Walid Fazeli

1.8k total citations
17 papers, 308 citations indexed

About

Walid Fazeli is a scholar working on Genetics, Molecular Biology and Clinical Biochemistry. According to data from OpenAlex, Walid Fazeli has authored 17 papers receiving a total of 308 indexed citations (citations by other indexed papers that have themselves been cited), including 7 papers in Genetics, 5 papers in Molecular Biology and 4 papers in Clinical Biochemistry. Recurrent topics in Walid Fazeli's work include Metabolism and Genetic Disorders (4 papers), Epilepsy research and treatment (4 papers) and Genomics and Rare Diseases (3 papers). Walid Fazeli is often cited by papers focused on Metabolism and Genetic Disorders (4 papers), Epilepsy research and treatment (4 papers) and Genomics and Rare Diseases (3 papers). Walid Fazeli collaborates with scholars based in Germany, United States and France. Walid Fazeli's co-authors include Dirk Isbrandt, Christophe Bernard, Monique Esclapez, Younis Baqi, Sanja Darmopil, Yuri Zilberter, Rodrigo A. Cunha, Carla G. Silva, Antoine Ghestem and Christa E. Müller and has published in prestigious journals such as Human Molecular Genetics, Science Translational Medicine and Experimental Neurology.

In The Last Decade

Walid Fazeli

17 papers receiving 303 citations

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Walid Fazeli Germany	9	99	87	64	60	54	17	308
Oleg Kambur Finland	12	91 0.9×	94 1.1×	19 0.3×	15 0.3×	61 1.1×	19	417
Géza Nagy Hungary	12	60 0.6×	56 0.6×	63 1.0×	46 0.8×	13 0.2×	17	360
R.B. Lu Taiwan	7	186 1.9×	92 1.1×	59 0.9×	16 0.3×	22 0.4×	12	377
Julie A. Mattison United States	8	94 0.9×	27 0.3×	32 0.5×	18 0.3×	10 0.2×	13	379
Ciara A. Torres United States	5	88 0.9×	78 0.9×	57 0.9×	29 0.5×	84 1.6×	5	389
Nobuya Harayama Japan	10	142 1.4×	165 1.9×	8 0.1×	85 1.4×	20 0.4×	27	424
Maria Carolina Bittencourt Gonçalves Brazil	7	69 0.7×	28 0.3×	33 0.5×	110 1.8×	10 0.2×	12	240
Adelina Holguin United States	8	87 0.9×	190 2.2×	20 0.3×	9 0.1×	42 0.8×	9	564
Adriana Pelegrini-da-Silva Brazil	12	101 1.0×	197 2.3×	5 0.1×	99 1.6×	42 0.8×	15	487
José M. Navarro‐Pando Spain	9	231 2.3×	16 0.2×	16 0.3×	15 0.3×	20 0.4×	12	445

Countries citing papers authored by Walid Fazeli

Since Specialization

Citations

This map shows the geographic impact of Walid Fazeli'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 Walid Fazeli with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Walid Fazeli more than expected).

Fields of papers citing papers by Walid Fazeli

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Walid Fazeli. 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 Walid Fazeli. The network helps show where Walid Fazeli may publish in the future.

Co-authorship network of co-authors of Walid Fazeli

This figure shows the co-authorship network connecting the top 25 collaborators of Walid Fazeli. A scholar is included among the top collaborators of Walid Fazeli 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 Walid Fazeli. Walid Fazeli is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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17 of 17 papers shown

Fazeli, Walid, et al.. (2024). Significant Seizure Reduction in Pediatric Participants with Early-Onset SCN2A Developmental and Epileptic Encephalopathy Following Treatment with Elsunersen, a Novel Antisense Oligonucleotide: Findings from the EMBRAVE Study. Neuropediatrics. 55(S 01). S1–S25. 1 indexed citations

Ali, Yasir, Umme Habiba, Sadia Saeed, et al.. (2023). Whole-Exome sequencing identifies GYS2 biallelic variants in individuals with suspected epilepsy. Seizure. 116. 74–80. 2 indexed citations

