Going senile

My grandfather has, more than once, left my stove on for hours until a pan burns and a cloud sets off the smoke alarm. The other day he forgot to turn off the faucet and flooded my bathroom. I fear I can’t leave him alone. He could hurt himself or he could burn down my house.

Dementia is a symptom used in a broad way to describe any loss of ordered neural function. It affects my grandfather as senility—its cause being his age of 82. It is a relief that my grandmother, just as old, does not show similar signs. And I just hope my parents don’t get it. I hope I don’t get it. Worst case scenario would be Alzheimer’s disease—the slow progression of dementia to the point that mental function is surrendered. If you happen to live with a parent or grandparent who is one of the 6 percent of the population that has Alzheimer’s, then, yes, I feel for you. My situation doesn’t come close.

Depending on the pathological cause, dementia can be reversible. If altered mental function is due to depression, impaired heart function, or anemia, it can be helped. We know now that Pick’s and Alzheimer’s disease are different because they affect the cerebral cortex.

Although symptoms may be indistinguishable to Alzheimer’s, Pick’s causes atrophy of the gyri, which at autopsy is called “walnut brain.” Alzheimer’s doesn’t just affect the cerebral cortex. It also affects the hippocampus, the amygdale and the basal nucleus of Meynert. This is because of widespread depletion of acetylcholine (and other chemicals) resulting from loss of cells in the nucleus of Meynert. Neurons called pyramidal cells die, their associated axons die and the brain loses its white matter. The gyri shrinks and ventricals expand worsening the atrophy.

The severity and progression of Alzheimer’s depends on three findings: 1) neurofibrillary tangles that encircle or displace the nucleus of pyramidal cells; 2) neuritic plaques that contain a cluster of neural processes filled with filaments; 3) amyloid precursor protein, which is normal in cells, but is elevated in the brains of patients with Alzheimer’s. Ten percent of cases are familial due to a gene that produces amyloid protein, which may be related to Down syndrome. Most of those with Down syndrome do develop Alzheimer’s if they live beyond 45. A mutation of another gene called APP may be related to early-onset Alzheimer’s. And research also has identified enzyme (secretases) abnormalities that may result in increased conversion of abnormal APP to amyloid beta protein.

No, there are no practical treatments for Alzheimer’s, unfortunately. Someday maybe we’ll have something to degrade amyloid protein. Elevated aluminum levels found in patients who’ve had Alzheimer’s raises concerns that those with a genetic predisposition shouldn’t use aluminum cookware or other products such as deodorants containing aluminum. To remove aluminum, chelating agents have been used to reverse symptoms. Another experimental treatment is tetrahydroaminoacridine to enhance memory, but may cause liver damage. Aspirin also appears to slow inflammation that is part of Alzheimer’s.Healthy diet and exercise as well as exercise of cognitive skills remain the most important ways to help slow the progression of dementia and Alzheimer’s.

Reference List

Nowak TJ, Handford AG. Pathophysiology: Concepts and Applications for Health Professionals. New York: McGraw-Hill, 2004.

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