Extracellular amyloid β (Aβ) that confers neurotoxicity and modulates synaptic plasticity and memory function has been central to the amyloid hypothesis of Alzheimer's disease (AD) pathology. Like many other misfolded proteins identified in neurodegenerative disorders, Aβ also accumulates inside the AD neurons. This intracellular Aβ affects a variety of cellular physiology from protein degradation, axonal transport, autophagy to apoptosis, further documenting the role of Aβ in AD. Therapeutics targeting intracellular Aβ could be effective treatment for AD.