
	1999 Summer Scholars Program

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Neuronal and Glial Cell Numbers in the Subgenual Prefrontal Cortex in Relation to Aging and Alzheimer's Disease

By Jessica Straatmann
Mentor: Dr. Joseph Price
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO

Alzheimer's Disease (AD) is the most common form of dementia. An estimated four million people in the United States suffer from this disease. It affects one in ten people over the age of sixty-five. AD is most commonly characterized by memory loss. Previous studies examining the hippocampus, the area of the brain long associated with memory, indicate neuronal cell loss due to AD. Normal aging is characterized by similar, less pronounced symptoms. There is subtle memory impairment and slight, if any, cell loss.

Another characteristic of AD and aging is a change in personality. Thus, we chose to look at an area of the brain that relates to personality, the prefrontal cortex. The medial prefrontal cortex is associated with visceromotor control (Price), but it has also been linked to the behavioral guidance and mood disorders. Damage to this area results in inability to judge the consequences of one's actions and, as in the case of Phineas Gage, a complete change in personality.

We chose to examine area 24 in the subgenual prefrontal cortex because previous studies indicate that mood disorders cause glial cell loss in this area and because area sg24 is relatively easy to delineate. Dr. Price delineated the area of cortex extending from the anterior tip of the corpus callosum caudally to the appearance of the putamen. The superior border was the corpus callosum and the extending white matter, and the inferior border was the transition from a granular to an agranular cortical layer 4. The brain tissue was stained with Nissl in order to view the cell bodies.

In this study, we used stereological techniques to determine if area sg24 experienced cell loss due to Alzheimer's and/or aging. Stereology is a method of estimating the total number of cells or other structures within a certain region. It is designed to eliminate double counting, to eliminate the effect of tissue shrinkage, and to make the process as unbiased as possible. After the area to be counted is delineated, the computer selects twenty regularly spaced, randomly located fields. In each slide field, the number of neurons and the number of glial cells were counted. The total volume of the area being examined was summed, and the densities and total numbers of both neurons and glial cells were calculated.

AD patients are tested and rated on a scale called the Clinical Dementia Rating (CDR) ranging from 0.0 to 3.0. We examined ten brains that showed no signs of dementia (CDR 0.0). Four brains were examined with very mild dementia (CDR 0.5). Two brains were examined with slightly more serious cases of dementia (CDR 1.0). Six brain sections, each fifty microns in thickness, were examined per brain.

We found no correlation between age and neuronal or glial cell loss in area sg24. This is further evidence that, contrary to popular belief, age alone does not induce significant cell loss. We did find a significant increase (p<0.05) in both neuronal and glial cell number in very mild to mild cases of AD. The increase in glial cell number could indicate cell death, since glia usually consume cell debris. The increased number of neurons, however, contradicts that evidence. Because of this and because of the limited number of cases studied, this data is not conclusive. More studies with a larger number of subjects are needed.

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