Currently $200 billion/year is spent in the US to care for 5.4 million individuals afflicted with Alzheimer's disease (AD).  Subsequently, new techniques for diagnosis and treatment of AD is at the forefront of biomedical research.  The most favored explanation for the disease pathology is the �amyloid cascade hypothesis� where increased concentration of beta amyloids (A�) leads to its aggregation and deposition in key areas of the brain associated with memory; the mechanisms of which remain elusive.  One key hypothesis is that oligomeric A�'s disrupt membranes, while another is that it binds to redox active metals to generate reactive oxygen species that lead to weakened synaptic signaling or neuronal cell death.  While model membranes have provide insight into A� membrane interactions, there are still many questions that remain.  We hypothesize that biomimetic models comprised of lipid-coated nanoparticles can serve as investigative probes to elucidate the mechanisms by which A� induce membrane disruption and lipid peroxidation in the presence of metal ions.  We will demonstrate that nanoparticles when combined with a fluorophore affinity probe specific to A�, can serve as sensors of A� and as cellular mimics to determine how membrane curvature and composition influence its affinity to membranes.  We will provide insight into the role of metal ions and chelators in A� oligomerization and membrane interactions.

Investigating beta amyloid interactions with lipid-coated nanoparticles

246th National Meeting (2013)

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