Introduction
Alois was born on June 14, 1864 to Edward and Therese Alzheimer. Their family lived in southern Germany. After graduating with his medical doctor degree, Alzheimer took a position at the Community Hospital for Mental and Epileptic Patients in 1888. In 1902, he and a colleague, Emil Kraepelin, took positions at the Royal Psychiatric Clinic of the University of Munich.
How Was Alzheimer’s Disease Identified?
One of Alzheimer’s patients was a woman named Auguste D, who had been hospitalized since 1901. This patient was 51 years old and showed signs of dementia, including memory loss, disorientation, aphasia, confusion, hallucinations and delusions. Alzheimer treated her and documented her symptoms in depth, as well as his conversations with her. He noted that at one point when Auguste was unable to correctly write something, she stated, “I have lost myself.”
After Auguste died in 1906 at the age of 55, Alzheimer asked that her brain be sent to him for his research. When he studied it, he discovered that it contained the characteristics that we now think of as hallmarks of Alzheimer’s disease, specifically a buildup of amyloid plaques and neurofibrillary tangles. Her brain also showed cerebral atrophy, another finding typical in Alzheimer’s disease (Heerema:2019)
When time is spent time with individuals affected with Alzheimer’s disease (AD), one might notice that some people lose their memory and other cognitive skills more slowly than others. The reason for this is that new findings indicate that at least part of the answer may lie in differences in their immune responses.
New research has now found that slower loss of cognitive skills in people with AD correlates with higher levels of a protein that helps immune cells clear plaque-like cellular debris from the brain (Ewers: 2019). According to him increased soluble TREM2 in cerebrospinal fluid is associated with reduced cognitive and clinical decline in Alzheimer’s disease). Science Translational Medicine. The efficiency of this clean-up process in the brain can be measured via fragments of the protein that shed into the cerebrospinal fluid (CSF). This suggests that the protein, called TREM2, and the immune system as a whole, may be promising targets to help fight Alzheimer’s disease.
Scientists reveal ground-breaking a plan to target the cause of Alzheimer’s disease by University of Cambridge
Conceptual image showing blurred brain with loss of neuronal networks. Credit: Kateryna. A breakthrough has been made in the fight against Alzheimer’s disease—researchers have found a new way to target the toxic particles that destroy healthy brain cells.
According to Holscher (2019) Johnson and Johnson recently announced that it was halting a clinical trial for a new Alzheimer’s drug after safety issues emerged. This latest failure adds to the dozens of large, costly clinical trials that have shown no effect in treating this devastating disease. Despite the continued failure of new drugs to make a difference has to be interpreted as evidence that the amyloid protein is not the cause of Alzheimer’s disease, some companies continue to spend money on more research. Some companies have changed their target to the tau protein. But again, drugs companies are assuming that a single protein is the cause of the disease.
Holscher (2019) also urges potential researchers that it is time to rethink the disease altogether. One alternative is to look for genes that increase the risk of developing the disease. The problem however is that there are in fact few of these genes, and they are rare. Alzheimer’s does not appear to be driven by gene mutations, so this option is no longer on board.
Another option is to look at the risk factors for developing Alzheimer’s. Another alternative is type 2 diabetes. Clearly, diabetes is very different from Alzheimer’s disease, so what’s the connection? In diabetes, insulin becomes less effective at controlling blood sugar levels. But insulin does a lot more than just control blood sugar; it is a “growth factor”. Neurons (brain cells) are very dependent on growth factors, and if they don’t get enough, they die.
The loss of insulin’s growth factor effects in the brain appear to make neurons vulnerable to stress and reduce the brain’s ability to repair damage that accumulates over time. (Neurons live as long as we do, so there is a lot of damage to accrue). When looking at brain tissue taken from deceased Alzheimer’s patients, researchers found that insulin lost its effectiveness as a growth factor, even in people who were not diabetic. This observation suggests that diabetes drugs might be an effective treatment for people with Alzheimer’s. Some experiments showed impressive results in animal studies, and several clinical trials have started.).
