Abraham Acevedo‐Arozena

16.3k total citations · 1 hit paper
42 papers, 2.2k citations indexed

About

Abraham Acevedo‐Arozena is a scholar working on Molecular Biology, Neurology and Cellular and Molecular Neuroscience. According to data from OpenAlex, Abraham Acevedo‐Arozena has authored 42 papers receiving a total of 2.2k indexed citations (citations by other indexed papers that have themselves been cited), including 18 papers in Molecular Biology, 16 papers in Neurology and 15 papers in Cellular and Molecular Neuroscience. Recurrent topics in Abraham Acevedo‐Arozena's work include Genetic Neurodegenerative Diseases (9 papers), Amyotrophic Lateral Sclerosis Research (9 papers) and Autophagy in Disease and Therapy (9 papers). Abraham Acevedo‐Arozena is often cited by papers focused on Genetic Neurodegenerative Diseases (9 papers), Amyotrophic Lateral Sclerosis Research (9 papers) and Autophagy in Disease and Therapy (9 papers). Abraham Acevedo‐Arozena collaborates with scholars based in United Kingdom, Spain and Italy. Abraham Acevedo‐Arozena's co-authors include Steve D. M. Brown, David C. Rubinsztein, Brinda Ravikumar, Sara Imarisio, Cahir J. O’Kane, Silvia Corrochano, Fiona M. Menzies, Elizabeth Fisher, Ashley R. Winslow and Chien‐Wen Chen and has published in prestigious journals such as Nature Genetics, The Journal of Experimental Medicine and The Journal of Cell Biology.

In The Last Decade

Abraham Acevedo‐Arozena

40 papers receiving 2.2k citations

Hit Papers

α-Synuclein impairs macroautophagy: implications for Park... 2010 2026 2015 2020 2010 200 400 600
What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

  1. α-Synuclein impairs macroautophagy: implications for Parkinson’s disease
    2010 651 citations Silvia Corrochano, Abraham Acevedo‐Arozena et al. profile →

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Abraham Acevedo‐Arozena United Kingdom 20 882 870 759 497 452 42 2.2k
Sandra Maday United States 18 442 0.5× 1.0k 1.2× 1.1k 1.4× 602 1.2× 530 1.2× 24 2.6k
Mala V. Rao United States 26 721 0.8× 240 0.3× 1.0k 1.4× 817 1.6× 434 1.0× 37 2.7k
Caty Casas Spain 26 277 0.3× 324 0.4× 1.1k 1.5× 678 1.4× 505 1.1× 51 2.4k
Jacqueline A. Sluijs Netherlands 22 354 0.4× 211 0.2× 1.4k 1.8× 471 0.9× 694 1.5× 42 2.4k
Rika Suzuki-Migishima Japan 14 604 0.7× 2.4k 2.8× 2.1k 2.7× 527 1.1× 696 1.5× 17 4.5k
Paula Dietrich United States 28 747 0.8× 266 0.3× 1.4k 1.9× 1.3k 2.6× 378 0.8× 38 2.7k
Lynnette J. Cook United Kingdom 12 213 0.2× 499 0.6× 624 0.8× 409 0.8× 210 0.5× 12 1.4k
Kishore R. Kumar Australia 23 882 1.0× 195 0.2× 726 1.0× 647 1.3× 255 0.6× 95 1.9k
Matthieu Y. Pasco France 11 193 0.2× 534 0.6× 482 0.6× 418 0.8× 243 0.5× 11 1.4k
Oleg S. Gorbatyuk United States 24 550 0.6× 317 0.4× 1.4k 1.8× 892 1.8× 304 0.7× 41 2.6k

Countries citing papers authored by Abraham Acevedo‐Arozena

Since Specialization
Citations

This map shows the geographic impact of Abraham Acevedo‐Arozena's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Abraham Acevedo‐Arozena with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Abraham Acevedo‐Arozena more than expected).

Fields of papers citing papers by Abraham Acevedo‐Arozena

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Abraham Acevedo‐Arozena. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Abraham Acevedo‐Arozena. The network helps show where Abraham Acevedo‐Arozena may publish in the future.

