Alzheimer’s disease (AD) is the most common form of dementia in the elderly. Currently there is no effective treatment available. Senile plaques and neurofibrillary tangles are hallmarks of AD pathology, and patients demonstrate cognitive complaints with deficits in various neuropsychological domains. Familial AD (FAD) accounts for 0.5% of all AD cases and usually presents before the age of 65 years. Approximately 50% of the FAD patients carry mutations in one of the following genes: APP, PSEN1, and PSEN2. Inheriting any of these genetic mutations increases Aβ42 production, which has been linked to AD pathogenesis. Late-onset AD represents the majority of AD cases, with evidence suggesting impaired Aβ clearance. However, the etiology of late-onset AD is more complex. Several findings suggest that multiple risk genes and factors may contribute to the pathogenesis of LOAD. In this chapter, we elaborate some of these factors and their involvements in the development of AD.
Part of the book: Update on Dementia