What is happening in the brain of an Alzheimer's patient to cause all of the unpleasant cognitive and behavioral symptoms of the sickness? Alois Alzheimer was the first to find the strange plaques and tangles characteristic of the sickness in the brain of one of his patients during an autopsy.
He gave his name to the sickness despite the contribution his associate Emil Kraepelin made by isolating and identifying the symptoms of the disease. For years, Alzheimer's disease could only be diagnosed with a high degree of accuracy post-mortem. Now researchers are learning more about what exactly is happening in the brain to cause the sickness and why those strange plaques and tangles develop in the first place.
Neurofibrillary tangles are one characteristic of Alzheimer's disease. Brain damage occurs as a result of neurons being clogged with microscopic filaments, which are made up of an abnormal type of Tau protein. Normally functioning Tau protein sends chemical messages from neuron to neuron by bonding to microtubules, while the type of Tau protein found in an Alzheimer's disease brain bonds with itself and goes nowhere.
Clogged neurons are no longer able to do their job and pass along the impulses they receive from the environment; therefore, disabled neurons are one cause of the cognitive impairment associated with Alzheimer's disease. Brain damage due to neurofibrillary tangles is also found in associated diseases, such as Parkinson's disease. Scientists aren't sure why the Tau protein malfunctions and causes the tangles.
Some researchers believe that Tau malfunctions as a result of beta amyloid protein, which is what causes the second form of damage in an Alzheimer's disease brain-plaques between neurons.
Senile plaque, which is considered to be the more detrimental of the two abnormalities in an Alzheimer's disease brain, consists of large, abnormal, sticky patches containing beta amyloid protein. These patches block communication between neurons, causing the learning and memory problems consistent with the cognitive impairment associated with Alzheimer's disease.
The more plaque there is in the brain, the worse the impairment becomes because plaque is thought to interfere with the functioning of acetylcholine, which transmits nerve impulses in the brain and body. The only FDA-approved medications used to treat Alzheimer's are acetylcholinesterase inhibitors, which block the enzymes that eat away at acetylcholine. These medications work best, however, in the earliest stages of the disease before the amount of plaque in an Alzheimer's disease brain has caused considerable damage.
Recent research has begun to clarify the possible cause-and-effect connection between plaques and tangles. A study that used proteins from the immune system of mice to get rid of the beta amyloid that causes plaque discovered that the proteins ate away at the tangles as well. Other medications used to lower levels of beta amyloid also worked on the tangles. Some researchers believe that plaques and tangles may themselves be the result of some other disease process in the brain, such as swollen axons.
In research done on mice that were genetically engineered to have a disease similar to Alzheimer's, the swollen axons, which are important in communicating between neurons, caused a "traffic" jam of sorts that may, over time, lead to the neuronal degeneration, plaques and tangles apparent in the brains of Alzheimer's patients. Researchers hope that, by focusing on the disease process in the brain of Alzheimer's patients, they can one day find a cause and, ultimately, a cure for the sickness.
