Conclusion: Henry Omer

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1. How do anticholinesterase drugs delay the progression of Alzheimer symptoms?

Mr. Omer's progress was monitored using another set of tests:

• Structural neuroimaging: Magnetic resonance imaging (MRI) showed possible cerebral atrophy.
• Functional neuroimaging: Single photon emission computed tomography (SPECT) indicated equivocal parietal hypoperfusion.
• Cerebrospinal fluid (CSF): low levels of amyloid-beta (<500) and elevated and tau protein (> 500).
• APOE genotyping indicated the presence of the apoE4 gene on chromosome 19.

2. What is the significance of the CSF results for amyloid-beta and tau protein? In other words, how do the low level of amyloid and the increased level of tau protein contribute to the neurologic changes associated with SDAT?

3. What implications does the positive ApoE gene testing have for Virginia and her family?

The treatment was successful for several years, but Mr. Omer's condition continued to deteriorate. Eventually he was placed in a nursing home, where he died of cardiac arrythmia related to the mitral stenosis caused by his bout with rheumatic fever.

4. The family requested an autopsy following Mr. Omer's death. What brain tissue changes would confirm a diagnosis of SDAT?

Generalized cerebral hypertrophy

Multiple areas of infracted brain tissue throughout the cerebellum.

Neurofibrillary tangles and amyloid plaques

Vascular insufficiency

The postmortem exam revealed the following:

• Gross findings
  • Cerebral atrophy
  • Ventricular dilation associated with loss of the cortex
• Microscopic evaluation : Histologic studies reveal the presence of the following:
  • Senile plaques
  • Neurofibrillary tangles.
  • Neuritic plaques with amyloid deposition
  • Magnification of a single plaque

5. Imagine you are researching Alzheimer's disease for a close friend. If you had only two pieces of paper, which of the above images would you print out to help you explain the pathophysiology and signs of Alzheimer's disease? Why?