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Tania F. Gendron

Tania F. Gendron

D-Index & Metrics

Biology and Biochemistry

D-Index
70
Citations
18543
World Ranking
6973
National Ranking
3209

Overview

Tania F. Gendron is affiliated with the Mayo Clinic in the United States. Their research primarily spans the fields of Medicine and Biochemistry, Genetics and Molecular Biology, with significant contributions to Neurology, Molecular Biology, and Genetics subfields.

The central topics of their work include Amyotrophic Lateral Sclerosis (ALS) Research, Neurogenetic and Muscular Disorders Research, Parkinson's Disease Mechanisms and Treatments, Alzheimer's Disease research and treatments, Genetic Neurodegenerative Diseases, Prion Diseases and Protein Misfolding, and RNA Research and Splicing.

Gendron has coauthored numerous publications with recurring collaborators, including Leonard Petrucelli, Bradley F. Boeve, Dennis W. Dickson, Hilary W. Heuer, and Adam M. Staffaroni.

Their scientific output is frequently published in several key venues, including:

  • bioRxiv (Cold Spring Harbor Laboratory)
  • Science Translational Medicine
  • Alzheimer's & Dementia
  • Molecular Neurodegeneration
  • Brain

Their notable recent papers encompass:

  • "Truncated stathmin-2 is a marker of TDP-43 pathology in frontotemporal dementia" (2020), Journal of Clinical Investigation
  • "Reduced C9ORF72 function exacerbates gain of toxicity from ALS/FTD-causing repeat expansion in C9orf72" (2020), Nature Neuroscience
  • "C9orf72 poly(GR) aggregation induces TDP-43 proteinopathy" (2020), Science Translational Medicine
  • "Temporal order of clinical and biomarker changes in familial frontotemporal dementia" (2022), Nature Medicine
  • "Preventing amyotrophic lateral sclerosis: insights from pre-symptomatic neurodegenerative diseases" (2021), Brain

Best Publications

  • 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

  • Targeting RNA Foci in iPSC-Derived Motor Neurons from ALS Patients with a C9ORF72 Repeat Expansion

    Dhruv Sareen;Jacqueline G. O’Rourke;Pratap Meera;A. K. M. G. Muhammad

  • Aberrant Cleavage of TDP-43 Enhances Aggregation and Cellular Toxicity

    Yong Jie Zhang;Ya Fei Xu;Casey Cook;Tania F. Gendron

  • Wild-Type Human TDP-43 Expression Causes TDP-43 Phosphorylation, Mitochondrial Aggregation, Motor Deficits, and Early Mortality in Transgenic Mice

    Ya Fei Xu;Tania F. Gendron;Yong Jie Zhang;Wen Lang Lin

  • Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS

    Tania F Gendron;Kevin F. Bieniek;Yong-Jie Zhang;Karen Jansen-West

  • The role of tau in neurodegeneration

    Tania F Gendron;Leonard Petrucelli

  • Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

    Jie Jiang;Jie Jiang;Qiang Zhu;Tania F. Gendron;Shahram Saberi

  • C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits

    Jeannie Chew;Tania F. Gendron;Mercedes Prudencio;Hiroki Sasaguri

  • Distinct brain transcriptome profiles in C9orf72-associated and sporadic ALS

    Mercedes Prudencio;Veronique V Belzil;Ranjan Batra;Christian A Ross

  • Poly(GR) in C9ORF72-Related ALS/FTD Compromises Mitochondrial Function and Increases Oxidative Stress and DNA Damage in iPSC-Derived Motor Neurons.

    Rodrigo Lopez-Gonzalez;Yubing Lu;Tania F. Gendron;Anna Karydas

  • Discovery of a Biomarker and Lead Small Molecules to Target r(GGGGCC)-Associated Defects in c9FTD/ALS

    Zhaoming Su;Yongjie Zhang;Tania F. Gendron;Peter O. Bauer

  • Modeling key pathological features of frontotemporal dementia with C9ORF72 repeat expansion in iPSC-derived human neurons

    Sandra Almeida;Eduardo Gascon;Hélène Tran;Hsin Jung Chou

  • Aggregation-prone c9FTD/ALS poly(GA) RAN-translated proteins cause neurotoxicity by inducing ER stress

    Yong Jie Zhang;Karen Jansen-West;Ya Fei Xu;Tania F. Gendron

  • Reduced C9orf72 gene expression in c9FTD/ALS is caused by histone trimethylation, an epigenetic event detectable in blood.

    Veronique V. Belzil;Peter O Bauer;Mercedes Prudencio;Tania F Gendron

  • Autophagic-lysosomal perturbation enhances tau aggregation in transfectants with induced wild-type tau expression.

    Tadanori Hamano;Tania F. Gendron;Ena Causevic;Shu Hui Yen

  • C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins

    Yong Jie Zhang;Tania F. Gendron;Jonathan C. Grima;Hiroki Sasaguri

  • Amyotrophic Lateral Sclerosis: An Update for 2018

    Bjorn E Oskarsson;Tania F. Gendron;Nathan P. Staff

  • Poly(GR) impairs protein translation and stress granule dynamics in C9orf72-associated frontotemporal dementia and amyotrophic lateral sclerosis

    Yong Jie Zhang;Tania F. Gendron;Mark T.W. Ebbert;Aliesha D. O’Raw

  • Acetylation of the KXGS motifs in tau is a critical determinant in modulation of tau aggregation and clearance

    Casey Cook;Yari Carlomagno;Tania F. Gendron;Judy Dunmore

  • Human C9ORF72 Hexanucleotide Expansion Reproduces RNA Foci and Dipeptide Repeat Proteins but Not Neurodegeneration in BAC Transgenic Mice

    Owen Morgan Peters;Gabriela Toro Cabrera;Helene Tran;Tania F. Gendron

Frequent Co-Authors

Rosa Rademakers
Rosa Rademakers University of Antwerp
Bradley F. Boeve
Bradley F. Boeve Mayo Clinic
Dieter Edbauer
Dieter Edbauer German Center for Neurodegenerative Diseases
David S. Knopman
David S. Knopman Mayo Clinic
Keith A. Josephs
Keith A. Josephs Mayo Clinic
Fen-Biao Gao
Fen-Biao Gao University of Massachusetts Chan Medical School
Ronald C. Petersen
Ronald C. Petersen University of Pennsylvania

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