Alzheimer’s disease is one of the greatest forms of dementia, a general term used for memory loss and other cognitive abilities that interfere with daily life. It causes problems with thinking, behaviour, and memory, and accounts for around 70 percent of dementia cases. Alzheimer’s is a progressive disease, where symptoms usually develop slowly and get worse over time, eventually interfering with day-to-day tasks.

In early stages of Alzheimer’s disease memory loss is mild, as it progresses, individuals may lose the ability to even carry on a conversation. This disease has no current cure, but treatments and research are continuing to develop. While current treatments for Alzheimer’s can’t stop the disease from progressing, it can temporarily slow the worsening of the symptoms to improve quality of life. There are 5 FDA (Food and Drug Administration) approved drugs that are used to treat different levels of Alzheimer’s disease depending on severity. Donepezil, galantamine, and rivastigmine are three FDA approved drugs that are cholinesterase inhibitors – medication that prevent the breakdown of acetylcholine in the body. The brand name for these drugs are Aricept, Razadyne, and Exelon. They are taken in the form of tablets or through patches (only rivastigmine). Cholinesterase inhibitors are said to reduce the symptoms of Alzheimer’s disease by increasing communication between nerve cells in the brain. It is still unknown as to whether any of these three medications are more effective than the other, but some people with Alzheimer’s disease are able to better remember things when they take cholinesterase inhibitors. [1] These medications are used for all stages of Alzheimer’s disease, except Galantamine which is only used from mild to moderate stages. All three of the medications have side effects such as vomiting, diarrhea, nausea, and dizziness. Higher- dose Rivastigmine patches that release 9.5 mg of rivastigmine in 24 hours are shown to improve brain function. [1] Memantine is another FDA approved drug for the treatment of moderate to severe Alzheimer’s disease, it is said to prevent excess amounts glutamate from damaging the brain. The brand name for this drug is Namenda. Glutamate is a chemical messenger which carries nerve signals and plays a crucial role in our learning and memory. People with Alzheimer’s disease are known to have too much glutamate in their brains, causing the death of nerve cells. It is unknown as to whether memantine affects the duration that patients with Alzheimer’s disease can be given home care, but memantine can delay the deterioration of cognitive performance in about 1 out of 10 people over a six-month time frame. [1] Evidence also suggests that some people who take this drug can carry on doing daily activities such as brushing their teeth. Memantine is overall well tolerated with rarely occurring side effects. Donepezil and memantine are combined together for a drug known as Namzaric, which treats moderate to severe illness. It has shown similar results and efficiency to other name brand names which consist of donepezil and memantine.

Until recently, only two monoclonal antibodies showed potential for the treatment of Alzheimer’s disease. None of the monoclonal antibodies for use against Alzheimer’s disease have succeeded in clinical trials. These two drugs are solanezumab (Eli Lilly) and aducanumab (Biogen), along with BAN2401 (Biogen, Eisai), gantenerumab (Chugai, Hoffmann La-Roche), and crenezumab (AC Immune, Genentech, Hoffmann La-Roche). Solanezumab is a humanized monoclonal antibody, which are biological drugs used to treat lupus, cancer, and certain types of arthritis. The final results failed the phase 3 trial of solanezumab in patients with mild Alzheimer’s disease, and did not meet its primary outcome. Aducanumab (Biogen) has also failed to treat Alzheimer’s disease as it failed to meet the goal mid-stage trail. The difference in mechanism used by these treatments, caused scientists to think these drugs failed to perform as they were proposed to.

A novel relation between clearance of senescent glial cells and tau aggregation reduction inside the brain may be essential in treating Alzheimer’s disease. Scientists have found that destroying senescent cells can reduce tau aggregation. Any approach that manages to destroy a large fraction of senescent cells results in significant health improvement. The treatments cost very little, are easily accessible globally, and show promising results of consistency in the future. The removal of senescent cells works really well because of the low percent by number in aged tissues, therefore making selective destruction (destroying ‘bad’ cells, so that ‘good’ cells are not harmed) not disruptive. With little debris to clean up the lost cells may be replaced rapidly. The senescent cells are harmful through their continuous secretion of inflammatory/harmful signals. The moment this signalling is cut back, the brain switches to a less inflammatory, and less disrupted state. The accumulation of senescent cells in Alzheimer’s disease causes this age-related inflammatory condition. In the mouse model, the scientists proved that the removal of senescent cells showed to reverse aging measures in Alzheimer’s near all major organs.

There is a great focus now on Alzheimer’s disease research than ever before, and the last few years have shown an immense increase in discovery of the roles of amyloid, cholinesterase, and glutamate in Alzheimer’s disease, along with FDA’s approval. As a result of such research, there are an array of drugs in development that scientists believe have great potential to effectively treat Alzheimer’s. We may not be close to finding a cure to the disease, but advances are now allowing us to better understand Alzheimer’s pathology in the brain. With more cutting-edge research performed along with promising interventions and newly funded prevention trails, we will ultimately near the cure for Alzheimer’s disease in the next decade.

References:

• [1] Medications for the treatment of Alzheimers disease. (2017, June 29). Retrieved April 3, 2019
• [2] Marco, D., V., & A. (2018, January 01). Volume and Connectivity of the Ventral Tegmental Area are Linked to Neurocognitive Signatures of Alzheimer’s Disease in Humans. Retrieved April 3, 2019
• [3] Budd Haeberlein, S., O’Gorman, J., Chiao, P., Bussière, T., von Rosenstiel, P., Tian, Y., … Sandrock, A. (2017). Clinical Development of Aducanumab, an Anti-Aβ Human Monoclonal Antibody Being Investigated for the Treatment of Early Alzheimer’s Disease.
  
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