H-Index & Metrics Best Publications

H-Index & Metrics

Discipline name H-index Citations Publications World Ranking National Ranking
Medicine D-index 79 Citations 21,108 268 World Ranking 9880 National Ranking 5318

Overview

What is she best known for?

The fields of study she is best known for:

  • Gene
  • Mutation
  • Internal medicine

Her primary areas of study are Frontotemporal dementia, Genetics, Pathology, Frontotemporal lobar degeneration and Amyotrophic lateral sclerosis. Her biological study spans a wide range of topics, including Alzheimer's disease, Tau protein and Neuroscience. As a part of the same scientific study, Rosa Rademakers usually deals with the Pathology, concentrating on Internal medicine and frequently concerns with Oncology.

Her Frontotemporal lobar degeneration research integrates issues from Charged multivesicular body protein 2B, RNA-Binding Protein FUS, Haploinsufficiency, Allele and Parkinsonism. The concepts of her Amyotrophic lateral sclerosis study are interwoven with issues in C9orf72 Protein, C9orf72, Neurodegeneration and Gene. Her C9orf72 Protein study combines topics in areas such as Translation, DNA Repeat Expansion and Gene expression.

Her most cited work include:

  • Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS (3097 citations)
  • TREM2 Variants in Alzheimer's Disease (1646 citations)
  • Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17 (1484 citations)

What are the main themes of her work throughout her whole career to date?

Her primary areas of investigation include Frontotemporal dementia, Pathology, Frontotemporal lobar degeneration, Genetics and C9orf72. Her work investigates the relationship between Frontotemporal dementia and topics such as Amyotrophic lateral sclerosis that intersect with problems in Neurodegeneration. Her Frontotemporal lobar degeneration research includes themes of Primary progressive aphasia, Haploinsufficiency and Asymptomatic.

Genetics is represented through her Mutation, Gene, Allele, Haplotype and Genome-wide association study research. Rosa Rademakers combines subjects such as C9orf72 Protein, DNA Repeat Expansion, RNA and Age of onset with her study of C9orf72. Her Progressive supranuclear palsy research is multidisciplinary, incorporating perspectives in Tau protein and Tauopathy.

She most often published in these fields:

  • Frontotemporal dementia (38.46%)
  • Pathology (34.71%)
  • Frontotemporal lobar degeneration (28.40%)

What were the highlights of her more recent work (between 2018-2021)?

  • Frontotemporal dementia (38.46%)
  • Frontotemporal lobar degeneration (28.40%)
  • Pathology (34.71%)

In recent papers she was focusing on the following fields of study:

Rosa Rademakers mainly focuses on Frontotemporal dementia, Frontotemporal lobar degeneration, Pathology, C9orf72 and Disease. Her Frontotemporal dementia study combines topics from a wide range of disciplines, such as Asymptomatic, Neuroscience and Atrophy. Her studies deal with areas such as Mutation, Clinical Dementia Rating, Microgliosis and Genetics as well as Frontotemporal lobar degeneration.

Rosa Rademakers interconnects Gyrification and Entorhinal cortex in the investigation of issues within Pathology. Her C9orf72 study introduces a deeper knowledge of Trinucleotide repeat expansion. She focuses mostly in the field of Disease, narrowing it down to topics relating to Gene and, in certain cases, Computational biology.

Between 2018 and 2021, her most popular works were:

  • Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report. (300 citations)
  • Heterochromatin anomalies and double-stranded RNA accumulation underlie C9orf72 poly(PR) toxicity (91 citations)
  • Systematic analysis of dark and camouflaged genes reveals disease-relevant genes hiding in plain sight (60 citations)

In her most recent research, the most cited papers focused on:

  • Gene
  • Internal medicine
  • Mutation

Her main research concerns Frontotemporal dementia, Frontotemporal lobar degeneration, C9orf72, Pathology and Disease. Her Frontotemporal dementia study integrates concerns from other disciplines, such as Neuropathology, Asymptomatic and Atrophy. Her Frontotemporal lobar degeneration research incorporates themes from Audiology, Motor neuron, Spinal cord, Primary progressive aphasia and Microgliosis.

The study incorporates disciplines such as Symptom onset, Functional magnetic resonance imaging, Neuroscience and Cell biology in addition to C9orf72. Her Pathology research is multidisciplinary, relying on both Hippocampal formation, Hippocampus, Entorhinal cortex and Neuroimaging. Amyotrophic lateral sclerosis is closely attributed to Genetics in her work.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

Mariely DeJesus-Hernandez;Ian R. Mackenzie;Bradley F. Boeve;Adam L. Boxer.
Neuron (2011)

3949 Citations

Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17

Matt Baker;Ian R. Mackenzie;Stuart M. Pickering-Brown;Jennifer Gass.
Nature (2006)

1860 Citations

TREM2 Variants in Alzheimer's Disease

Rita Guerreiro;Rita Guerreiro;Aleksandra Wojtas;Jose Bras;Minerva Carrasquillo.
The New England Journal of Medicine (2013)

1821 Citations

Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21

Marc Cruts;Ilse Gijselinck;Julie van der Zee;Sebastiaan Engelborghs.
Nature (2006)

1354 Citations

Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS

Hong Joo Kim;Nam Chul Kim;Yong Dong Wang;Emily A. Scarborough.
Nature (2013)

1089 Citations

Unconventional Translation of C9ORF72 GGGGCC Expansion Generates Insoluble Polypeptides Specific to c9FTD/ALS

Peter E.A. Ash;Kevin F. Bieniek;Tania F. Gendron;Thomas Caulfield.
Neuron (2013)

891 Citations

TDP-43 and FUS in amyotrophic lateral sclerosis and frontotemporal dementia

Ian R.A. Mackenzie;Rosa Rademakers;Manuela Neumann.
Lancet Neurology (2010)

880 Citations

A new subtype of frontotemporal lobar degeneration with FUS pathology.

Manuela Neumann;Rosa Rademakers;Sigrun Roeber;Matt Baker.
Brain (2009)

695 Citations

TDP-43 A315T Mutation in Familial Motor Neuron Disease

Michael A. Gitcho;Robert H. Baloh;Sumi Chakraverty;Kevin Mayo.
Annals of Neurology (2008)

692 Citations

Mutations in progranulin are a major cause of ubiquitin-positive frontotemporal lobar degeneration

Jennifer Gass;Ashley Cannon;Ian R. Mackenzie;Bradley Boeve.
Human Molecular Genetics (2006)

575 Citations

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