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Late-Onset Alzheimer’s Disease (AD) is a complex disease with multifactorial genetic
and environmental etiologies. As such, there is a pressing need to understand the
full molecular complexity of the disease, in order to develop therapeutics that target
multiple orthogonal AD etiologies. There are three major challenges associated with
this endeavor: 1) identifying new molecular hypotheses and mechanisms, 2) vetting
those hypotheses via independent experimental assessments, and 3) prioritizing which
new molecular mechanisms to recommend for therapeutic development. We posit that technologies
developed to empower community-driven solutions in a radically open way will be key
to the overall success of creating new AD therapeutics.
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