Altered Cholesterol Intracellular Trafficking and the Development of Pathological Hallmarks of Sporadic AD

Journal Title: Journal of Parkinson’s Disease and Alzheimer’s Disease - Year 2014, Vol 1, Issue 1

Abstract

Compared to the rare familial early onset Alzheimer’s disease (AD) that results from gene mutations in AbPP and presenilin-1, the pathogenesis of sporadic AD is much more complex and is believed to result from complex interactions between nutritional, environmental, epigenetic and genetic factors. Among those factors, the presence APOE4 is still the single strongest genetic risk factor for sporadic AD. However, the exact underlying mechanism whereby apoE4 contributes to the pathogenesis of sporadic AD remains unclear. Here, we discuss how altered cholesterol intracellular trafficking as a result of apoE4 might contribute to the development of pathological hallmarks of AD including brain deposition of amyloid beta (Ab), neurofibrillary tangles, and synaptic dysfunction.

Authors and Affiliations

Xuesong Chen

Keywords

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  • EP ID EP207462
  • DOI 10.13188/2376-922X
  • Views 119
  • Downloads 0

How To Cite

Xuesong Chen (2014). Altered Cholesterol Intracellular Trafficking and the Development of Pathological Hallmarks of Sporadic AD. Journal of Parkinson’s Disease and Alzheimer’s Disease, 1(1), 1-8. https://europub.co.uk./articles/-A-207462