Volume 3 Issue 6

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Page 25 of 63

Alzheimer's Disease Alzheimer's disease is a neurodegenerative disorder characterized by a decline in cognitive function that eventually leads to death. 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. 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. 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. Emerging, intriguing research implicates chronic infection with several pathogenic organisms in the development and progression of Alzheimer's disease as well. Moreover, age-related changes such as declining hormone levels and vascular dysfunction are thought to contribute to some aspects of Alzheimer's disease. 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. 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. Theories of Alzheimer's Disease Research into the potential causes of Alzheimer's disease has been frustrating. A number of processes are believed to contribute to the cognitive decline observed in Alzheimer's disease. Brain deterioration in Alzheimer's disease is thought to begin decades before symptoms become evident. Outlined below are several factors postulated to contribute to Alzheimer's disease; each also represents a potential therapeutic target. Senile Plaques A prominent finding in Alzheimer's disease is that senile plaques, which are comprised of "clumps" of the protein fragment amyloid beta, accumulate and cause cellular damage in key areas of the brain, especially the hippocampus, which is involved in memory consolidation and spatial navigation. Aggregates of amyloid beta have been shown to contribute to oxidative damage, excitotoxicity, inflammation, cell death, and formation of neurofibrillary tangles (NFTs) Page 26 | Abby's Magazine -

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