Original Publication Date: >8 May, 2015
Publication / Source: Future Neurology
Authors: Jee Hoon Roh & David M. Holtzman
Alzheimer’s disease (AD) has become a leading cause of morbidity and mortality and is even a greater cause of socio-economic burden as the average length of clinical disease spans more than 10 years . While beneficial effects have been observed following administration of disease modifying treatments targeting amyloid-β (Aβ) in AD transgenic animal models, most clinical trials in human AD have not achieved such success . The discrepancy between results in animal models versus what has been observed in humans may be related to the fact that there exists a longer period of preclinical AD in humans when the pathology of AD begins to accumulate before the onset of clinical symptoms . By the time cognitive decline begins in humans, there is already substantial amyloid plaque deposition, tau tangles, and both neuronal and synaptic loss . Therefore, detecting human subjects who are developing AD pathology but still asymptomatic (preclinical AD), as well as defining and modulating factors that can contribute to the pathophysiology during the period leading up to and during the period of preclinical AD are major goals in the field.