Abstract Title:

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

Abstract Source:

Biochem Pharmacol. 2023 Oct ;216:115792. Epub 2023 Sep 7. PMID: 37689271

Abstract Author(s):

Jee Hyun Yi, Eunbi Cho, Soowon Lee, Kyoung Ja Kwon, Seungheon Lee, Juyong Lee, Changyeol Lee, Chan Young Shin, Dong Hyun Kim, Sang Hee Shim

Article Affiliation:

Jee Hyun Yi


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 Aβantibody 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 Aβaggregation and Aβ-induced toxicity. Pectolinarin demonstrated concentration-dependent inhibition of Aβaggregation and had the ability to break down pre-formed Aβaggregates, thereby reducing their neurotoxicity. Furthermore, pectolinarin suppressed Aβaggregates-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 Aβinjection in the hippocampus. These results indicate that pectolinarin may reduce toxic Aβspecies and Aβ-induced memory impairments and synaptic dysfunction.

Study Type : Animal Study

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