Evidence map›Paper›PMID 41350438›Full record

ArticlePsychopharmacology2026

7,8-Dihydroxyflavone ameliorates bone loss by regulating TRKB/AKT/FOXO3a pathway in a mouse model of alzheimer's disease.

Dong Liu, Xiaoxiong Li, Peng Shi, Wenjuan Hong, Jie Huang, Mingliang Hou, Linqiu Ma, Qirong Liao, Hongyan Yang, Xiaoyan Fu and 6 more

Abstract read
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In one paragraph

Article in Psychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Dong LiuThe State Key Laboratory of Molecular Biology of Trauma, Department of Trauma, Daping Hospital, Ministry of Science and Technology, Army Medical University, Chongqing, China.
Xiaoxiong LiDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Peng ShiDepartment of Neurology, The First Affiliated Hospital of Bengbu Medical University, Bengbu Medical University, Anhui, China.
Wenjuan HongDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Jie HuangDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Mingliang HouDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Linqiu MaDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Qirong LiaoDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Hongyan YangDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Xiaoyan FuDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Huadong ZhouDepartment of Neurology, Daping Hospital, Army Medical University, Chongqing, China.
Jing LuDepartment of Neurology, The First Affiliated Hospital of Bengbu Medical University, Bengbu Medical University, Anhui, China.
Yating LiuDepartment of Neurology, The First Affiliated Hospital of Bengbu Medical University, Bengbu Medical University, Anhui, China.
Xiangqian FengDepartment of Neurology, The First Affiliated Hospital of Bengbu Medical University, Bengbu Medical University, Anhui, China.
Donglin WangDepartment of Neurology, The First Affiliated Hospital of Bengbu Medical University, Bengbu Medical University, Anhui, China.
Rui ZhouDepartment of Orthopedics, Southwest Hospital, The Orthopedic Surgery Center of Chinese PLA, Army Medical University, Chongqing, 400038, China. zhourui519@tmmu.edu.cn.ORCID http://orcid.org/0000-0002-2861-7964

Funding

National Natural Science Foundation of China 81972112
6 · The paper itself

Abstract

backgroundThe incidence of osteoporosis is increased in Alzheimer's disease (AD). The pathogenesis of AD with osteoporosis is still unknown, there is no ideal treatment as yet for it. 7,8-Dihydroxyflavone (7,8-DHF), a functional brain-derived neurotrophic factor (BDNF) mimetic, shows therapeutic potential for neurological and orthopedic disorders.

objectivesThis research investigated the molecular mechanisms by which 7,8-DHF mitigates bone loss and cognitive dysfunction in osteoporotic AD mice.

methodsMicro-CT analysis quantified bone loss in AD mice. The Morris water maze (MWM) assessed mouse cognitive function, and immunohistochemical analysis measured Aβ plaque deposition. qPCR and Western blotting measured expression levels of APP, Aβ42, TRKB, and FOXO3a in osteoblasts isolated from femoral bone marrow mesenchymal stem cells (BMSCs) and brain tissue. ELISA determined the levels of IL-1β, IL-6, osteocalcin (OCN), fibroblast growth factor 23 (FGF23) and sclerostin. For in vitro experiments, osteoblast differentiation was monitored in MC3T3-E1 cells co-cultured with Aβ42, with concurrent measurement of TRKB, AKT, and FOXO3a expression. The efficacy of 7,8-DHF against bone loss and osteoblast differentiation was systematically evaluated.

resultsCognitive impairment and bone loss manifested in APP/PS1 mice. 7,8-DHF treatment ameliorated bone mass reduction, decreased Aβ42 expression in bone tissue, and enhanced TRKB expression. Concurrently, 7,8-DHF improved cognitive function and accelerated clearance of [¹²⁵I]-Aβ42 from the brain. In in-vitro, Aβ42 increased inflammatory cytokine levels, suppressed TRKB expression, and impaired osteoblast differentiation. 7,8-DHF reduced the levels of AKT and pFOXO3a by TRKB.

conclusion7,8-DHF could alleviate bone mass loss in AD mice by regulating the TRKB/AKT/FOXO3a pathway. This finding provides new ideas for the treatment strategy of AD with osteoporosis and is beneficial to the health of the elderly.

Indexed as

Alzheimer DiseaseFlavonesOsteoporosisAmyloid beta-PeptidesAnimalsCell DifferentiationDisease Models, AnimalForkhead Box Protein O3MaleMiceMice, Inbred C57BLMice, TransgenicOsteoblastsPeptide FragmentsProtein-Tyrosine KinasesProto-Oncogene Proteins c-akt6,7-dihydroxyflavoneAmyloid beta-PeptidesFlavonesForkhead Box Protein O3FoxO3 protein, mouseNtrk2 protein, mousePeptide FragmentsProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktReceptor, trkB7,8-DHFAlzheimer's diseaseOsteoblastsOsteoporosisTRKB

Identifiers

PMID41350438

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.