Quiz: The Aging Brain and Neurodegeneration¶
Test your understanding of Chapter 13. Choose the best answer, then click Show Answer to check.
Question 1¶
Where are amyloid plaques found in the brain of a person with Alzheimer's disease?
- Inside the nucleus of neurons, wrapped around the DNA
- Outside neurons, in the spaces between cells
- Inside the axon, attached to the microtubules
- Inside the myelin sheath that surrounds axons
Show Answer
The correct answer is B. Amyloid plaques are clumps of misfolded beta-amyloid that build up between neurons, outside the cells. The main distractor, C, describes where tau normally works: tau tangles form inside neurons after tau lets go of the microtubules.
Concept Tested: Amyloid Plaque Bloom's Level: Remember
Question 2¶
What is the normal job of the protein tau in a healthy neuron?
- It carries neurotransmitters across the synapse
- It forms the myelin that insulates axons
- It stabilizes microtubules, the "tracks" that move cargo along the axon
- It breaks down beta-amyloid so plaques cannot form
Show Answer
The correct answer is C. Tau normally binds to and stabilizes microtubules, which act like railroad tracks for transport inside the neuron. In Alzheimer's disease, tau detaches and clumps into tangles. Option D is wrong because clearing beta-amyloid is a job of microglia, not tau.
Concept Tested: Tau Tangle Bloom's Level: Remember
Question 3¶
Which statement correctly describes the FDA approval of tofersen (Qalsody) for SOD1-ALS?
- Traditional approval in 2016, after a trial showed it cured ALS
- Traditional approval in 2023, after its phase 3 trial met its primary clinical endpoint
- It has not been approved and is available only in clinical trials
- Accelerated approval in April 2023, based on lowering neurofilament light, a blood biomarker of nerve injury
Show Answer
The correct answer is D. The FDA granted tofersen accelerated approval on April 25, 2023, because it lowered plasma neurofilament light, a biomarker reasonably likely to predict clinical benefit. Option B is the most tempting mistake: the phase 3 VALOR trial did not meet its primary clinical endpoint.
Concept Tested: Biomarker Bloom's Level: Remember
Question 4¶
Why is trouble forming new memories usually the first symptom of Alzheimer's disease?
- The damage usually begins in the entorhinal cortex and hippocampus, which are needed to form new memories
- The damage usually begins in the motor cortex, which controls writing things down
- Amyloid plaques block the eyes and ears from sending new information to the brain
- Old memories take up all the brain's storage space, leaving no room for new ones
Show Answer
The correct answer is A. Alzheimer's disease usually damages the entorhinal cortex and hippocampus first, and the hippocampus is essential for turning new experiences into lasting memories. Option D reflects a common but wrong idea that memory is like a full hard drive. The problem is damaged neurons, not lack of space.
Concept Tested: Alzheimer's Disease Bloom's Level: Understand
Question 5¶
How does an antisense oligonucleotide (ASO) such as tofersen reduce the amount of a harmful protein?
- It replaces the faulty gene in the DNA with a healthy copy using a virus
- It binds to the finished protein in the blood and marks it for removal
- It blocks the receptor that the protein normally binds at the synapse
- It binds to the protein's specific mRNA so that less of the protein is made
Show Answer
The correct answer is D. An ASO is a short, lab-made strand of genetic letters that sticks to one specific mRNA. Tofersen binds SOD1 mRNA, so cells make less SOD1 protein. Option A describes gene therapy, and option B describes how an antibody such as lecanemab works.
Concept Tested: Antisense Oligonucleotide Bloom's Level: Understand
Question 6¶
Which statement best explains the idea of cognitive reserve?
- Healthy habits prevent amyloid plaques from ever forming
- The brain stores spare neurons that replace any neurons that die
- Some brains cope with damage better by using networks efficiently or switching to backup routes, so symptoms appear later
- Older adults have a reserve supply of memories that they can use after dementia begins
Show Answer
The correct answer is C. Cognitive reserve is the brain's ability to tolerate damage by using its networks more efficiently or flexibly, built through experiences such as education and mentally stimulating activities. Option A is a common overstatement: reserve changes how much damage the brain can absorb, not whether plaques form.
Concept Tested: Cognitive Reserve Bloom's Level: Understand
Question 7¶
A 78-year-old woman says it takes her longer to remember people's names than it used to, and sometimes she forgets a word but recalls it later. She manages her own money, cooks, drives to familiar places without getting lost, and learned to use a new phone last month. What is the most likely explanation?
- Normal brain aging
- Moderate Alzheimer's disease
- Huntington's disease
- Dementia, because any memory change after age 75 is dementia
Show Answer
The correct answer is A. Slower name and word recall is a normal part of aging, and the key point is that her daily life is not affected. She can even learn new skills. Option D is the misconception that memory changes in older adults always mean dementia, but dementia requires problems severe enough to interfere with daily life.
Concept Tested: Normal Brain Aging Bloom's Level: Apply
Question 8¶
Jordan is 22. His mother was recently diagnosed with Huntington's disease, and his father does not carry the gene variant. What is the chance that Jordan inherited the Huntington's gene variant?
- 25 percent, because both parents must pass on a copy
- 50 percent, because one altered copy from one parent is enough
- 100 percent, because the disease runs in his family
- Nearly 0 percent, because the disease skips a generation
Show Answer
The correct answer is B. Huntington's disease is autosomal dominant, so each child of an affected parent has a 50 percent chance of inheriting the expanded CAG repeat in HTT. Option A confuses it with recessive inheritance, which needs a copy from both parents.
Concept Tested: Huntington's Disease Bloom's Level: Apply
Question 9¶
A 70-year-old man with early Alzheimer's disease starts an anti-amyloid antibody. A routine MRI a few weeks later shows a small area of swelling in his brain, though he feels fine. Genetic testing before treatment showed he carries two copies of APOE e4. What is the best analysis?
- The drug has failed, because swelling means the plaques are growing faster
- He has had a stroke caused by high blood pressure, unrelated to the drug
- This is likely ARIA, a known side effect of anti-amyloid antibodies, and two copies of APOE e4 raise its risk
- The swelling shows that the drug is curing his Alzheimer's disease
Show Answer
The correct answer is C. Amyloid-related imaging abnormalities (ARIA) appear on MRI as temporary swelling, sometimes with small bleeds, and often cause no symptoms. People with two copies of APOE e4 have a higher risk, which is why doctors test for it and monitor with MRI. Option D is wrong because these drugs modestly slow decline. They do not cure the disease.
Concept Tested: Anti-Amyloid Antibody Bloom's Level: Analyze
Question 10¶
A 58-year-old man has a weak, thin right hand with twitching muscles, and his leg muscles are stiff with overactive reflexes. His memory and thinking are normal. Which analysis of the findings is best?
- Only lower motor neurons are damaged, which points to Huntington's disease
- Only upper motor neurons are damaged, which points to Alzheimer's disease
- The striatum is damaged, which explains the stiffness and twitching
- Both lower motor neuron signs (weakness, wasting, twitching) and upper motor neuron signs (stiffness, overactive reflexes) are present, which points to ALS
Show Answer
The correct answer is D. Weakness, muscle wasting, and fasciculations are lower motor neuron signs, while spasticity and overactive reflexes are upper motor neuron signs. Finding both together is a key clue for ALS. Option C is tempting because the striatum is involved in movement, but striatal damage in Huntington's disease causes chorea, not muscle wasting and twitching.
Concept Tested: Amyotrophic Lateral Sclerosis Bloom's Level: Analyze