Regulation of amyloid-β molecular composition by altering spiking patterns in vivo.
Accumulated genetic evidence suggests that attenuation in the ratio between cerebral amyloid-β isoforms, Aβ40 and Aβ42, is central to familial Alzheimer’s disease pathogenesis. The composition of Aβ, namely Aβ40/42 ratio, has been shown to regulate the aggregation kinetics of the peptide in vitro and correlate with severity of the symptoms in AD patients. In order to understand the experience-dependent mechanism leading to AD I explore the relationship between spiking pattern and Aβ40/42 dynamics in vivo and molecular mechanisms underlying change in the Aβ composition by neuronal pattern of activity.
The 23rd ISFN Annual Meeting, 2014 – Presented poster
Vertkin I, Styr B, Slomowitz E, Ofir N, Shapira I, Berner D, Fedorova T, Laviv T, Barak-Broner N, Greitzer-Antes D, Gassmann M, Bettler B, Lotan I, Slutsky I. GABAB receptor deficiency causes failure of neuronal homeostasis in hippocampal networks; PNAS 2015; 112(25):E3291-9.
Shulman Y, Stavsky A, Fedorova T, Mikulincer D, Atias M, Radinsky I, Kahn J, Slutsky I, Gitler D. ATP binding to synaspsin IIa regulates usage and clustering of vesicles in terminals of hippocampal neurons; J Neuroscience 2015; 35(3):985-98
Mitkevich V.A., Petrushanko I.Y., Spirin P.V., Fedorova T.V., Kretova O.V., Tchurikov N.A., Prassolov V.S., Ilinskaya O.N., Makarov A.A.; Sensitivity of acute myeloid leukemia Kasumi-1 cells to binase toxic action depends on the expression of KIT and АML1-ETO oncogenes; Cell Cycle 2011 12-1; 10(23).
Dan David Prize scholarship recipient; 2014-2015 year
Research Categories: Brain Disorders, Cellular/molecular neuroscience