Evidence map›Paper›PMID 26742522›Full record

ArticleMolecular neurobiology2017

Clozapine Improves Memory Impairment and Reduces Aβ Level in the Tg-APPswe/PS1dE9 Mouse Model of Alzheimer's Disease.

Yura Choi, Ha Jin Jeong, Quan Feng Liu, Seung Tack Oh, Byung-Soo Koo, Yeni Kim, In-Won Chung, Yong Sik Kim, Songhee Jeon

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

Who cites it

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  5. Drug repurposing for neurodegenerative diseases using Zebrafish behavioral profiles.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024
    Article
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  15. Animal Models of Psychosis in Alzheimer Disease.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2020
    Review
  16. mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders.International journal of molecular sciences · 2018
    Review
  17. Article
  18. Article
4 · The record

Corrections and comments

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

9 authors at 2 institutions in 1 country.

Yura ChoiDepartment of Biomedical Engineering, Dongguk University, Gyeonggi-do, 10326, Republic of Korea.
Ha Jin JeongDongguk University Research Institute of Bio-Medi Integration, Sangyoung-Bio, Biomedi-Campus, Dongguk-ro 32, Goyang-si, Gyeonggi-do, 10326, Republic of Korea.
Quan Feng LiuDepartment of Neuropsychiatry, Graduate School of Oriental Medicine, Dongguk University, Gyeongju, 38066, Republic of Korea.
Seung Tack OhDepartment of Biomedical Engineering, Dongguk University, Gyeonggi-do, 10326, Republic of Korea.
Byung-Soo KooDepartment of Neuropsychiatry, Graduate School of Oriental Medicine, Dongguk University, Gyeongju, 38066, Republic of Korea.
Yeni KimDepartment of Child Psychiatry, National Center for Child and Adolescent Psychiatry, Seoul National Hospital, Seoul, 04933, Republic of Korea.
In-Won ChungDepartment of Neuropsychiatry, Dongguk University International Hospital, Dongguk University Medical School, Gyeonggi-do, 10326, Republic of Korea.
Yong Sik KimDepartment of Neuropsychiatry, Dongguk University International Hospital, Dongguk University Medical School, Gyeonggi-do, 10326, Republic of Korea. kys@snu.ac.kr.
Songhee JeonDongguk University Research Institute of Bio-Medi Integration, Sangyoung-Bio, Biomedi-Campus, Dongguk-ro 32, Goyang-si, Gyeonggi-do, 10326, Republic of Korea. jsong0304@dongguk.edu.
Dongguk University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive degenerative condition. In order to treat AD, the use of a "drug repositioning" or "repurposing" approach with potential disease-modifying compounds has been increased. The new generation antipsychotics are commonly used in AD and other dementias for the treatment of psychosis and behavioral symptoms, and several animal models have shown the effects of these potential disease-modifying compounds. In this study, we examined whether long-term clozapine treatment could reduce amyloid beta (Aβ) deposition and cognitive impairment in transgenic mice of AD, Tg-APPswe/PS1dE9. AD mice were fed clozapine at 20 mg/kg/day for 3 months from 4.5 months of age. Intake of clozapine improved the Aβ-induced memory impairment and suppressed Aβ levels and plaque deposition in the brain of AD mice. Clozapine upregulated Trk, brain-derived neurotrophic factor, cyclin-dependent kinase-5, and p35 in the cortex and hippocampus of AD mice and activated AMP-activated protein kinase (AMPK). As a downstream effector of AMPK, beta-secretase expression was decreased by clozapine administration. Moreover, clozapine-phosphorylated synapsin I at Ser9 and Ser549 sites in the hippocampus and cortex of AD mice, which may be involved in synaptic strength. This study suggests that as one of candidate for multi-target approach of AD treatment, clozapine is proposed as a therapeutic drug for treatment of AD patients.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsClozapineMaleMemory DisordersMiceMice, Inbred C57BLMice, TransgenicPeptide FragmentsPresenilin-1Amyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Amyloid beta-Protein PrecursorClozapinePeptide FragmentsPresenilin-1presenilin 1, mouseAlzheimer’s diseaseAMPKBACECDK5ClozapineSynapsin

Identifiers

PMID26742522
OpenAlexW2228991189

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.