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Abstract
Alzheimer disease (AD) is a heterogeneous disease with a complex pathobiology. The
presence of extracellular amyloid-β deposition as neuritic plaques and intracellular
accumulation of hyperphosphorylated tau as neurofibrillary tangles remain the primary
neuropathologic criteria for AD diagnosis. However, a number of recent fundamental
discoveries highlight important pathological roles for other critical cellular and
molecular processes. Despite this, no disease modifying treatment currently exists
and numerous phase 3 clinical trials have failed to demonstrate benefit. We review
here recent advances in our understanding of AD pathobiology and discuss current treatment
strategies, highlighting recent clinical trials and opportunities for developing future
disease modifying therapies.