In a 2015 study, Umeda et al. found that Intracellular Amyloid Beta (Aβ) oligomers impair organelle transport and induce dendritic spine loss in primary neurons. Amyloid beta (Aβ) oligomers may contribute to early synaptic pathology in Alzheimer’s disease and argued against the consensus that Aβ-induced spine loss and transport defects require Tau protein. Amyloid Beta E22P ( 11A1 ) Aβ Anti-Human Mouse IgG MoAb(#10379) antibodies were used to stain their mouse primary neurons during their study (page 3).

Introduction: Synaptic dysfunction and intracellular transport defects are early events in Alzheimer's disease (AD). Extracellular amyloid β (Aβ) oligomers cause spine alterations and impede the transport of proteins and organelles such as brain-derived neurotrophic factor (BDNF) and mitochondria that are required for synaptic function. Meanwhile, intraneuronal accumulation of Aβ precedes its extracellular deposition and is also associated with synaptic dysfunction in AD. However, the links between intracellular Aβ, spine alteration, and mechanisms that support synaptic maintenance such as organelle trafficking are poorly understood.