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Mapping trends and hotspots of mitochondrial dysfunction in Alzheimer's disease from 2013 to 2022: a bibliometric analysis of global research.

作者信息

Guo Wang, Hassan Liban Abdulle, Chu Yu-Hao, Yang Xue-Ping, Wang Sheng-Xue, Zhu Han-Xiao, Li Yun

机构信息

Clinical Medical School, Dali University, Dali, China.

Department of Neurology, The First Affiliated Hospital of Dali University, Dali, China.

出版信息

Front Neurosci. 2023 Jun 26;17:1199625. doi: 10.3389/fnins.2023.1199625. eCollection 2023.


DOI:10.3389/fnins.2023.1199625
PMID:37434768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10330782/
Abstract

OBJECTIVE: Alzheimer's disease (AD), a prevalent neurodegenerative affliction that predominantly affects the elderly population, imposes a substantial burden on not only patients but also their families and society at large. Mitochondrial dysfunction plays an important role in its pathogenesis. In this study, we conducted a bibliometric analysis of research on mitochondrial dysfunction and AD over the past 10 years, with the aim of summarizing current research hotspots and trends in this field. METHODS: On February 12, 2023, we searched for publications about mitochondrial dysfunction and AD in the Web of Science Core Collection database from 2013 to 2022. VOSview software, CiteSpace, SCImago, and RStudio were used to analyze and visualize countries, institutions, journals, keywords, and references. RESULTS: The number of publications on mitochondrial dysfunction and AD were on the rise until 2021 and decreased slightly in 2022. The United States ranks first in the number of publications, H-index, and intensity of international cooperation in this research. In terms of institutions, Texas Tech University in the United States has the most publications. The has the most publications in this field of research, while have the highest number of citations. Mitochondrial dysfunction is still an important direction of current research. Autophagy, mitochondrial autophagy, and neuroinflammation are new hotspots. The article from Lin MT is the most cited by analyzing references. CONCLUSION: Research on mitochondrial dysfunction in AD is gaining significant momentum as it provides a crucial research avenue for the treatment of this debilitating condition. This study sheds light on the present research trajectory concerning the molecular mechanisms underlying mitochondrial dysfunction in AD.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/ba6b04995338/fnins-17-1199625-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/8683718d4bb4/fnins-17-1199625-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/88031299bdb9/fnins-17-1199625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/393675d51fc5/fnins-17-1199625-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/dacf7b721b36/fnins-17-1199625-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/7dba0757c180/fnins-17-1199625-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/df2b1cc89a49/fnins-17-1199625-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/b0756923fc1a/fnins-17-1199625-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/ba6b04995338/fnins-17-1199625-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/8683718d4bb4/fnins-17-1199625-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/88031299bdb9/fnins-17-1199625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/393675d51fc5/fnins-17-1199625-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/dacf7b721b36/fnins-17-1199625-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/7dba0757c180/fnins-17-1199625-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/df2b1cc89a49/fnins-17-1199625-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/b0756923fc1a/fnins-17-1199625-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20c9/10330782/ba6b04995338/fnins-17-1199625-g008.jpg

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引用本文的文献

[1]
Gene therapy in Aβ-induced cell and mouse models of Alzheimer's disease through compensating defective mitochondrial complex I function.

J Transl Med. 2024-8-14

[2]
Bibliometric analysis of studies on stress urinary incontinence surgery.

Heliyon. 2023-11-4

本文引用的文献

[1]
Trends of mitochondrial changes in AD: a bibliometric study.

Front Aging Neurosci. 2023-5-16

[2]
Neuroinflammation in Alzheimer's disease: microglial signature and their relevance to disease.

Inflamm Regen. 2023-5-10

[3]
Molecular Regulation Mechanism of Microglial Autophagy in the Pathology of Alzheimer's Disease.

Aging Dis. 2023-8-1

[4]
Mitochondrial mechanisms in Alzheimer's disease: Quest for therapeutics.

Drug Discov Today. 2023-5

[5]
Mortality of Alzheimer's Disease and Other Dementias in China: Past and Future Decades.

Int J Public Health. 2023

[6]
Aberrant Energy Metabolism in Alzheimer's Disease.

J Transl Int Med. 2022-9-24

[7]
Distinct Effects of Beta-Amyloid, Its Isomerized and Phosphorylated Forms on the Redox Status and Mitochondrial Functioning of the Blood-Brain Barrier Endothelium.

Int J Mol Sci. 2022-12-22

[8]
Hypothesis on ontogenesis and pathophysiology of Alzheimer's disease.

Einstein (Sao Paulo). 2022

[9]
Pathophysiology of Alzheimer's Disease.

Psychiatr Clin North Am. 2022-12

[10]
Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex.

Front Aging Neurosci. 2022-10-6

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