Synaptic Function and Dysfunction in Alzheimer’s Disease

1. Early onset Familial Alzheimer Disease (eFAD). Abnormalities of the amyloid precursor protein (APP) that render it more amyloidogenic, or defects of processing normal APP cause genetic forms of AD. The literature estimates that eFAD accounts for approximately 2% of all people with dementia (approximately 3-5% of all Alzheimer cases) [1,2]. In these patients, autosomal dominant AD usually develops before age 65 due to mutations of the APP gene on chromosome 21 or the presenilin 1 and 2 genes (PSEN1 and PSEN2) on chromosomes 14 and 1, respectively.