Photo of Mel Feany,  MD, PhD

Mel Feany, MD, PhD

Brigham And Women's Hospital

Brigham And Women's Hospital
Phone: (617) 525-4405
Fax: (617) 525-4422


mel_feany@hms.harvard.edu

Mel Feany, MD, PhD

Brigham And Women's Hospital

EDUCATIONAL TITLES

  • Professor, Pathology, Harvard Medical School
  • Associate Pathologist and Neuropathologist, Pathology, Brigham And Women's Hospital

DF/HCC PROGRAM AFFILIATION

Research Abstract

My laboratory has created models of diseases, including models of progressive neurological degenerations and cancer, in Drosophila. We are now exploiting genetic analysis in Drosophila with confirmatory studies in a variety of model organisms and in patients to investigate the role of various cellular pathways, including control of cell cycle, in these disorders. My clinical research has also focused on the control of cell cycle with studies of the proliferative potential of human astrocytes in the adult and pediatric brain.

Publications

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  • Hegde VR, Vogel R, Feany MB. Glia are critical for the neuropathology of complex I deficiency in Drosophila. Hum Mol Genet 2014. PubMed
  • Frost B, Hemberg M, Lewis J, Feany MB. Tau promotes neurodegeneration through global chromatin relaxation. Nat Neurosci 2014; 17:357-66. PubMed
  • Chen L, Periquet M, Wang X, Negro A, McLean PJ, Hyman BT, Feany MB. Tyrosine and serine phosphorylation of alpha-synuclein have opposing effects on neurotoxicity and soluble oligomer formation. J Clin Invest 2009; 119:3257-65. PubMed
  • McFarland NR, Fan Z, Xu K, Schwarzschild MA, Feany MB, Hyman BT, McLean PJ. alpha-Synuclein S129 Phosphorylation Mutants Do Not Alter Nigrostriatal Toxicity in a Rat Model of Parkinson Disease. J Neuropathol Exp Neurol 2009; 68:515-524. PubMed
  • Zhang S,Feany MB,Saraswati S,Littleton JT,Perrimon N. Inactivation of Drosophila Huntingtin affects long-term adult functioning and the pathogenesis of a Huntington's disease model. Dis Model Mech 2009; 2:247-66. PubMed
  • Cullen V,Lindfors M,Ng J,Paetau A,Swinton E,Kolodziej P,Boston H,Saftig P,Woulfe J,Feany MB,Myllykangas L,Schlossmacher MG,Tyynela J. Cathepsin D expression level affects alpha-synuclein processing, aggregation, and toxicity in vivo. Mol Brain 2009; 2:5. PubMed
  • Dufty BM, Warner LR, Hou ST, Jiang SX, Gomez-Isla T, Leenhouts KM, Oxford JT, Feany MB, Masliah E, Rohn TT. Calpain-Cleavage of {alpha}-Synuclein: Connecting Proteolytic Processing to Disease-Linked Aggregation. Am J Pathol 2007; 170:1725-38. PubMed
  • Steinhilb ML, Dias-Santagata D, Mulkearns EE, Shulman JM, Biernat J, Mandelkow EM, Feany MB. S/P and T/P phosphorylation is critical for tau neurotoxicity in Drosophila. J Neurosci Res 2007; 85:1271-8. PubMed
  • Khurana V, Feany MB. Connecting cell-cycle activation to neurodegeneration in Drosophila. Biochim Biophys Acta 2006; 1772:446-56. PubMed
  • Periquet M, Fulga T, Myllykangas L, Schlossmacher MG, Feany MB. Aggregated alpha-synuclein mediates dopaminergic neurotoxicity in vivo. J Neurosci 2007; 27:3338-46. PubMed
  • Fulga TA, Elson-Schwab I, Khurana V, Steinhilb ML, Spires TL, Hyman BT, Feany MB. Abnormal bundling and accumulation of F-actin mediates tau-induced neuronal degeneration in vivo. Nat Cell Biol 2006; 9:139-48. PubMed
  • Dias-Santagata D, Fulga TA, Duttaroy A, Feany MB. Oxidative stress mediates tau-induced neurodegeneration in Drosophila. J Clin Invest 2006; 117:236-45. PubMed
  • Gavin BA, Dolph MJ, Deleault NR, Geoghegan JC, Khurana V, Feany MB, Dolph PJ, Supattapone S. Accelerated accumulation of misfolded prion protein and spongiform degeneration in a Drosophila model of Gerstmann-Str舫ssler-Scheinker syndrome. J Neurosci 2006; 26:12408-14. PubMed
  • Kontopoulos E, Parvin JD, Feany MB. Alpha-synuclein acts in the nucleus to inhibit histone acetylation and promote neurotoxicity. Hum Mol Genet 2006; 15:3012-23. PubMed
  • Khurana V, Lu Y, Steinhilb ML, Oldham S, Shulman JM, Feany MB. TOR-mediated cell-cycle activation causes neurodegeneration in a Drosophila tauopathy model. Curr Biol 2006; 16:230-41. PubMed
  • Orso G, Martinuzzi A, Rossetto MG, Sartori E, Feany M, Daga A. Disease-related phenotypes in a Drosophila model of hereditary spastic paraplegia are ameliorated by treatment with vinblastine. J Clin Invest 2005; 115:3026-34. PubMed
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