Ilya Bezprozvanny, Ph.D.

Our goal is to understand the importance of calcium signaling in development of neurodegenerative disorders. Calcium ion (Ca2+) acts as an intracellular second messenger in living cells. Changes in the cytosolic Ca2+ level influence most fundamental cellular processes. Deranged calcium signaling results in a number of disorders. Local and rapid changes in cytosolic Ca2+ are evoked by activation of plasma membrane voltage-gated Ca2+ channels in response to membrane depolarization. Global changes in cytosolic Ca2+ are supported by intracellular Ca2+ release channels - the inositol (1,4,5)-trisphosphate receptor (InsP3R) and the ryanodine receptor(RyanR). The connection between abnormal neuronal calcium signaling and neurodegenerative disorders (Huntington's disease, ataxias, Alzheimer's disease) is the main focus of our research. We hope that our work will help in developing much needed cures for these lethal disorders.

Graduate School

Leningrad Polytechnic Institut (1988), Physics

Graduate School

St Petersburg Technical Instit (1992), Cell Biology

• Alzheimers disease
• Calcium channels and synaptic function
• Calcium signaling
• Huntingtons disease
• Neurodegeneration

Featured Publications

Reduced Synaptic STIM2 Expression and Impaired Store-Operated Calcium Entry Cause Destabilization of Mature Spines in Mutant Presenilin Mice.

Sun S, Zhang H, Liu J, Popugaeva E, Xu NJ, Feske S, White CL, Bezprozvanny I Neuron 2014 Apr 82 1 79-93

The synaptic maintenance problem: membrane recycling, Ca2+ homeostasis and late onset degeneration.

Bezprozvanny I, Hiesinger PR Mol Neurodegener 2013 8 23

Selective positive modulator of calcium-activated potassium channels exerts beneficial effects in a mouse model of spinocerebellar ataxia type 2.

Kasumu AW, Hougaard C, Rode F, Jacobsen TA, Sabatier JM, Eriksen BL, Strøbæk D, Liang X, Egorova P, Vorontsova D, Christophersen P, Rønn LC, Bezprozvanny I Chem. Biol. 2012 Oct 19 10 1340-53

Neuronal Store-Operated Calcium Entry Pathway as a Novel Therapeutic Target for Huntington's Disease Treatment.

Wu J, Shih HP, Vigont V, Hrdlicka L, Diggins L, Singh C, Mahoney M, Chesworth R, Shapiro G, Zimina O, Chen X, Wu Q, Glushankova L, Ahlijanian M, Koenig G, Mozhayeva GN, Kaznacheyeva E, Bezprozvanny I Chem. Biol. 2011 Jun 18 6 777-93

Role of presenilins in neuronal calcium homeostasis.

Zhang H, Sun S, Herreman A, De Strooper B, Bezprozvanny I J. Neurosci. 2010 Jun 30 25 8566-80

Familial Alzheimer's disease mutations in presenilins: effects on endoplasmic reticulum calcium homeostasis and correlation with clinical phenotypes.

Nelson O, Supnet C, Liu H, Bezprozvanny I J. Alzheimers Dis. 2010 21 3 781-93

Secondary structure of Huntingtin amino-terminal region.

Kim MW, Chelliah Y, Kim SW, Otwinowski Z, Bezprozvanny I Structure 2009 Sep 17 9 1205-12

Calcium signaling and neurodegenerative diseases.

Bezprozvanny I Trends Mol Med 2009 Mar 15 3 89-100

Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease.

Bezprozvanny I, Mattson MP Trends Neurosci. 2008 Sep 31 9 454-63

Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations.

Tu H, Nelson O, Bezprozvanny A, Wang Z, Lee SF, Hao YH, Serneels L, De Strooper B, Yu G, Bezprozvanny I Cell 2006 Sep 126 5 981-93

• Member of J. Biological Chemistry Editorial Board (2014)
• Member of Messenger Editorial Board (2012)
• Member of FACULTY of 1000 (2010)
• Member of Cell Calcium Editorial Board (2006)
• Biophysical Society, Member
• Society for Neuroscience, Member