Anna H. Hakonen

1.6k total citations
16 papers, 794 citations indexed

About

Anna H. Hakonen is a scholar working on Molecular Biology, Clinical Biochemistry and Cellular and Molecular Neuroscience. According to data from OpenAlex, Anna H. Hakonen has authored 16 papers receiving a total of 794 indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Molecular Biology, 8 papers in Clinical Biochemistry and 6 papers in Cellular and Molecular Neuroscience. Recurrent topics in Anna H. Hakonen's work include Mitochondrial Function and Pathology (10 papers), Metabolism and Genetic Disorders (8 papers) and Genetic Neurodegenerative Diseases (6 papers). Anna H. Hakonen is often cited by papers focused on Mitochondrial Function and Pathology (10 papers), Metabolism and Genetic Disorders (8 papers) and Genetic Neurodegenerative Diseases (6 papers). Anna H. Hakonen collaborates with scholars based in Finland, Norway and Australia. Anna H. Hakonen's co-authors include Anu Suomalainen, Anders Paetau, Tuula Lönnqvist, Pirjo Isohanni, Petri Luoma, Riitta Herva, Gert Van Goethem, Laurence A. Bindoff, Sofia Ahola and Maria Rantamäki and has published in prestigious journals such as Brain, Neurology and Scientific Reports.

In The Last Decade

Anna H. Hakonen

13 papers receiving 781 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Anna H. Hakonen Finland 10 687 425 211 87 71 16 794
Victoria Nesbitt United Kingdom 13 641 0.9× 414 1.0× 101 0.5× 38 0.4× 68 1.0× 22 741
L. He United Kingdom 9 665 1.0× 374 0.9× 127 0.6× 43 0.5× 55 0.8× 10 751
Maria Rantamäki Finland 8 512 0.7× 294 0.7× 238 1.1× 60 0.7× 62 0.9× 9 581
Marianna Bugiani Italy 9 600 0.9× 343 0.8× 98 0.5× 39 0.4× 48 0.7× 10 720
Anna Rubegni Italy 15 329 0.5× 110 0.3× 132 0.6× 38 0.4× 44 0.6× 47 493
Ese Mudanohwo United Kingdom 7 340 0.5× 165 0.4× 184 0.9× 190 2.2× 37 0.5× 10 495
Zarazuela Zolkipli‐Cunningham United States 14 406 0.6× 232 0.5× 64 0.3× 32 0.4× 79 1.1× 25 566
Marjan E. Steenweg Netherlands 11 509 0.7× 160 0.4× 42 0.2× 37 0.4× 31 0.4× 16 621
Alfonso Oyarzábal Spain 11 242 0.4× 156 0.4× 38 0.2× 76 0.9× 79 1.1× 18 452
Isabel Fineza Portugal 11 225 0.3× 89 0.2× 98 0.5× 29 0.3× 26 0.4× 25 341

Countries citing papers authored by Anna H. Hakonen

Since Specialization
Citations

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

Fields of papers citing papers by Anna H. Hakonen

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Anna H. Hakonen. 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 Anna H. Hakonen. The network helps show where Anna H. Hakonen may publish in the future.

Co-authorship network of co-authors of Anna H. Hakonen

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

All Works

16 of 16 papers shown
1.
Hakonen, Anna H., Ulla Wartiovaara‐Kautto, Sakari Kakko, et al.. (2024). Biallelic hexokinase 1 (HK1) variants causative of non‐spherocytic haemolytic anaemia: A case series with emphasis on the HK1 promoter variant and literature review. British Journal of Haematology. 204(5). 2040–2048.
2.
Sulonen, Anna-Maija, Henrikki Almusa, Vilma‐Lotta Lehtokari, et al.. (2024). Haplotype information of large neuromuscular disease genes provided by linked-read sequencing has a potential to increase diagnostic yield. Scientific Reports. 14(1). 4306–4306.
3.
Pardo, Luba M., et al.. (2023). Adding to the evidence of gene‐disease association of RAP1B and syndromic thrombocytopenia. Clinical Genetics. 105(2). 196–201.
4.
Hakonen, Anna H., Sirpa Kivirikko, Riikka Keski‐Filppula, et al.. (2020). Recessive MYH3 variants cause “Contractures, pterygia, and variable skeletal fusions syndrome 1B” mimicking Escobar variant multiple pterygium syndrome. American Journal of Medical Genetics Part A. 182(11). 2605–2610. 5 indexed citations
5.
Hakonen, Anna H., Anne Polvi, Carola Saloranta, et al.. (2019). SLC18A3 variants lead to fetal akinesia deformation sequence early in pregnancy. American Journal of Medical Genetics Part A. 179(7). 1362–1365. 8 indexed citations
6.
Lindeque, Jeremie Zander, Shayne Mason, Francois H. van der Westhuizen, et al.. (2018). A urinary biosignature for mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes (MELAS). Mitochondrion. 45. 38–45. 16 indexed citations
7.
Buzková, Jana, Joni Nikkanen, Sofia Ahola, et al.. (2018). Metabolomes of mitochondrial diseases and inclusion body myositis patients: treatment targets and biomarkers. EMBO Molecular Medicine. 10(12). 54 indexed citations
8.
Palin, Eino, et al.. (2011). Mitochondrial recessive ataxia syndrome mimicking dominant spinocerebellar ataxia. Journal of the Neurological Sciences. 315(1-2). 160–163. 14 indexed citations
9.
Isohanni, Pirjo, Anna H. Hakonen, Liliya Euro, et al.. (2011). POLG1 manifestations in childhood. Neurology. 76(9). 811–815. 38 indexed citations
10.
Hakonen, Anna H., Pirjo Isohanni, Maria Rantamäki, et al.. (2010). [Mitochondrial recessive ataxia syndrome (MIRAS) and valproate toxicity].. PubMed. 126(13). 1552–9. 11 indexed citations
11.
Hakonen, Anna H., Pirjo Isohanni, Maria Rantamäki, et al.. (2010). Mitokondriaalinen resessiivinen ataksiasyndrooma ja valproaattihoidon toksisuus. Tampere University Institutional Repository (Tampere University). 126(13). 1552–1559. 9 indexed citations
12.
Hakonen, Anna H., Steffi Goffart, Sanna Marjavaara, et al.. (2008). Infantile-onset spinocerebellar ataxia and mitochondrial recessive ataxia syndrome are associated with neuronal complex I defect and mtDNA depletion. Human Molecular Genetics. 17(23). 3822–3835. 94 indexed citations
13.
Hakonen, Anna H., Pirjo Isohanni, Anders Paetau, et al.. (2007). Recessive Twinkle mutations in early onset encephalopathy with mtDNA depletion. Brain. 130(11). 3032–3040. 145 indexed citations
14.
Hakonen, Anna H., Guido Davidzon, Renato Salemi, et al.. (2007). Abundance of the POLG disease mutations in Europe, Australia, New Zealand, and the United States explained by single ancient European founders. European Journal of Human Genetics. 15(7). 779–783. 60 indexed citations
15.
Luoma, Petri, Johanna Eerola, Sofia Ahola, et al.. (2007). Mitochondrial DNA polymerase gamma variants in idiopathic sporadic Parkinson disease. Neurology. 69(11). 1152–1159. 113 indexed citations
16.
Hakonen, Anna H., Vesa Juvonen, Petri Luoma, et al.. (2005). Mitochondrial DNA Polymerase W748S Mutation: A Common Cause of Autosomal Recessive Ataxia with Ancient European Origin. The American Journal of Human Genetics. 77(3). 430–441. 227 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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