1. Answer: C. The lifetime risk for Alzheimer’s disease is approximately 1:4. It is estimated that more than 14% to 15% of people older than 65 have AD, and this figure increases to 40% in the over-80 age group.

2. Answer: D. Patients with AD have atrophy of the association areas, particularly the medial aspect of the temporal lobe.

3. Answer: E. All of the above choices are associated with AD. In addition, senile plaques are also seen. The neurofibrillary tangles and senile plaques are often thought of as the hallmark of the disease but are not pathognomonic.

4. Answer: A. Neurofibrillary tangles are initially and most densely distributed in the medial aspect of the temporal lobe and mostly affect the entorhinal cortex and the hippocampus.

5. Answer: D. The most common and primary cause of death in AD patients is concurrent illnesses (e.g., pneumonia), especially in patients who have had AD for many years and are debilitated by the disease.

6. Answer: A. Alzheimer’s disease is typically sporadic (about 90%). Early-onset AD occurs in the familial form and has about 10% or less prevalence. This can occur as early as the patient’s third decade in life.

7. Answer: E. Memory loss is the most common presenting symptom. After memory loss, the patient often develops anomia and aphasia. Impairment of executive function and visuospatial skills follows as well.

8. Answer: E. All of the above are necessary to be ruled out before anyone is labeled with AD.

9. Answer: B. Spastic paraparesis and right parietal lobe syndrome along with the other features of AD are associated with the visual variant of AD. This presentation of AD is extremely unusual.

10. Answer: C. Mutations that alter the way amyloid precursor protein is processed is thought to be the mechanism for AD. The amyloid precursor protein leads to aggregation of the 40 to 43 amino acid residues also known as beta-amyloid peptide. This peptide is thought to have neurotoxic effects.

11. Answer: C. The amyloid precursor protein is associated with chromosome 21.

12. Answer: A. Up until now, there has been no convincing treatment that can prevent or even delay the onset or slow the progression of AD.

13. Answer: E. Currently, the FDA has not approved any agent for the treatment of AD behavioral manifestations.

14. Answer: F. All of the above as well as RPR are often part of the routine screening for dementia workup. Current recommendations from the AAN recommend cobalamin and thyroid function as screening tests; all other tests are left to the physician’s discretion.

15. Answer: B. The tau protein test is advocated by some experts. It can be measured in the CSF to help diagnose AD. This protein is seen in neurofibrillary tangles and amyloid protein. This test, however, is not a reliable test or mandatory.

16. Answer: B. AD is thought of as a disease process that is caused by depletion of acetylcholine in the cerebral cortex. The subcortical cholinergic neurons are thought to be primarily depleted in AD. The basal nucleus of Meynert and the medial septal nuclei in the hippocampus are the main cholinergic neurons that send projections to the cortex.

17. Answer: E. NMDA antagonists are approved for the advanced stages of AD that cholinesterase inhibitors are not approved for (however, cholinesterase inhibitors do help improve cognitive function in late-stage AD). Also, NMDA antagonists may also be helpful in treating Huntington’s disease, dementia associated with AIDS, and vascular dementia (cholinesterase inhibitors may be helpful in this situation as well).

18. Answer: B. More than 30% of patients with AD develop depression. Often, the depression may precede the diagnosis of AD. Treatment of the depression often improves both the cognitive and noncognitive performance.

19. Answer: B. Both physical and mental activity should be recommended to patients with AD. Often, crossword puzzles and brainteasers are recommended to mentally challenge patients. These puzzles, however, should not be too challenging, which would end in frustration and less motivation for the patient to continue.

20. Answer: B. Patients with Down syndrome have clinically and neuropathologically indistinguishable characteristics from patients with AD.

21. Answer: D. All patients with AD have been found to have limited education or diminished baseline cognitive abilities and are at a higher risk for AD. In Down syndrome, patients are often mentally retarded and have poor baseline cognition.

22. Answer: B. Once patients with Down syndrome develop AD, they often have a sharp decline in survival after age 45. The mean age at the time of clinical diagnosis of AD in Down syndrome is around age 51.

23. Answer: B. Behavioral changes are usually the early signs of dementia in Down syndrome. These changes are usually subtle early on, and the family or individuals that are close to him or her would recognize them. These changes are typically considered an exaggeration of long-standing behavioral traits.

24. Answer: B. Down syndrome patients with advanced-stage dementia as well as non-Down syndrome patients are usually in a comatose/vegetative state and usually require 100% assistance and interact minimally with the environment.

25. Answer: B. Age is the most important risk factor of those listed above. The others are all risk factors but are not as important.

26. Answer: C. A Mediterranean diet as well as an active lifestyle have been associated with decreased risk of AD.

27. Answer: A. Aphasia is an acquired disorder of language caused by a lesion or damage to the brain. All of the others are not true aphasia.

28. Answer: C. Approximately 60% of left-handed people are language dominant on the left side. About 96% to 99% of right-handed people are language dominant on the left. Of the 40% of the left-handed people, 50% are mixed language and the 50% are right- hemisphere dominant.

29. Answer: B. Stroke is the most common cause of aphasia, and about 20% of stroke patients develop aphasia.

30. Answer: D. There are few studies that evaluate gender differences regarding aphasia. Some studies suggest, however, that women develop aphasia less often than men, and it is thought that women may have more bilateral language function. It has also been suggested that women develop Wernicke’s aphasia more than men.

31. Answer: E. All of the above as well as many others are part of aphasic syndromes or language syndromes. The classics are Broca’s and Wernicke’s, conduction, and global aphasia. Anomic, transcortical sensory, transcortical motor, and mixed transcortical aphasias, however, are also included. Some of the more specific language deficits are aphemia, alexia with and without agraphia, and pure word deafness.