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Researcher · Universitat de Barcelona · Spain

EDUARDO S. TOLOSA

EDUARDO S. TOLOSA publishes mostly in Neurology, Cellular and Molecular Neuroscience and Neurology, on topics such as Parkinson's Disease Mechanisms and Treatments, Neurological disorders and treatments and Genetic Neurodegenerative Diseases.

ORCID 0000-0002-3781-0854 OpenAlex
World rank
#43,885
of 7,710,434 ranked researchers
Rank in Spain
#460
of 204,306
Works
578
Citations
53k
Citations per work
92.1
h-index
113
i10-index 404Top 0.1% in Neurology (Medicine)
EDUARDO S. TOLOSA

What does EDUARDO S. TOLOSA research?

EDUARDO S. TOLOSA's work is mostly in Medicine (54%), Neuroscience (18%), Biochemistry, Genetics and Molecular Biology (4%).

Health Sciences: 309 works · 53.5% of their workMedicine: 309 works · 53.5% of their workNeurology: 282 works · 48.8% of their workPhysiology: 27 works · 4.7% of their workEverything else: 141 works · 24.4% of their workLife Sciences: 128 works · 22.1% of their workNeuroscience: 107 works · 18.5% of their workCellular and Molecular Neuroscience: 51 works · 8.8% of their workNeurology: 31 works · 5.3% of their workCognitive Neuroscience: 25 works · 4.4% of their workBiochemistry, Genetics and Molecular Biology: 21 works · 3.6% of their workMolecular Biology: 21 works · 3.6% of their workTHEIR WORKEDUARDO S. TOLOSA578works
Life Sciences22%Health Sciences54%

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. Medicine30953.5%
  2. Everything else14124.4%
    1. Neuroscience10718.5%
    2. Biochemistry, Genetics and Molecular Biology213.6%
  1. 1Neurology49% of their works
  2. 2Cellular and Molecular Neuroscience9% of their works
  3. 3Neurology5% of their works
  4. 4Physiology5% of their works
  5. 5Cognitive Neuroscience4% of their works
  6. 6Molecular Biology4% of their works

Research topics

Which keywords describe EDUARDO S. TOLOSA's research?

The keywords of their largest research topics: Parkinson's Disease, Mitochondrial Dysfunction, Neurodegeneration, Oxidative Stress, Diagnostic Criteria, a-Synuclein, Dopaminergic Neurons and Neurological Disorders.

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 23 words, with their numbers
  1. Parkinson's Disease6673 topics
  2. Mitochondrial Dysfunction5063 topics
  3. Neurodegeneration4743 topics
  4. Oxidative Stress4242 topics
  5. Diagnostic Criteria4202 topics
  6. Dopaminergic Neurons3871 topic
  7. a-Synuclein3871 topic
  8. Neurological Disorders3694 topics
  9. Deep Brain Stimulation2802 topics
  10. Basal Ganglia2401 topic
  11. Subthalamic Nucleus2401 topic
  12. Huntington's Disease691 topic
  13. Protein Aggregation691 topic
  14. Botulinum Toxin561 topic
  15. Neurotoxins561 topic
  16. Brain Iron Accumulation501 topic
  17. Pantothenate Kinase501 topic
  18. Camptocormia401 topic
  19. Dropped Head Syndrome401 topic
  20. Amyloid Hypothesis371 topic
  21. Tau Pathology371 topic
  22. Epidemiology331 topic
  23. Restless Legs Syndrome331 topic

Where does EDUARDO S. TOLOSA work?

EDUARDO S. TOLOSA's main affiliation in the publication record is Universitat de Barcelona, Spain.

How many publications and citations does EDUARDO S. TOLOSA have?

OpenAlex counts 578 works and 53,229 citations for EDUARDO S. TOLOSA, an h-index of 113, ranking #43,885 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.

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