Paeonol ameliorates scopolamine- and β-amyloid 1–42 oligomer-induced cognitive impairments through modulation of the TGR5–PKA–cAMP response element-binding–brain-derived neurotrophic factor pathway and inhibition of acetylcholinesterase

Ye-Won Lee

doi:10.1016/j.neuint.2026.106188

Paeonol ameliorates scopolamine- and β-amyloid 1–42 oligomer-induced cognitive impairments through modulation of the TGR5–PKA–cAMP response element-binding–brain-derived neurotrophic factor pathway and inhibition of acetylcholinesterase

2026-05-20

0

PRE

AI

Y

Ye-Won Lee

Y

Ye Eun Cho

S

So-Yeon Kim

S

So-Young Cho

S

Su Jung Lee

Y

Young-Ju Do

N

Na-Hyun Lee

D

Dong Hyun Kim

J

Jong Hoon Ryu

H

Ho Jung Bae *

S

Se Jin Park *

DOI：10.1016/j.neuint.2026.106188

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• Paeonol improves cognitive deficits in scopolamine and Aβ1–42 mouse models. • Paeonol activates the TGR5–PKA–CREB–BDNF signaling pathway in the brain. • Molecular docking identifies TGR5 as a potential binding target of paeonol. • Paeonol suppresses acetylcholinesterase activity comparable to donepezil.

Keywords:

Paeonol

cognitive impairment

TGR5

PKA

CREB

BDNF

acetylcholinesterase

Paeonol ameliorates scopolamine- and β-amyloid 1–42 oligomer-induced cognitive impairments through modulation of the TGR5–PKA–cAMP response element-binding–brain-derived neurotrophic factor pathway and inhibition of acetylcholinesterase

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