Co-authorship network of co-authors of Abraham Acevedo‐Arozena

This figure shows the co-authorship network connecting the top 25 collaborators of Abraham Acevedo‐Arozena. A scholar is included among the top collaborators of Abraham Acevedo‐Arozena based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Abraham Acevedo‐Arozena. Abraham Acevedo‐Arozena is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Moreno‐Martínez, Laura, Núria Gaja‐Capdevila, Mireia Herrando‐Grabulosa, et al.. (2025). Novel FKBP prolyl isomerase 1A (FKBP12) ligand promotes functional improvement in SOD1G93A amyotrophic lateral sclerosis (ALS) mice. British Journal of Pharmacology. 182(11). 2466–2486.
2.
Armas, José Miguel Brito, et al.. (2025). Challenges of modelling TDP-43 pathology in mice. Mammalian Genome. 36(2). 465–481.
3.
Stewart, Michelle, Petrina Lau, Gareth Banks, et al.. (2019). Loss of Frrs1l disrupts synaptic AMPA receptor function, and results in neurodevelopmental, motor, cognitive and electrographical abnormalities. Disease Models & Mechanisms. 12(2). 19 indexed citations
4.
Nair, R., Silvia Corrochano, Charlotte Tibbit, et al.. (2019). Uses for humanised mouse models in precision medicine for neurodegenerative disease. Mammalian Genome. 30(7-8). 173–191. 23 indexed citations
5.
Rodríguez‐Rodríguez, Ana Elena, Javier Donate‐Correa, Jordi Rovira, et al.. (2019). Inhibition of the mTOR pathway: A new mechanism of β cell toxicity induced by tacrolimus. American Journal of Transplantation. 19(12). 3240–3249. 31 indexed citations
6.
Luis-Ravelo, Diego, Pedro Barroso‐Chinea, Domingo Afonso‐Oramas, et al.. (2017). Pramipexole reduces soluble mutant huntingtin and protects striatal neurons through dopamine D3 receptors in a genetic model of Huntington's disease. Experimental Neurology. 299(Pt A). 137–147. 15 indexed citations
7.
Ricketts, Thomas C., Philip McGoldrick, Pietro Fratta, et al.. (2014). A Nonsense Mutation in Mouse Tardbp Affects TDP43 Alternative Splicing Activity and Causes Limb-Clasping and Body Tone Defects. PLoS ONE. 9(1). e85962–e85962. 16 indexed citations
8.
Cortese, Andrea, Vincent Plagnol, Stefen Brady, et al.. (2014). Widespread RNA metabolism impairment in sporadic inclusion body myositis TDP43-proteinopathy. Neurobiology of Aging. 35(6). 1491–1498. 33 indexed citations
9.
Renna, Maurizio, Carla F. Bento, Angeleen Fleming, et al.. (2013). IGF-1 receptor antagonism inhibits autophagy. Human Molecular Genetics. 22(22). 4528–4544. 72 indexed citations
10.
Corrochano, Silvia, Maurizio Renna, Cristina Tomás‐Zapico, et al.. (2012). α-synuclein levels affect autophagosome numbers in vivo and modulate Huntington disease pathology. Autophagy. 8(3). 431–432. 19 indexed citations
11.
Joyce, Peter I., Pietro Fratta, Elizabeth Fisher, & Abraham Acevedo‐Arozena. (2011). SOD1 and TDP-43 animal models of amyotrophic lateral sclerosis: recent advances in understanding disease toward the development of clinical treatments. Mammalian Genome. 22(7-8). 420–448. 90 indexed citations
12.
Corrochano, Silvia, Maurizio Renna, Sarah Carter, et al.. (2011). α-Synuclein levels modulate Huntington's disease in mice. Human Molecular Genetics. 21(3). 485–494. 33 indexed citations
13.
Acevedo‐Arozena, Abraham, Bernadett Kalmár, Thomas C. Ricketts, et al.. (2011). A comprehensive assessment of the SOD1G93A low-copy transgenic mouse, which models human amyotrophic lateral sclerosis. Disease Models & Mechanisms. 4(5). 686–700. 79 indexed citations
14.
Rose, Claudia, Fiona M. Menzies, Maurizio Renna, et al.. (2010). Rilmenidine attenuates toxicity of polyglutamine expansions in a mouse model of Huntington's disease. Human Molecular Genetics. 19(11). 2144–2153. 163 indexed citations
15.
Ravikumar, Brinda, Abraham Acevedo‐Arozena, Sara Imarisio, et al.. (2005). Dynein mutations impair autophagic clearance of aggregate-prone proteins. Nature Genetics. 37(7). 771–776. 366 indexed citations
16.
Rubinsztein, David C., Brinda Ravikumar, Abraham Acevedo‐Arozena, et al.. (2005). Dyneins, Autophagy, Aggregation and Neurodegeneration. Autophagy. 1(3). 177–178. 40 indexed citations
17.
Rodrı́guez, Manuel, Pedro Barroso‐Chinea, Abraham Acevedo‐Arozena, & Tomás González‐Hernández. (2002). Effects of dopaminergic cell degeneration on electrophysiological characteristics and GAD65/GAD67 expression in the substantia nigra: Different action on GABA cell subpopulations. Movement Disorders. 18(3). 254–266. 15 indexed citations
18.
Santos, Javíer, Xavier Montagutelli, Abraham Acevedo‐Arozena, et al.. (2002). A new locus for resistance to γ-radiation-induced thymic lymphoma identified using inter-specific consomic and inter-specific recombinant congenic strains of mice. Oncogene. 21(43). 6680–6683. 31 indexed citations
19.
González‐Hernández, Tomás, Pedro Barroso‐Chinea, Abraham Acevedo‐Arozena, Eduardo Salido, & Manuel Rodrı́guez. (2001). Colocalization of tyrosine hydroxylase and GAD65 mRNA in mesostriatal neurons. European Journal of Neuroscience. 13(1). 57–67. 17 indexed citations
20.
Acevedo‐Arozena, Abraham, et al.. (1991). [Severe ischemia of the hand. Treatment with regional intravenous sympathicolysis with reserpine].. PubMed. 119(4). 412–7. 1 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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