Dora M. Kovacs, Ph.D.

Headshot photo

Neurobiology of Disease Laboratory
Genetics and Aging Research Unit
Massachusetts General Hospital

Dr. Kovacs has over fifteen years of molecular and cell biology research experience. She joined the Genetics and Aging Research Unit in 1993 as a postdoctoral fellow, to study the role of the amyloid precursor protein (APP) in Alzheimer's disease. She has since co-authored over fifteen original articles in peer-reviewed journals, over ten chapters or reviews, and is co-inventor on three patents. She has served for several years on the Review Board of the Medical and Scientific Advisory Council of the Alzheimer's Association, and most recently on the Editorial Board of The Scientific World. For her contributions to research on the molecular basis of Alzheimer's disease, she received the Britton Fellowship for Research in Alzheimer's disease, the French Foundation for Alzheimer Research Fellowship, and the Neurosciences Education and Research Foundation Award.

Dr. Kovacs received a summa cum laude BS-MS degree in Biology from the University of Bologna, Italy, and a Ph.D. in Pharmacology and Toxicology from the University of Padova, Italy, in 1991. While earning her Ph.D. degree in Italy, she performed her research at the Division of Neuropathology, Case Western Reserve University, Cleveland.

Funded Research

Project Description Researchers Funding
Optimization of Novel ACAT Inhibitors for Alzheimer's Disease

The goal of this project is to test three novel ACAT inhibitors to determine whether they will prevent development of amyloid pathology and alter APP processing in AD mice in order to prevent and treat AD.

Three Studies of ACAT Inhibitors as Potential Therapies for AD

It is known that high cholesterol is associated with cardiovascular disease. Cholesterol also regulates the production of the toxic amyloid beta (Aβ) peptide in Alzheimer’s disease (AD). Therapies already developed or in development for dyslipidemia and atherosclerosis are becoming attractive for reducing Aβ in the brains of patients affected by AD. We have previously reported that drugs specifically targeting one step of the cholesterol pathway, acyl-coenzyme A: cholesterol acyltransferase (ACAT) inhibitors, reduced generation of toxic Aβ peptide in cells and an animal model of AD.

2004 to 2010


Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.
Carla D’Avanzo, Christopher Sliwinski, Steven L. Wagner, Rudolph E. Tanzi, Doo Yeon Kim, and Dora M. Kovacs, γ-Secretase modulators reduce endogenous amyloid β42 levels in human neural progenitor cells without altering neuronal differentiation, The FASEB Journal, 29(8), 22 April 2015, 3335-3341
Raja Bhattacharyya, Cory Barren, Dora M. Kovacs, Palmitoylation of Amyloid Precursor Protein Regulates Amyloidogenic Processing in Lipid Rafts, The Journal of Neuroscience, 33(27), 3 July 2013, 11169-83
Sachse CC, Kim YH, Agsten M, Huth T, Alzheimer C, Kovacs DM, Kim DY, BACE1 and presenilin/γ-secretase regulate proteolytic processing of KCNE1 and 2, auxiliary subunits of voltage-gated potassium channels, FASEB J, 27(6), June 2013, 2458-67
Dong Y, Wu X, Zhang G, Xu Z, Zhang Y, Gautam V, Kovacs DM, Wu A, Yue Y, Xie Z, Isoflurane facilitates synaptic NMDA receptor endocytosis in mice primary neurons, Curr Mol Med., Sep 3, 2012
Huttunen HJ, Hutter-Paier B, Barren C, Peach C, Havas D, Duller S, Xia W, Frosch MP, Windisch M, Kovacs DM., The acyl-coenzyme A: cholesterol acyltransferase inhibitor CI-1011 reverses diffuse brain amyloid pathology in aged amyloid precursor protein transgenic mice, Journal of Neuropathology and Experimental Neurology, 69(8), August 2010, 777-88