Aβ dissociation by pectolinarin may counteract against Aβ-induced synaptic dysfunction and memory impairment.

Alzheimer's disease (AD) is a degenerative brain disorder characterised by various neurological symptoms, including memory impairment and mood disorders, associated with the abnormal accumulation of amyloid b(Aβ) and tau proteins in the brain. There is still no definitive treatment available for AD, and the Aβ antibody drugs, which are expected to be approved by the FDA, have many limitations. Therefore, there is an urgent need to develop low-molecular-weight therapeutic agents for the management of AD. In this study, we investigated whether pectolinarin, a flavonoid, regulates Aβ aggregation and Aβ-induced toxicity. Pectolinarin demonstrated concentration-dependent inhibition of Aβ aggregation and had the ability to break down pre-formed Aβ aggregates, thereby reducing their neurotoxicity. Furthermore, pectolinarin suppressed Aβ aggregates-induced reduction in long-term potentiation (LTP) in the hippocampus. Oral administration of pectolinarin in experimental animals inhibited memory impairment and LTP deficits induced by Aβ injection in the hippocampus. These results indicate that pectolinarin may reduce toxic Aβ species and Aβ-induced memory impairments and synaptic dysfunction.