Evidence map›Paper›PMID 37344916›Full record

ArticleActa neuropathologica communications2023

DHCR24 reverses Alzheimer's disease-related pathology and cognitive impairment via increasing hippocampal cholesterol levels in 5xFAD mice.

Wen-Bin Zhang, Yue Huang, Xiao-Rou Guo, Meng-Qi Zhang, Xiang-Shan Yuan, Heng-Bing Zu

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Alzheimer's Amyloid Hypothesis and Antibody Therapy: Melting Glaciers?International journal of molecular sciences · 2024
    Review
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  18. Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023
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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

6 authors at 2 institutions in 1 country.

Wen-Bin Zhang *Department of Neurology, Jinshan Hospital Affiliated to Fudan University, No.1508 Long-Hang Road, Jinshan District, Shanghai, 201508, China.
Yue Huang *Department of Neurology, Jinshan Hospital Affiliated to Fudan University, No.1508 Long-Hang Road, Jinshan District, Shanghai, 201508, China.
Xiao-Rou GuoDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No.1508 Long-Hang Road, Jinshan District, Shanghai, 201508, China.
Meng-Qi ZhangDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No.1508 Long-Hang Road, Jinshan District, Shanghai, 201508, China.
Xiang-Shan YuanDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No.1508 Long-Hang Road, Jinshan District, Shanghai, 201508, China. yuanxiangshan1999@163.com.
Heng-Bing ZuDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No.1508 Long-Hang Road, Jinshan District, Shanghai, 201508, China. hbzyy666@163.com.ORCID 0000-0002-0150-744X
Jinshan Hospital of Fudan University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidences reveal that cellular cholesterol deficiency could trigger the onset of Alzheimer's disease (AD). As a key regulator, 24-dehydrocholesterol reductase (DHCR24) controls cellular cholesterol homeostasis, which was found to be downregulated in AD vulnerable regions and involved in AD-related pathological activities. However, DHCR24 as a potential therapeutic target for AD remains to be identified. In present study, we demonstrated the role of DHCR24 in AD by employing delivery of adeno-associated virus carrying DHCR24 gene into the hippocampus of 5xFAD mice. Here, we found that 5xFAD mice had lower levels of cholesterol and DHCR24 expression, and the cholesterol loss was alleviated by DHCR24 overexpression. Surprisingly, the cognitive impairment of 5xFAD mice was significantly reversed after DHCR24-based gene therapy. Moreover, we revealed that DHCR24 knock-in successfully prevented or reversed AD-related pathology in 5xFAD mice, including amyloid-β deposition, synaptic injuries, autophagy, reactive astrocytosis, microglial phagocytosis and apoptosis. In conclusion, our results firstly demonstrated that the potential value of DHCR24-mediated regulation of cellular cholesterol level as a promising treatment for AD.

Indexed as

Alzheimer DiseaseCognitive DysfunctionOxidoreductases Acting on CH-CH Group DonorsAmyloid beta-PeptidesAnimalsCholesterolDisease Models, AnimalHippocampusMiceMice, TransgenicNerve Tissue ProteinsAmyloid beta-PeptidesCholesterolDhcr24 protein, mouseNerve Tissue ProteinsOxidoreductases Acting on CH-CH Group Donors24-dehydrocholesterol reductase (DHCR24)Alzheimer’s diseaseCholesterolGene therapyNeurodegenerationNeuroprotectionPathogenesis

Identifiers

PMID37344916
PMCPMC10286507
OpenAlexW4381548264

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.