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Alzheimer’s disease is a neurodegenerative disorder characterized by a decline in cognitive function that eventually leads to death (Upadhyaya 2010; Stern 2008; Knopman 2011; Mayo Clinic 2011). Research in Alzheimer’s disease has not yet identified a cure for the disease. Advanced age is a risk factor for development of the disease (Alzheimer’s Association 2012b; Knopman 2011).
With an increase in the aging population, the worldwide prevalence of Alzheimer’s disease has increased remarkably and is expected to continue to do so. Estimates suggest that in the United States alone there will be 11-16 million individuals aged 65 and older diagnosed with Alzheimer’s disease by 2050 (Zhao 2012; Tarawneh 2012).
Alzheimer’s disease appears to be the consequence of several convergent factors including oxidative stress, inflammation, mitochondrial dysfunction, and accumulation of toxic protein aggregates in and around neurons (Luan 2012; Teng 2012; Rosales-Corral 2012; Wang 2007; Fonte 2011; Ittner 2011). Emerging, intriguing research implicates chronic infection with several pathogenic organisms in the development and progression of Alzheimer’s disease as well (Miklossy 2011). Moreover, age-related changes such as declining hormone levels and vascular dysfunction are thought to contribute to some aspects of Alzheimer’s disease (Vest 2012; Barron 2012; Baloyannis 2012).
Conventional pharmacologic interventions target symptoms, but fall short of addressing underlying, contributing factors for Alzheimer’s disease. This results in a small reduction of symptoms, but does not halt or reverse disease progression (Sadowsky 2012; Alkadhi 2011).
A comprehensive approach to Alzheimer’s disease treatment is required that acknowledges and targets the many possible factors underlying the changes in brain structure and function that drive this complex condition (Sadowsky 2012).