Evidence map›Paper›PMID 35732869›Full record

ArticleMolecular neurobiology2022

Hippocampal Iron Accumulation Impairs Synapses and Memory via Suppressing Furin Expression and Downregulating BDNF Maturation.

Yating Zhang, Xue Bai, Yi Zhang, Shanshan Yao, Yiduo Cui, Lin-Hao You, Peng Yu, Yan-Zhong Chang, Guofen Gao

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  13. Amyloid Precursor Protein and Alzheimer's Disease.International journal of molecular sciences · 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

9 authors at 1 institution in 1 country.

Yating ZhangMinistry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China.
Xue Bai *Ministry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China.
Yi Zhang *Ministry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China.
Shanshan YaoMinistry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China.
Yiduo CuiMinistry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China.
Lin-Hao YouMinistry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China.
Peng YuMinistry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China. yupeng0311@163.com.ORCID http://orcid.org/0000-0002-0991-2976
Yan-Zhong ChangMinistry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China. chang7676@163.com.ORCID http://orcid.org/0000-0002-6386-9649
Guofen GaoMinistry of Education Key Laboratory of Molecular and Cellular Biology, Laboratory of Molecular Iron Metabolism, College of Life Sciences, Hebei Normal University, No. 20 Nanerhuan Eastern Road, Shijiazhuang, 050024, Hebei Province, China. guofen83@hotmail.com.ORCID http://orcid.org/0000-0002-2707-0792
Hebei Normal University · CN

Funding

National Natural Science Foundation of China 32170979Science and Technology Project of Hebei Education Department ZD2021327
6 · The paper itself

Abstract

Brain iron overload is positively correlated with the pathogenesis of Alzheimer's disease (AD). However, the role of iron in AD pathology is not completely understood. Furin is the first identified mammalian proprotein convertase that catalyzes the proteolytic maturation of large numbers of prohormones and proproteins. The correlation between altered furin expression and AD pathology has been suggested, but the underlying mechanism remains to be clarified. Here, we found that the expression of furin in the hippocampus of Alzheimer's model APP/PS1 mice was significantly reduced, and we demonstrated that the reduction of furin was directly caused by hippocampal iron overload using wild-type mice with intrahippocampal injection of iron. In cultured neuronal cells, this suppression effect was observed as transcriptional inhibition. Regarding the changes of furin-mediated activities caused by hippocampal iron overload, we found that the maturation of brain-derived neurotrophic factor (BDNF) was impeded and the expression levels of synaptogenesis-related proteins were downregulated, leading to cognitive decline. Furthermore, iron chelation or furin overexpression in the hippocampus of APP/PS1 mice increased furin expression, restored synapse plasticity, and ameliorated cognitive decline. Therefore, the inhibitory effect of hippocampal iron accumulation on furin transcription may be an important pathway involved in iron-mediated synapse damage and memory loss in AD. This study provides new insights into the molecular mechanisms of the toxic effects of iron in neurons and AD pathophysiology and renders furin as a potential target for treatment of iron overload-related neurodegenerative diseases.

Indexed as

Alzheimer DiseaseIron OverloadAmyloid beta-Protein PrecursorAnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalFurinHippocampusIronMammalsMiceMice, TransgenicSynapsesAmyloid beta-Protein PrecursorBrain-Derived Neurotrophic FactorFurinIronAlzheimer’s diseaseBrain-derived neurotrophic factorCognitive dysfunctionFurinIron

Identifiers

PMID35732869
OpenAlexW4283313316

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.