Boßelmann, Christian M., Ingo Borggräfe, Walid Fazeli, et al.. (2023). Genetische Diagnostik der Epilepsien: Empfehlung der Kommission Epilepsie und Genetik der Deutschen Gesellschaft für Epileptologie (DGfE). 36(3). 224–237. 7 indexed citations

Yavuz, Süleyman Tolga, et al.. (2022). Aseptic Meningitis, Mucocutaneous Lesions and Arthritis after COVID-19 Vaccination in a 15-Year-Old Boy. Vaccines. 10(2). 325–325. 8 indexed citations

Saffari, Afshin, Thomas Bast, Knut Brockmann, et al.. (2022). Efficacy, Tolerability, and Retention of Antiseizure Medications in PRRT2 -Associated Infantile Epilepsy. Neurology Genetics. 8(5). e200020–e200020. 8 indexed citations

Fazeli, Walid, Somayeh Bakhtiari, Abbas Tafakhori, et al.. (2021). The phenotypic spectrum of PCDH12 associated disorders - Five new cases and review of the literature. European Journal of Paediatric Neurology. 36. 7–13. 5 indexed citations

Fazeli, Walid, Somayeh Bakhtiari, Abbas Tafakhori, et al.. (2021). The Phenotypic Spectrum of PCDH12-Associated Disorders: Five New Cases and Review of the Literature. Neuropediatrics. 1 indexed citations

Mangold, Elisabeth, et al.. (2019). Cleft Palate as Distinguishing Feature in a Patient with GABRB3 Epileptic Encephalopathy. Neuropediatrics. 50(6). 378–381. 3 indexed citations

Xia, Li, Qiuyun Chen, Walid Fazeli, et al.. (2018). De novo BK channel variant causes epilepsy by affecting voltage gating but not Ca2+ sensitivity. European Journal of Human Genetics. 26(2). 220–229. 41 indexed citations

10.

Becker, Kerstin, Peter Herkenrath, Friederike Körber, et al.. (2018). Dominant SCN2A Mutation Causes Familial Episodic Ataxia and Impairment of Speech Development. Neuropediatrics. 49(6). 379–384. 8 indexed citations

11.

Fazeli, Walid, Peter Herkenrath, Barbara Stiller, et al.. (2017). A TUBB6 mutation is associated with autosomal dominant non-progressive congenital facial palsy, bilateral ptosis and velopharyngeal dysfunction. Human Molecular Genetics. 26(20). 4055–4066. 15 indexed citations

12.

Fazeli, Walid, Stefania Zappettini, Stephan Lawrence Marguet, et al.. (2017). Early-life exposure to caffeine affects the construction and activity of cortical networks in mice. Experimental Neurology. 295. 88–103. 24 indexed citations

13.

Fazeli, Walid, Mert Karakaya, Peter Herkenrath, et al.. (2016). Mendeliome sequencing enables differential diagnosis and treatment of neonatal lactic acidosis. PubMed. 3(1). 22–22. 10 indexed citations

14.

Schattling, Benjamin, Walid Fazeli, Birgit Engeland, et al.. (2016). Activity of NaV1.2 promotes neurodegeneration in an animal model of multiple sclerosis. JCI Insight. 1(19). e89810–e89810. 23 indexed citations

15.

Fazeli, Walid, et al.. (2015). A novel mutation within the lactase gene (LCT): the first report of congenital lactase deficiency diagnosed in Central Europe. BMC Gastroenterology. 15(1). 90–90. 17 indexed citations

16.

Silva, Carla G., Christine Métin, Walid Fazeli, et al.. (2013). Adenosine Receptor Antagonists Including Caffeine Alter Fetal Brain Development in Mice. Science Translational Medicine. 5(197). 197ra104–197ra104. 134 indexed citations

17.

Fazeli, Walid, Birgit Engeland, Yi‐Chu Liao, et al.. (2013). A mutation in the SCN2A gene associated with BFNIS leads to seizures and behavioral impairment in a mouse model. Neuropediatrics. 44(2). 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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