Alzheimer’s disease is one of the most fearful sicknesses of old age. The prospect of gradually losing your mental facilities is scary for many. It doesn’t help that the mechanisms by which this disease acts are still relatively unknown.
Treatment options currently exist but only serve to control symptoms instead of directly acting on the condition. However, several experimental treatments show potential, providing hope for the millions of people who suffer worldwide from Alzheimer’s disease.
Current Status Of Alzheimer’s Disease
What we know so far about Alzheimer’s disease is that it starts decades before symptoms appear. There are yet no specific causes, but the disease is suspected to be influenced by a variety of genetic and environmental factors.
The Alzheimer’s Association claims that between 2000 and 2008 deaths from Alzheimer’s increased by 66% while every other major cause of death decreased. — Jeanne Murray Walker Ph. D.
In all cases, microscopic examination of the brain tissue reveals plaques and tangles which disrupt neurons, causing them to die. These objects are made out of beta-amyloid and tau proteins, which are found generally in all humans but are present in high amounts in people with the disease. These proteins steadily accumulate, causing slow but irreversible brain damage.
Current treatments consist of drugs that regulate the neurotransmitters used by neurons to communicate signals with each other. These drugs help alleviate symptoms, although the disease mechanism itself isn’t stopped or reversed.
Cognitive therapy also works by stimulating the mind and helping the person retain some of their mental skills, but it also addresses symptoms only instead of the disease itself. There is no treatment yet that has been proven to be effective in stopping the disease. But, several researchers are investigating numerous experimental methods.
Targeting Plaques And Tangles With Drugs
Clearing the plaques and tangles will stop the disease from progressing. One approach is to use antibodies, which mark certain substances for elimination by the immune system. One drug that has plaque-clearing potential is Aducanumab, which is an antibody that targets beta-amyloid plaques, causing them to break apart.
Another approach is to inhibit beta-secretase, one of two enzymes responsible for producing beta-amyloid from the amyloid precursor protein. A drug that seems to be able to do this is JNJ-54861911, which is currently being tested if it can slow down cognitive decline in people with elevated beta-amyloid who haven’t yet been diagnosed with Alzheimer’s.
Aside from plaques, the second distinct marker of Alzheimer’s disease is the formation of tangles out of defective tau protein. A particular drug that shows promise is AADvac1, which is a vaccine that caused the immune system to seek out and destroy defective tau proteins.
The daily metabolic waste (dirt) accumulates in the area (floor) between the neurons. The space where the metabolic waste lodges is narrower during waking hours, with less brain fluid (clean water) present for movement; however, this condition changes when we are asleep (drain). Increased pathways allow more disposal of metabolic waste. — Mylea Charvat, Ph.D.
Protection From Inflammation
When plaques and tangles form, they cause an inflammatory response that can further damage neurons. A potential drug that can help protect neurons from inflammation is Sargramostim, which has already been approved to stimulate the bone marrow in cases of leukemia. The stimulation enhances the immune system, which plays a part in shielding neurons from the inflammatory response.
Medicines, even those approved for general use, may still have varying intensities of effect among different people. This instance can also be seen in clinical trials for Alzheimer’s disease, where not all treatment routes work.
Genetics play a role in determining how people will respond to medicines, so analyzing the genetic makeup of people can shed light on the particular drugs that are most likely to work on them. Precision medicine does just that, and while current work is still cutting-edge, it can prove useful in assigning people in clinical trials to treatment paths that are most likely to work.
Inheriting one copy of the APOE e4 gene results in a two-to-four times greater likelihood of developing Alzheimer’s, while inheriting two copies (one from each parent) results in a 9-to12-fold increase in risk. However, about 50 percent of individuals with one copy of APOE e4 do not go on to develop Alzheimer’s. — Michelle Braun Ph.D., ABPP-CN
These therapies are still years away from public implementation, but they represent the best hope we have so far of finally obtaining a way to stop Alzheimer’s disease for good.