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Researcher · North Carolina Central University · United States

Tomas T. Ding

Tomas T. Ding publishes mostly in Neurology, Molecular Biology and Neurology, on topics such as Parkinson's Disease Mechanisms and Treatments, Genetic Neurodegenerative Diseases and Neurological disorders and treatments.

OpenAlex
World rank
#1,424,919
of 7,710,434 ranked researchers
Rank in United States
#449,242
of 1,627,098
Works
16
Citations
3.5k
Citations per work
216.2
h-index
10
i10-index 10Top 60% in Neurology (Medicine)
Tomas T. Ding

What does Tomas T. Ding research?

Tomas T. Ding's work is mostly in Medicine (31%), Biochemistry, Genetics and Molecular Biology (23%), Neuroscience (21%).

Life Sciences: 8 works · 47.9% of their workBiochemistry, Genetics and Molecular Biology: 4 works · 22.9% of their workMolecular Biology: 4 works · 22.9% of their workNeuroscience: 3 works · 20.8% of their workCellular and Molecular Neuroscience: 2 works · 10.4% of their workNeurology: 2 works · 10.4% of their workAgricultural and Biological Sciences: 1 works · 4.2% of their workPlant Science: 1 works · 4.2% of their workHealth Sciences: 5 works · 31.3% of their workMedicine: 5 works · 31.3% of their workNeurology: 4 works · 25.0% of their workPhysiology: 1 works · 6.3% of their workEverything else: 3 works · 20.8% of their workTHEIR WORKTomas T. Ding16works
Life Sciences48%Health Sciences31%

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 Biology422.9%
    2. Neuroscience320.8%
    3. Agricultural and Biological Sciences14.2%
    1. Medicine531.3%
  3. Everything else320.8%
  1. 1Neurology25% of their works
  2. 2Molecular Biology23% of their works
  3. 3Neurology10% of their works
  4. 4Cellular and Molecular Neuroscience10% of their works
  5. 5Physiology6% of their works
  6. 6Plant Science4% of their works

Research topics

Which keywords describe Tomas T. Ding's research?

The keywords of their largest research topics: Mitochondrial Dysfunction, Oxidative Stress, Neurodegeneration, Parkinson's Disease, a-Synuclein, Dopaminergic Neurons, Neurodegenerative Diseases and Deep Brain Stimulation.

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 21 words, with their numbers
  1. Mitochondrial Dysfunction154 topics
  2. Oxidative Stress144 topics
  3. Neurodegeneration113 topics
  4. Parkinson's Disease102 topics
  5. Dopaminergic Neurons61 topic
  6. a-Synuclein61 topic
  7. Neurodegenerative Diseases52 topics
  8. Deep Brain Stimulation41 topic
  9. Huntington's Disease41 topic
  10. Protein Aggregation41 topic
  11. Subthalamic Nucleus41 topic
  12. Amyloid Hypothesis31 topic
  13. Mitochondria31 topic
  14. Muscle Regeneration31 topic
  15. Reactive Oxygen Species31 topic
  16. Skeletal Muscle Atrophy31 topic
  17. Tau Pathology31 topic
  18. Brain Iron Accumulation21 topic
  19. Cerebral Hypoperfusion21 topic
  20. Pantothenate Kinase21 topic
  21. Vascular Cognitive Impairment21 topic

Where does Tomas T. Ding work?

Tomas T. Ding's main affiliation in the publication record is North Carolina Central University, United States.

How many publications and citations does Tomas T. Ding have?

OpenAlex counts 16 works and 3,459 citations for Tomas T. Ding, an h-index of 10, ranking #1,424,919 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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