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OpenAlex Citation Counts

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OpenAlex is a bibliographic catalogue of scientific papers, authors and institutions accessible in open access mode, named after the Library of Alexandria. It's citation coverage is excellent and I hope you will find utility in this listing of citing articles!

If you click the article title, you'll navigate to the article, as listed in CrossRef. If you click the Open Access links, you'll navigate to the "best Open Access location". Clicking the citation count will open this listing for that article. Lastly at the bottom of the page, you'll find basic pagination options.

Requested Article:

Mislocalisation of TDP‐43 to the cytoplasm causes cortical hyperexcitability and reduced excitatory neurotransmission in the motor cortex
Marcus S. Dyer, Laura A. Reale, Katherine E. Lewis, et al.
Journal of Neurochemistry (2020) Vol. 157, Iss. 4, pp. 1300-1315
Open Access | Times Cited: 51

Showing 1-25 of 51 citing articles:

Amyotrophic lateral sclerosis: a neurodegenerative disorder poised for successful therapeutic translation
Richard J. Mead, Ning Shan, H. Joseph Reiser, et al.
Nature Reviews Drug Discovery (2022) Vol. 22, Iss. 3, pp. 185-212
Open Access | Times Cited: 250
TDP-43 pathology: From noxious assembly to therapeutic removal
Sean S. Keating, Rebecca San Gil, Molly E. V. Swanson, et al.
Progress in Neurobiology (2022) Vol. 211, pp. 102229-102229
Closed Access | Times Cited: 52
The Role of TDP-43 in Neurodegenerative Disease
Yan-Zhe Liao, Jing Ma, Jie-Zhi Dou
Molecular Neurobiology (2022) Vol. 59, Iss. 7, pp. 4223-4241
Closed Access | Times Cited: 51
UNC13Ain amyotrophic lateral sclerosis: from genetic association to therapeutic target
Sean W. Willemse, Peter Harley, Ruben P.A. van Eijk, et al.
Journal of Neurology Neurosurgery & Psychiatry (2023) Vol. 94, Iss. 8, pp. 649-656
Open Access | Times Cited: 35
Aggregation-prone TDP-43 sequesters and drives pathological transitions of free nuclear TDP-43
Sean S. Keating, Adekunle T. Bademosi, Rebecca San Gil, et al.
Cellular and Molecular Life Sciences (2023) Vol. 80, Iss. 4
Open Access | Times Cited: 31
Pathologically mislocalised TDP-43 in upper motor neurons causes a die-forward spread of ALS-like pathogenic changes throughout the mouse corticomotor system
Laura A. Reale, Marcus S. Dyer, Sharn Perry, et al.
Progress in Neurobiology (2023) Vol. 226, pp. 102449-102449
Closed Access | Times Cited: 22
A transient protein folding response targets aggregation in the early phase of TDP-43-mediated neurodegeneration
Rebecca San Gil, Dana Pascovici, Juliana Venturato, et al.
Nature Communications (2024) Vol. 15, Iss. 1
Open Access | Times Cited: 9
How do we get from hyperexcitability to excitotoxicity in amyotrophic lateral sclerosis?
G. Lorenzo Odierna, Steve Vucic, Marcus S. Dyer, et al.
Brain (2024) Vol. 147, Iss. 5, pp. 1610-1621
Open Access | Times Cited: 8
Synaptic dysfunction in ALS and FTD: anatomical and molecular changes provide insights into mechanisms of disease
Pauline A. Gelon, Paul A. Dutchak, Chantelle F. Sephton
Frontiers in Molecular Neuroscience (2022) Vol. 15
Open Access | Times Cited: 35
Pathways to healing: Plants with therapeutic potential for neurodegenerative diseases
Sheena E.B. Tyler, Luke D.K. Tyler
IBRO Neuroscience Reports (2023) Vol. 14, pp. 210-234
Open Access | Times Cited: 16
Aberrant axon initial segment plasticity and intrinsic excitability of ALS hiPSC motor neurons
Peter Harley, Caoimhe Kerins, Ariana Gatt, et al.
