Stabilized Low-n Amyloid-beta Oligomers Induce Robust Novel Object Recognition Deficits Associated with Inflammatory, Synaptic, and GABAergic Dysfunction in the Rat

摘要

Background: With current treatments for Alzheimer's disease (AD) only providing temporary symptomatic benefits, disease modifying drugs are urgently required. This approach relies on improved understanding of the early pathophysiology of AD. A new hypothesis has emerged, in which early memory loss is considered a synapse failure caused by soluble amyloid-beta oligomers (A beta o). These small soluble A beta o, which precede the formation of larger fibrillar assemblies, may be the main cause of early AD pathologies.