Alzheimer’s Disease, a progressive neurodegenerative disease resulting in dementia, affects about 5.4 million people over the age of 65 in the United States, with an estimated 476,000 new diagnoses in people aged 65+ in 2016.1 It is safe to say that most people either know someone who has struggled with Alzheimer’s Disease or know someone whose life has been otherwise touched by its often-difficult consequences. As the plight of infectious disease has become far less deadly in the 21st century, with the introduction of antibiotics (the overuse of which is a sensitive subject for many scientists), vaccines, public works projects like water-treatment and public sanitation, and regulation by agencies like the USDA and FDA, the expected longevity of human life has increased dramatically over the past half-century. The life expectancy (at-birth) in the united states has risen from 47.3 in 1900 to 79.3 years in 2015.2,3 In a similar fashion, it is estimated that the number of people with Alzheimer’s Disease will increase to 13.8 million by 2050.1
As longevity increased, diseases of old age that had previously gone neglected began to replace infectious diseases as the most common causes of death – heart disease, cancer, Alzheimer’s, and many more all fall in this category. Of course, not all those struggling with Alzheimer’s Disease are of old age; of the 5.4 million with Alzheimer’s, about 200,000 are young enough to be considered to have an early-onset.1 Early-onset Alzheimer’s Disease is most commonly associated with a genetic predisposition for its development. Some people are born with or develop differences or mutations in their DNA that predispose them to diseases like early-onset Alzheimer’s Disease, whereas normal-onset Alzheimer’s Disease appears to be a relatively ‘normal’ process in human aging, with some people more resilient to it than others.
The amyloid-β and tau proteins are most commonly cited as being the primary culprits of the pathogenesis of Alzheimer’s Disease. In the case of amyloid-β, a protein that is expressed on the cell surface of neurons and is involved in normal physiological function, is cleaved at the cell surface, normally forming the amyloid-β40 protein, a segment of the amyloid precursor protein (APP), an oligomer, 40 amino acids in length. It has been found that when the APP is cleaved in an incorrect position, it forms the cleavage product amyloid- β42, a protein 42 amino acids in length. This slight difference in amino acid composition is enough to cause the protein to fold incorrectly (misfolded) and aggregate with other misfolded amyloid-β oligomers. This aggregation forms ‘plaques’ in the brain which grow to the point where they damage neurons, causing cell death and the characteristic cognitive challenge and brain lesions found in someone challenged with Alzheimer’s Disease.
 Alzheimer’s Association. “2016 Alzheimer’s disease facts and figures.” Alzheimer’s & Dementia 12.4 (2016): 459-509.
 CDC/NCHS, National Vital Statistics System; Grove RD, Hetzel AM. Vital statistics rates in the United States, 1940–1960. Washington, DC: U.S. Government Printing Office, 1968; Arias E, Rostron BL, Tejada-Vera B. United States life tables, 2005. National vital statistics reports; vol 58 no 10. Hyattsville, MD: NCHS. 2010. Xu J, Kochanek KD, Murphy SL, Tejada-Vera B. Deaths: Final Data for 2007. National vital statistics reports; vol 58 no 19. Hyattsville, MD: NCHS. 2010.
 World Health Organization. “World health statistics 2016: monitoring health for the SDGs, sustainable development goals.” (2016).
For More Information:
Alzheimer’s Association: http://www.alz.org
Center for Disease Control: https://www.cdc.gov/aging/aginginfo/alzheimers.htm