Cell Reports (2023) Vol. 42, Iss. 12, pp. 113509-113509
Open Access | Times Cited: 15
Molecular Chaperones’ Potential against Defective Proteostasis of Amyotrophic Lateral Sclerosis
Sumit Kinger, Ankur Rakesh Dubey, Prashant Kumar, et al.
Cells (2023) Vol. 12, Iss. 9, pp. 1302-1302
Open Access | Times Cited: 13
Neuronal TDP-43 aggregation drives changes in microglial morphology prior to immunophenotype in amyotrophic lateral sclerosis
Molly E. V. Swanson, Miran Mrkela, Clinton Turner, et al.
Acta Neuropathologica Communications (2025) Vol. 13, Iss. 1
Open Access
TDP-43 pathology is sufficient to drive axon initial segment plasticity and hyperexcitability of spinal motoneurones in vivo in the TDP43-ΔNLS model of Amyotrophic Lateral Sclerosis
Svetlana Djukic, Zhenxiang Zhao, Lasse Mathias Holmsted Jørgensen, et al.
Acta Neuropathologica Communications (2025) Vol. 13, Iss. 1
Open Access
Targeting senescence in Amyotrophic Lateral Sclerosis: senolytic treatment improves neuromuscular function and preserves cortical excitability in a TDP-43Q331K mouse model.
W. David Arnold, Jose A. Viteri, Nathan R. Kerr, et al.
Research Square (Research Square) (2025)
Closed Access
Cytoplasmic TDP-43 accumulation drives changes in C-bouton number and size in a mouse model of sporadic Amyotrophic Lateral Sclerosis
Anna Normann Bak, Svetlana Djukic, Marion Kadlecova, et al.
Molecular and Cellular Neuroscience (2023) Vol. 125, pp. 103840-103840
Open Access | Times Cited: 10
Riluzole does not ameliorate disease caused by cytoplasmic TDP‐43 in a mouse model of amyotrophic lateral sclerosis
Amanda L. Wright, Paul A. Della Gatta, Sheng Le, et al.
European Journal of Neuroscience (2021) Vol. 54, Iss. 6, pp. 6237-6255
Open Access | Times Cited: 21
Neuronal dysfunction caused by FUSR521G promotes ALS-associated phenotypes that are attenuated by NF-κB inhibition
Mari Carmen Pelaez, Antoine Desmeules, Pauline A. Gelon, et al.
Acta Neuropathologica Communications (2023) Vol. 11, Iss. 1
Open Access | Times Cited: 8
Spatial enrichment and genomic analyses reveal the link of NOMO1 with amyotrophic lateral sclerosis
Jingyan Guo, Linya You, Yu Zhou, et al.
Brain (2024) Vol. 147, Iss. 8, pp. 2826-2841
Closed Access | Times Cited: 2
Neuronal Circuit Dysfunction in Amyotrophic Lateral Sclerosis
Andrea Salzinger, Vidya Ramesh, Shreya Das Sharma, et al.
Cells (2024) Vol. 13, Iss. 10, pp. 792-792
Open Access | Times Cited: 2
Cytoplasmic Human TDP-43 Mislocalization Induces Widespread Dendritic Spine Loss in Mouse Upper Motor Neurons
Marcus S. Dyer, Adele Woodhouse, Catherine A. Blizzard
Brain Sciences (2021) Vol. 11, Iss. 7, pp. 883-883
Open Access | Times Cited: 16
Loss of TBK1 activity leads to TDP-43 proteinopathy through lysosomal dysfunction in human motor neurons
Jin Hao, Michael F. Wells, Gengle Niu, et al.
bioRxiv (Cold Spring Harbor Laboratory) (2021)
Open Access | Times Cited: 15
Familial ALS-associated SFPQ variants promote the formation of SFPQ cytoplasmic aggregates in primary neurons
Jocelyn Widagdo, Saumya R. Udagedara, Nishita Bhembre, et al.
Open Biology (2022) Vol. 12, Iss. 9
Open Access | Times Cited: 10
Cortical Hyperexcitability in the Driver’s Seat in ALS
Zeynep I. Gunes, Vanessa W. Y. Kan, Shenyi Jiang, et al.
Clinical and Translational Neuroscience (2022) Vol. 6, Iss. 1, pp. 5-5
Open Access | Times Cited: 9
Breakdown of the central synapses in C9orf72-linked ALS/FTD
Layla T. Ghaffari, Davide Trotti, Aaron R. Haeusler, et al.
Frontiers in Molecular Neuroscience (2022) Vol. 15
Open Access | Times Cited: 9
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