Robert Max Friedlander
Robert Max Friedlander publishes mostly in Neurology, Molecular Biology and Cellular and Molecular Neuroscience, on topics such as Intracranial Aneurysms: Treatment and Complications, Mitochondrial Function and Pathology and Genetic Neurodegenerative Diseases.
- World rank
- #439,958 of 7,710,434 ranked researchers
- Rank in United States
- #154,842 of 1,627,098
- Works
- 321
- Citations
- 20k
- Citations per work
- 61.5
What does Robert Max Friedlander research?
Robert Max Friedlander's work is mostly in Medicine (29%), Biochemistry, Genetics and Molecular Biology (15%), Neuroscience (14%).
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
- Everything else13441.7%
- Life Sciences9529.6%
- Biochemistry, Genetics and Molecular Biology4815.1%
- Neuroscience4714.5%
- Health Sciences9228.7%
- Medicine9228.7%
- 1Neurology20% of their works
- 2Molecular Biology15% of their works
- 3Cellular and Molecular Neuroscience11% of their works
- 4Surgery6% of their works
- 5Neurology3% of their works
- 6Pulmonary and Respiratory Medicine3% of their works
Research topics
- Intracranial Aneurysms: Treatment and Complications
- Mitochondrial Function and Pathology
- Genetic Neurodegenerative Diseases
- Vascular Malformations Diagnosis and Treatment
- Traumatic Brain Injury and Neurovascular Disturbances
- Cerebrospinal fluid and hydrocephalus
- Neuroinflammation and Neurodegeneration Mechanisms
- Intracerebral and Subarachnoid Hemorrhage Research
Which keywords describe Robert Max Friedlander's research?
The keywords of their largest research topics: Endovascular Treatment, Mitochondrial Dysfunction, Neuroinflammation, Aneurysmal Subarachnoid Hemorrhage, Intracranial Aneurysms, Mitochondria, Reactive Oxygen Species and Huntington's Disease.
- Cerebral Amyloid Angiopathy
- Microglia
- Cerebrospinal Fluid
- Pathophysiology
- Arteriovenous Malformations
- Huntington's Disease
- Mitochondria
- Aneurysmal Subarachnoid Hemorrhage
- Mitochondrial Dysfunction
- Endovascular Treatment
- Neuroinflammation
- Intracranial Aneurysms
- Reactive Oxygen Species
- Protein Aggregation
- Cerebral Cavernous Malformations
- Traumatic Brain Injury
- Glymphatic System
- Neurodegeneration
- Intracerebral Hemorrhage
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 19 words, with their numbers
- Endovascular Treatment842 topics
- Mitochondrial Dysfunction832 topics
- Neuroinflammation643 topics
- Aneurysmal Subarachnoid Hemorrhage511 topic
- Intracranial Aneurysms511 topic
- Mitochondria471 topic
- Reactive Oxygen Species471 topic
- Huntington's Disease361 topic
- Protein Aggregation361 topic
- Arteriovenous Malformations331 topic
- Cerebral Cavernous Malformations331 topic
- Pathophysiology241 topic
- Traumatic Brain Injury241 topic
- Cerebrospinal Fluid211 topic
- Glymphatic System211 topic
- Microglia211 topic
- Neurodegeneration211 topic
- Cerebral Amyloid Angiopathy191 topic
- Intracerebral Hemorrhage191 topic
Where does Robert Max Friedlander work?
Robert Max Friedlander's main affiliation in the publication record is Neurological Surgery, United States.
How many publications and citations does Robert Max Friedlander have?
OpenAlex counts 321 works and 19,751 citations for Robert Max Friedlander, an h-index of 67, ranking #439,958 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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