Aggregation and deposition of amyloid β-protein (Aβ) in brain is an invariable and initial event in the pathological process of Alzheimer's disease. Thus, one of the fundamental challenges regarding pathogenesis of Alzheimer's disease is to elucidate how Aβ starts to aggregate and how aggregated Aβ causes its toxicities against neurons. Recently, a body of evidence is growing that Aβ aggregation is facilitated in the presence of particular membranes lipids such as gangliosides and cholesterol and furthermore, that Aβ toxicities emerge through interaction with specific neuronal membrane microdomains such as lipid rafts.

We invite investigators to contribute original research articles as well as review articles that will provide novel information on this research area and stimulate research activities to understand the basic mechanism underlying early pathogenesis of Alzheimer's disease.

Potential topics include, but are not limited to:

• Aβ interaction with cholesterol and sphingolipids
• Effect of cholesterol on Aβ-membrane interaction
• Aβ conformational changes on neuronal membranes (lipid rafts)
• Aβ aggregation/oligomerization on neuronal membranes (lipid rafts)
• Aβ toxicities on neuronal or intraneuronal membranes/organelles (e.g., mitochondria and ER)
• Aβ-induced ion channel formation
• Structure of Aβ oligomers in membranes: theoretical and experimental studies
• Internalization of Aβ in neuronal cells

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ijad/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: