SciTech

Health Talk: Alzheimer's disease

In 1906, Dr. Alois Alzheimer noticed a strange condition in one of his patients. She suffered from memory loss, language problems, and also showed behavioral changes. These symptoms are seen far more frequently now, and the condition has been given a name — Alzheimer’s disease. Those suffering from Alzheimer’s disease (AD) face memory problems and are unable to perform the most menial tasks necessary for living a normal life. What makes this disease all the more worrisome is that it is common among the elderly; statistics from the Mayo Clinic show that nearly 50 percent of people over the age of 85 years have AD. A rare form of the disease, called early onset Alzheimer’s disease, occurs in patients under the age of 65 years. Only 5 to 10 percent of people develop this form of the disease.

Early onset Alzheimer’s is even less common for those between 30 and 40 years of age, but cases of Alzheimer’s in patients between these ages have also been recorded. Research has shown that this form of the disease could be hereditary.
As of now, according to the National Institute of Aging, nearly 2.4 to 2.5 million Americans are suffering from AD. These statistics, coupled with the fact that currently there is no satisfactory cure for AD, have caused scientists across the world to study the disease and to try to delve into its root causes.

AD is caused by a gradual degradation of brain cells leading to memory loss at first, and then a steady decline in all mental capacities. Dr. Alzheimer studied the brain of his patient after she died and discovered various clumps and masses of tangled fibers within the brain. The clumps have now been discovered to be amyloid plaques, while the fibers are now called neurofibrillary tangles. Amyloid plaques are composed of a protein called beta-amyloid. Normally, a protein called the amyloid precursor protein (APP) is cut by an enzyme called alpha secretase. This cutting produces fragments that can be easily degraded. However, for reasons that are still not completely understood, alpha secretase activity reduces in patients with AD.
The task of degrading APP is then taken up by the enzymes beta secretase and gamma secretase. These enzymes cut APP in such a way that the fragments produced are hard to degrade. These fragments clump together, forming the plaques. Scientists have discovered that excessive beta-amyloid may interfere with the signaling between different neurons, ultimately causing the neurons to die. Plaques may also release free radicals, which are chemical species with unpaired electrons, that can harm the nearby cells.

Neurofibrillary tangles are the second feature of the disease. These are composed of a protein called tau. Tau is normally needed for maintaining the normal internal structure of neurons. Abnormal formation of tau leads to the production of twisted tau fibers that form the tangles. Since tau is critical for the neurons, this malfunction of tau can cause cell death. Although there have been significant advances in discovering the cause of AD, there still is no cure for the disease. Current treatments focus on reducing the symptoms of the disease and helping the patients retain the mental functions needed for daily living as long as possible. The most commonly prescribed medicines are cholinesterase inhibitors. Cholinesterase is an enzyme that degrades acetylcholine, a neurotransmitter. By inhibiting cholinesterase, the medicines seek to increase acetylcholine levels. This would enable better communication between neurons. This treatment involving cholinesterase inhibitors can help delay the onset of severe AD, but it is unable to completely cure patients. Researchers are therefore searching for factors that increase the risk of contracting the disease.

Studies involving early onset AD revealed that two genes could be possible for the disease. Last year, researchers from the Weill Medical College of Cornell University found a gene that could be linked to the more common late onset form of the disease. This gene has been named CALHM1 and could significantly increase the risk of contracting the disease. Another study, published last week in the journal Molecular Neurodegeneration, shows that a high protein diet could significantly increase the risk of contracting AD. The study was conducted by studying the brains of mice after feeding them different types of diets for a period of 14 weeks. After 18 weeks, the brains of the mice were studied and it was found that the mice on the high protein diet had brains that were 5 percent lighter than those on other diets. The researchers thus concluded that these mice were more susceptible to Alzheimer’s disease.