Author(s): Jennifer Madeo and Chris Elsayad
Alzheimer’s disease (AD) is a growing health care epidemic. It is the most common cause of dementia in the elderly and its incidence is rising. The disease is progressive, irreversible and debilitating. It is a great burden on both the patient and their caregivers. The two pathological hallmarks of the disease are aggregated beta-amyloid deposits and hyperphosphorylated neurofibrillary tangles. Although these lesions are found in the AD brain, their role in the pathogenesis leading to clinical dementia is largely unknown and still under debate. Age, which influences theoxidative and inflammatory states of the brain, is the most important risk factor. Recent research has highlighted the important role of oxidative stress, the role of the mitochondria in early disease and inflammation in the underlying molecular mechanism of AD. Oxidative damage predominately involves lipid peroxidation from reactive oxygen species derived from metabolism. Most patients are diagnosed after irreversible damage has been done. A better understanding of the role of these stressors could lead to early therapeutic interventions that better target the cause and have potential to modify disease course. Currently there is no disease modifying treatments available. This literature review highlights current knowledge regarding the role of oxidative stress, how it relates to the pathogenesis of AD and how further research in this field can benefit those who suffer from this debilitating disease.
