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Alzheimer’s General Summary
Alzheimer’s is a dementing illness (causes loss of mental functions like memory or thought), and between 60 and 80% of all dementing illness is produced by Alzheimer’s, making it the most common form of dementia in older people. Alzheimer’s first appears in people after the age of 60, and in all individuals over the age of 65, an estimated 5% have the disease. Just like dementia in general, the odds of getting Alzheimer’s doubles every five years after 65 years of age. While Alzheimer’s is sporadic (not genetic) there have been reports of familial links with the disease, and an autosomal dominant disorder linked to the mutation causing Alzheimer’s is not unheard of. In addition, Alzheimer’s affects men and women equally. Diabetes mellitus, cardiovascular disease, hypertension, and head trauma are reputed to be causes of Alzheimer’s; however the majority believes that at least diabetes and hypertension play a role in the development of the disease.
Men and women are equally affected by Alzheimer’s, but because women tend to live longer than men, women are more prevalent to it. The disease also has no predilection for a particular ethnicity. Approximately 5.1 million Americans have the disease, and the numbers continue to rise as the American populace becomes older.
Alzheimer’s eventually gets worse and worse, leading to the patient not recognizing family members, forgetting how to do simple things (like brushing their teeth), and other simple tasks. The patient may even become aggressive or anxious or walk away from home. He or she will eventually need total care, causing great stress for family members who must take care of their elderly burden.
There is no treatment. However, there are drugs to help repress the symptoms from worsening temporarily.

Dementia: A brain disorder that can seriously impair a person’s ability to carry out daily activities

Alzheimer’s Disease Current Research
At the moment, scientists are trying to discover new ways to counter the effect Alzheimer’s has on the brain. The aim of new drugs is to modify the process of Alzheimer’s by targeting the specific things that cause brain changes. The most well known proteins that cause these changes are Beta-amyloid, and Tau Protein.
Beta-amyloid is known to be the main component of the plaques that aggregate in the brain. It is a protein fragment that is created when two enzymes incorrectly clip it from the rest of the protein. Scientists are working to create drugs that can either block the enzymes’ activity, prevent the fragments from aggregating, or clear it from the brain entirely.
Tau Proteins are the main causes of tangles in the brain. When Tau molecules collapse, they twist and create tangles that result in cell death because it destroys a cell’s transport system. Currently, scientists are researching different ways to stop Tau Proteins from collapsing and twisting.
Various researchers from different fields of sciences are also working together to better understand the effect of Alzheimer’s. Psychologists are investigating the role of various stimulants, such as music and diet, on the brain to help their patients live through the disease. Scientists who are involved with producing newer and better drugs for Alzheimer’s are also exploring how inflammation affects the brain and how to prevent it from being harmful. This research can help them design anti-inflammatory drugs. Additionally, scientists want to understand how brain cells use insulin in relation to sugar to produce the necessary energy to function. These discoveries can aid the production of drugs that support cell function and prevent the changes brought upon by Alzheimer’s.
In one current research project, scientists attempted to determine whether β-Asarone has an effect on CaMKII cell pathway. The CaMKII enzyme (Calcium/calmodulin kinase II) has a wide variety of substrates and induces microtubule disassembly and neurite extention. Its main role is to promote the brain’s capacity for learning and memory. In the study, scientists used PC12 cells and cultures of cortical neurons treated with amyloid-β (Aβ)(1-40) or Aβ(1-42) peptide to demonstrate that the β-Asarone molecule did indeed protect the cells by activating the CaMKII cell pathway. They also administered β-Asarone intragastrically to AβPP/PS1 mice and noticed that β-Asarone improved their cognitive function and reduced neuronal apoptosis in the cortex. Their study revealed that β-Asarone can inhibit neuronal apoptosis by activating the CaMKII cell pathway and may be useful in the long-term treatment of Alzheimer’s Disease in the future.

Works Cited
"About Alzheimer 's Disease: Alzheimer 's Basics." National Institute on Aging. National Institute on Aging, n.d. Web. 25 Oct. 2013. .
"Alzheimer 's Disease." MedlinePlus. U.S. National Library of Medicine, 19 July 2013. Web. 25 Oct. 2013. .
Knopman, David. "Alzheimer 's Disease and Other Dementias." Goldman’s Cecil Medicine. Ed. Lee Goldman and Andrew I. Schafter. N.p.: n.p., n.d. N. pag. Print.
Lee, Frank. "Alzheimer 's Disease." Falselfo. Wordpress, 28 Jan. 2012. Web. 19 Oct. 2013. .
"Treatment Horizon." Alzheimer 's Association. Alzheimer 's Association, n.d. Web. 19 Oct. 2013. .
OpenWetWare. OpenWetWare, 25 Oct. 2006. Web. 23 Oct. 2013.

Cited:     2013. Web. 25 Oct. 2013. . Knopman, David Lee, Frank. "Alzheimer 's Disease." Falselfo. Wordpress, 28 Jan. 2012. Web. 19     Oct OpenWetWare. OpenWetWare, 25 Oct. 2006. Web. 23 Oct. 2013.