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Researcher · Siena Biotech (Italy) · Italy

Letizia Magnoni

Letizia Magnoni publishes mostly in Molecular Biology, Cellular and Molecular Neuroscience and Oncology, on topics such as Genetic Neurodegenerative Diseases, Muscle Physiology and Disorders and Glioma Diagnosis and Treatment.

ORCID 0000-0001-8525-033X OpenAlex
World rank
#2,995,147
of 7,710,434 ranked researchers
Rank in Italy
#101,166
of 242,206
Works
31
Citations
1k
Citations per work
32.7
h-index
14
i10-index 17Top 55% in Molecular Biology
Letizia Magnoni

What does Letizia Magnoni research?

Letizia Magnoni's work is mostly in Biochemistry, Genetics and Molecular Biology (35%), Neuroscience (14%), Medicine (13%).

Life Sciences: 15 works · 48.9% of their workBiochemistry, Genetics and Molecular Biology: 11 works · 34.9% of their workMolecular Biology: 11 works · 34.9% of their workNeuroscience: 4 works · 14.0% of their workCellular and Molecular Neuroscience: 4 works · 14.0% of their workEverything else: 9 works · 28.9% of their workHealth Sciences: 4 works · 12.8% of their workMedicine: 4 works · 12.8% of their workOncology: 3 works · 8.1% of their workGenetics: 1 works · 4.7% of their workPhysical Sciences: 3 works · 9.4% of their workChemistry: 1 works · 4.7% of their workSpectroscopy: 1 works · 4.7% of their workComputer Science: 1 works · 4.7% of their workArtificial Intelligence: 1 works · 4.7% of their workTHEIR WORKLetizia Magnoni31works
Life Sciences49%Physical Sciences9%Health Sciences13%

Their six largest subfields, inside their fields and domains; the grey slice is everything else they publish. The interactive view splits every one of their works down to single topics.

The fields and subfields, with their numbers
    1. Biochemistry, Genetics and Molecular Biology1134.9%
    2. Neuroscience414.0%
  2. Everything else928.9%
    1. Medicine412.8%
    1. Chemistry14.7%
    2. Computer Science14.7%
  1. 1Molecular Biology35% of their works
  2. 2Cellular and Molecular Neuroscience14% of their works
  3. 3Oncology8% of their works
  4. 4Spectroscopy5% of their works
  5. 5Artificial Intelligence5% of their works
  6. 6Genetics5% of their works

Research topics

Which keywords describe Letizia Magnoni's research?

The keywords of their largest research topics: Mitochondrial Dysfunction, Huntington's Disease, Protein Aggregation, Stem Cells, Mitochondria, Oxidative Stress, Cancer and Gene Expression.

Size is their works in the topics tagged with each word, from their 8 largest topics. Each links to the topic it comes from most. The words come from the keyword list OpenAlex gives each topic, not from the text of the papers, so a word can appear that none of the papers uses.

All 22 words, with their numbers
  1. Mitochondrial Dysfunction132 topics
  2. Huntington's Disease101 topic
  3. Protein Aggregation101 topic
  4. Stem Cells72 topics
  5. Mitochondria62 topics
  6. Oxidative Stress62 topics
  7. Cancer52 topics
  8. Gene Expression42 topics
  9. Glioblastoma41 topic
  10. Muscle Regeneration41 topic
  11. Skeletal Muscle Atrophy41 topic
  12. Temozolomide41 topic
  13. Cell Death31 topic
  14. Development31 topic
  15. Hedgehog Signaling31 topic
  16. Reactive Oxygen Species31 topic
  17. Resveratrol31 topic
  18. Sirtuins31 topic
  19. Data Analysis21 topic
  20. MicroRNA21 topic
  21. Microarray21 topic
  22. Regulation21 topic

Where does Letizia Magnoni work?

Letizia Magnoni's main affiliation in the publication record is Siena Biotech (Italy), Italy.

How many publications and citations does Letizia Magnoni have?

OpenAlex counts 31 works and 1,013 citations for Letizia Magnoni, an h-index of 14, ranking #2,995,147 of 7,710,434 researchers worldwide on the quality score.

Ranked on field-normalised citation excellence (50%), output (30%) and citations (20%). Counts come from OpenAlex author records, which occasionally merge different people who share a name or split one person into several.

Papers, co-authors, who cited this work and researchers on the nearest topics have tabs of their own, above. Is this your page? Claim it with your ORCID iD, or request a correction or removal.

Discussion

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