associated with the use of acetylcholinesterase inhibitors? a) Tachycardia b) Hypertension c) Nausea d) Hyperglycemia

c) Nausea

What is the proposed mechanism of action of acetylcholinesterase inhibitors in Alzheimer's disease? a) Increasing the production of acetylcholine b) Blocking the release of acetylcholine c) Inhibiting the degradation of acetylcholine d) Enhancing the reuptake of acetylcholine

c) Inhibiting the degradation of acetylcholine

Which formulation of rivastigmine is specifically mentioned as being available for the management of dementia in Parkinson's disease? a) Oral tablets b) Intravenous injection c) Transdermal patch d) Sublingual spray

c) Transdermal patch

Which of the following is NOT a common adverse effect associated with acetylcholinesterase inhibitors? a) Nausea b) Diarrhea c) Hypertension d) Tremors

c) Hypertension

True or False: Acetylcholinesterase inhibitors can completely halt the progression of Alzheimer's disease. a) True b) False

b) False

The reversible AChE inhibitors approved for the treatment of Alzheimer's disease include

Galantamine Rivastigmine ++dr.f Donepezil

Acetylcholinesterase inhibitors that used for ttt of Alzheimer’s disease A/E ?

Common adverse effects include • Nausea, diarrhea, vomiting, anorexia, • tremors, and muscle Cramps. • bradycardia.

Alzheimer's disease therapy ?

A. Acetylcholinesterase inhibitors Galantamine Rivastigmine B. NMDA receptor antagonist Memantine indicated for moderate-to- severe Alzheimer's disease. is often given in combination with an AChE inhibitor.

Memantine ( NMDA antagonist) A/E ?

• Confusion • Agitation • Restlessness

What is the role of glutamate NAMDA receptors in memory formation in the CNS? A. Inhibition of memory consolidation B. Excitotoxicity on neurons C. Critical for memory formation D. Induction of neurodegenerative processes

C. Critical for memory formation

Which of the following best describes the potential consequence of overstimulation of NMDA receptors? A. Facilitation of memory retrieval B. Excitotoxic damage to neurons C. Enhanced neuronal regeneration D. Promotion of synaptic plasticity

B. Excitotoxic damage to neurons

Overstimulation of NMDA receptors in Alzheimer’s disease is implicated in: A. Enhancing long-term memory B. Neuroprotective effects C. Excitotoxicity D. Decreasing synaptic plasticity

C. Excitotoxicity

G.R using NMDA receptor antagonist for ttt of Alzheimer’s disease?

Stimulation of glutamate receptors in the CNS appears to be critical for the formation of certain memories. However, overstimulation of glutamate receptors, particularly of the NMDA type, may result in excitotoxic effects on neurons and is suggested as a mechanism for neurodegenerative or apoptotic processes.

Which of the following is NOT a common goal of multiple sclerosis MS treatment? A. Slowing disease progression B. Reducing frequency of relapses C. Restoring lost neurological function D. Managing symptoms to improve quality of life

C. Restoring lost neurological function

• Multiple sclerosis (MS) is…

an autoimmune inflammatory demyelinating disease of the CNS. • Medications are used to modify the disease course, treat relapses (exacerbations or attacks), and manage symptoms.

Treatment for multiple sclerosis MS may include

the following: 1. Treating relapses of MS symptoms (with steroid medication dexamethasone ad prednisolone) 2. Treating specific MS symptoms 3. Treatment to reduce the number of relapses (disease- modifying therapies)

Treatment for MS may include

Which of the following best describes the purpose of disease-modifying therapies for MS? A. They primarily treat symptoms of MS. B. They aim to reverse existing damage to the myelin sheath. C. They target immune processes to reduce relapses and disability progression. D. They are designed to improve cognitive function in MS patients.

C. They target immune processes to reduce relapses and disability progression.

What is the primary mechanism of action of disease-modifying therapies in multiple sclerosis MS? A. Enhancing myelin regeneration B. Decreasing nerve cell apoptosis C. Modifying the immune response D. Stimulating oligodendrocyte function

C. Modifying the immune response Explanation: Disease-modifying therapies work by targeting immune processes, particularly inhibiting white blood cell-mediated inflammatory processes that lead to myelin sheath damage in MS.

In which types of MS are disease-modifying agents most useful? A. Primary progressive MS B. Relapse remitting MS and secondary progressive MS C. Progressive relapsing MS D. Clinically isolated syndrome (CIS)

B. Relapse remitting MS and secondary progressive MS Disease-modifying agents are useful in certain patients with relapse remitting MS or secondary progressive MS.

What is the primary goal of disease-modifying therapies in MS? A. To cure the disease B. To manage pain associated with MS C. To restore lost neurological function D. To decrease the number and severity of relapses

D. To decrease the number and severity of relapses

Disease-modifying therapies for MS “multiple sclerosis “ ?

