Origin of Alzheimer’s Disease

While working as a psychiatrist and neuropathologist in Frankfurt, Germany, Alois Alzheimer first met Auguste in 1901. The 51-year lady was affected by such an uncommon disease that forced her to forget everything. Other symptoms of the disease are misguided memory, sleep problems, doubtfulness, unnecessary fears, etc. After spending the rest of her life in the hospital, she died in 1906.

Alois Alzheimer was transferred to another hospital but he did not forget his patient back in Frankfurt. Auguste’s family dedicated her brain for the betterment of science. Alzheimer started microscopic examination to find out the hidden mystery in that brain.  

A contemporary scientist, Max Buyelcshky invented a new technique that is staining technique. Alzheimer used this method as it clearly shows brain cells. Monitoring brain cells became easier. He was surprised to see an unusual kind of substance spreading to the brain. There were tangles inside and plaques outside the brain cell. Scientists still use these two signs to detect the disease. 

He thought his research to be fruitful. In a conference of psychologists held in 1906, he released his research result. But it did not get much appreciation. Psycho-analysis was on the rise at that time. So, no one bothered about the findings on a particular patient’s brain. As a result, valuable research by Alzheimer was about to lose in the darkness of neglect.

Alzheimer's was too enthusiastic to stop his research. He kept his research going on the patients with more memory problems. He published another research paper in 1909 illustrating the brain conditions of three patients. Emil Kriplin was always an admirer of his work. In a famous treatise on psychology by Dr. Alzheimer, he contributed a chapter on the illness described and named it Alzheimer's Disease. 

In 1911, Alzheimer was working on the conditions of a patient named Joseph. He wrote a paper on this subject. His brain did not have the tangles, but the similar plaques were found. Although Alzheimer described this as a different disease, now we know that it is only a different phase of the same disease.

Alzheimer died in 1915 and his findings were hidden in the darkness for more than five decades. Alzheimer’s disease itself is a rare disease and did not become a subject of interest to other contemporary scientists. 

A new dimension to research

When Alzheimer was conducting his research, technology was not advanced enough to have detailed information on the structural mechanisms of cells. We have had to wait many years to know how the plaque that Alzheimer's saw underneath the microscope was made. The scientists got the result in the 1980s. They consider Amyloid β is the main culprit lying these plaques. It is also responsible for relating other diseases.  

After that wave, the rate of interest in Alzheimer's disease increased gradually. As the average life expectancy in the Western countries rises up, Alzheimer's disease is no more a rare disease. It is common now but the number of infected people is still huge. Infected people may live for long after being affected as the disease is slowly progressive. The worse their condition becomes, the more they need to spend. So, scientists needed to stop this. With a quick research, scientists were able to go a long way within a short time. 

Although John Hardy’s Amyloid theory was a great achievement in 1992, the source from where Alzheimer's originates was still a mystery. If the scientists could locate the initial source of this, they can stop this disease at the very beginning. Amyloid β is a very harmful peptide and alone can bring forth all the symptoms of Alzheimer's.   

Amyloid β is a long chain of Amino acid. They are very tall. For this reason, they often get folded. We know it is very difficult to use a tangled string. Similarly, scientists can not assess the chemical structure of the tangled Amyloid β. 

There are always possibilities for the breakdown of the long chain. If the breakdown happens because of a protein in the body, it results in releasing a smaller chain of Amyloid β. It is the main place where the harmful amyloid beta-peptide generates.