Evidence map›Paper›PMID 35296367›Full record

ReviewActa neuropathologica communications2022

The role of DHCR24 in the pathogenesis of AD: re-cognition of the relationship between cholesterol and AD pathogenesis.

Xiaojing Bai, Meiting Mai, Kai Yao, Mengqi Zhang, Yue Huang, Wenbin Zhang, Xiaorou Guo, Yixuan Xu, Ying Zhang, Atikam Qurban and 7 more

Open access · goldAbstract readReview
In one paragraph

Review in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

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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

17 authors at 2 institutions in 1 country.

Xiaojing BaiDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Meiting MaiDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Kai YaoDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Mengqi ZhangDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Yue HuangDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Wenbin ZhangDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Xiaorou GuoDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Yixuan XuDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Ying ZhangDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Atikam QurbanDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Lijie DuanDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Jimei BuDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Jianfeng ZhangDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Junfeng WuDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Yongfei ZhaoDepartment of Neurology, Jinshan Hospital Affiliated to Fudan University, No. 1508 Long-hang Road, Jinshan District, Shanghai, 201508, China.
Xiangshan YuanState Key Laboratory of Medical Neurobiology and Ministry of Education Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Hengbing 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 · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies show that 3β-hydroxysterol-Δ24 reductase (DHCR24) has a remarked decline in the brain of AD patients. In brain cholesterol synthetic metabolism, DHCR24 is known as the heavily key synthetase in cholesterol synthesis. Moreover, mutations of DHCR24 gene result in inhibition of the enzymatic activity of DHCR24, causing brain cholesterol deficiency and desmosterol accumulation. Furthermore, in vitro studies also demonstrated that DHCR24 knockdown lead to the inhibition of cholesterol synthesis, and the decrease of plasma membrane cholesterol and intracellular cholesterol level. Obviously, DHCR24 could play a crucial role in maintaining cholesterol homeostasis via the control of cholesterol synthesis. Over the past two decades, accumulating data suggests that DHCR24 activity is downregulated by major risk factors for AD, suggesting a potential link between DHCR24 downregulation and AD pathogenesis. Thus, the brain cholesterol loss seems to be induced by the major risk factors for AD, suggesting a possible causative link between brain cholesterol loss and AD. According to previous data and our study, we further found that the reduced cholesterol level in plasma membrane and intracellular compartments by the deficiency of DHCR24 activity obviously was involved in β-amyloid generation, tau hyperphosphorylation, apoptosis. Importantly, increasing evidences reveal that the brain cholesterol loss and lipid raft disorganization are obviously linked to neuropathological impairments which are associated with AD pathogenesis. Therefore, based on previous data and research on DHCR24, we suppose that the brain cholesterol deficiency/loss might be involved in the pathogenesis of AD.

Indexed as

CholesterolOxidoreductases Acting on CH-CH Group DonorsApoptosisCell MembraneCognitionHumansMembrane MicrodomainsNerve Tissue ProteinsCholesterolDHCR24 protein, humanNerve Tissue ProteinsOxidoreductases Acting on CH-CH Group DonorsAlzheimer’s diseaseCholesterolCholesterol deficiencyDHCR24HypothesisPathogenesis

Identifiers

PMID35296367
PMCPMC8925223
OpenAlexW4220741726

What OpenQuestion holds

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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.