1. Interferon beta 1a and interferon beta1b (injections): 2. Glatiramer (injections): 3. Fingolimod (oral): 4. Teriflunomide (oral): 5. Dimethyl fumarate (oral): 6. Monoclonal antibodies (injections): • Alemtuzumab • Daclizumab • Natalizumab • Ocrelizumab

Which mechanism of action is associated with interferon beta 1a and interferon beta-1b in the treatment of multiple sclerosis MS? A. Enhancing myelin regeneration B. Inhibiting axonal degeneration C. Diminishing inflammatory responses that leading to demyelination D. Blocking voltage-gated calcium channels

C. Diminishing inflammatory responses that leading to demyelination

How does glatiramer primarily function in the treatment of MS? A. By promoting remyelination of damaged axons B. By acting as an antioxidant to protect neurons C. By inhibiting B-cell proliferation D. By acting as a decoy to T-cell attack

D. By acting as a decoy to T-cell attack Explanation: Glatiramer resembles myelin protein and may act as a decoy to divert T-cell attack away from myelin, thus reducing autoimmune damage in MS.

What is the primary effect of fingolimod in the treatment of MS “multiple sclerosis” ? A. Inhibiting microglial activation B. Reducing astrocyte proliferation C. Altering lymphocyte migration into the CNS D. Enhancing oligodendrocyte differentiation

C. Altering lymphocyte migration into the CNS Explanation: Fingolimod alters lymphocyte migration, resulting in fewer lymphocytes entering the central nervous system (CNS), which helps to reduce autoimmune activity in MS.

What is the primary mechanism of action of teriflunomide in the treatment of MS? A. Inhibiting microglial activation B. Enhancing oligodendrocyte differentiation C. Blocking voltage-gated calcium channels D. Synthesis pyrimidine inhibitors leading to lower concentrations of active lymphocytes in the CNS

D. Synthesis pyrimidine inhibitors leading to lower concentrations of active lymphocytes in the CNS Explanation: Teriflunomide inhibits the synthesis of pyrimidines, which leads to a reduction in the number of active lymphocytes in the central nervous system (CNS) in MS.

How does dimethyl fumarate primarily affect disease progression in MS? A. By enhancing myelin repair mechanisms B. By reducing oxidative stress responses C. By promoting axonal regeneration D. By inhibiting T-cell proliferation

B. By altering the cellular response to oxidative stress to reduce disease progression Explanation: Dimethyl fumarate may alter the cellular response to oxidative stress, thereby reducing disease progression in MS.

Monoclonal antibodies (injections) used as disease modifying therapy for multiple sclerosis MS? “ 4”

• Alemtuzumab • Daclizumab • Natalizumab • Ocrelizumab

TTT of multiple sclerosis MS?

A.disease modifying therapy: 1. Interferon beta 1a and interferon beta1b (injections): 2. Glatiramer (injections): 3. Fingolimod (oral): 4. Teriflunomide (oral): 5. Dimethyl fumarate (oral): 6. Monoclonal antibodies (injections): • Alemtuzumab • Daclizumab • Natalizumab • Ocrelizumab B.symptomatic treatment: Dalfampridine • potassium channel blocker, improves walking speeds in patients with MS. It is the first drug approved for this use.

Which symptom of MS does Dalfampridine primarily target? A. Spasticity B. Constipation C. Bladder dysfunction D. Impaired walking speed

D. Impaired walking speed Explanation: Dalfampridine, a potassium channel blocker, is approved to improve walking speeds in patients with MS,

What is the primary mechanism of action of Dalfampridine in MS? A. Blocking acetylcholine receptors B. Enhancing neurotransmitter release C. Inhibiting voltage-gated calcium channels D. Blocking potassium channels

D. Blocking potassium channels Explanation : Dalfampridine works by blocking potassium channels, which can improve nerve conduction and enhance walking speed in MS patients.

Multiple sclerosis symptoms?

• Spasticity • Constipation • Bladder dysfunction • Depression

Which of the following best describes the primary mechanism of action of Riluzole in the treatment of ALS “ amyotrophic lateral sclerosis? A. Enhancing acetylcholine release at neuromuscular junctions B. Inhibiting glutamate release and blocking sodium channels C. Activating GABA receptors in motor neurons D. Stimulating dopamine production in the brain

B. Inhibiting glutamate release and blocking sodium channels Explanation: Riluzole acts as an NMDA receptor antagonist, inhibiting glutamate release and blocking sodium channels, which helps to reduce excitotoxicity and slow disease progression in ALS.

What is the proposed benefit of Riluzole for patients with ALS? A. It reverses motor neuron damage B. It alleviates muscle stiffness and spasticity C. It improves survival time D. It enhances muscle strength and coordination

C. It improves survival time Explanation: Riluzole may improve survival time in patients suffering from ALS by slowing down the progression of the disease.

How does Edaravone primarily function in the treatment of ALS? A. By enhancing neuromuscular transmission B. By inhibiting acetylcholinesterase activity C. By acting as a free radical scavenger and antioxidant D. By reducing inflammation in the central nervous system

C. By acting as a free radical scavenger and antioxidant Explanation: Edaravone functions as a free radical scavenger and antioxidant, which may help to slow the progression of ALS by reducing oxidative stress and neuronal damage.

Amyotrophic lateral sclerosis (ALS) is characterized by

progressive degeneration of motor neurons, resulting in the inability to initiate or control muscle movement.

Pharmacology of Neurodegenerative Disease Flashcards

(182 cards)