Dr. Arbel is a former Alzheimer’s Disease Research Unit fellow in the Neurology Department’s MassGeneral Institute for Neurodegenerative Disease, where she continues her research.

  • Lab Phone: 617-724-1259

Research Investigator Profile

Michal Arbel

Michal Arbel (Arbel-Ornath) MSc, PhD

  • Instructor in Neurology,
    Harvard Medical School

 

 

Research Description

Dr. Arbel's research interests include developing therapeutic strategies to neurodegenerative diseases in which protein misfolding is implicated.  Her research focuses on understanding the molecular mechanisms underlying Alzheimer’s disease (AD) that lead to neurodegeneration with the hope that our findings will reveal new therapeutic targets. 

Previous work in Dr. Bacskai's lab showed that AD mouse models exhibit calcium dysregulation in the presence of amyloid plaques. Plaques also serve as a reservoir rich in soluble oligomeric forms of Aβ.  It is still not known which species of Aβ, soluble oligomers or deposits are the culprit. We are also trying to understand the selective vulnerability of a subpopulation of neurons. My work has demonstrated that specific naturally occurring oligomeric species of Aβ are responsible for calcium dysregulation and involves the activation of NMDA receptors, and requires the presence of ApoE.

My second major project is related to the accumulation of Aβ within the wall of cerebral arteries and capillaries (CAA) that is associated with the majority of AD cases and on its own. 

 

Research interests PrPC Proteins, Amyloid Precursor Protein Secretases, Amyloid beta-Protein Precursor, Immunotherapy
Research techniques Multiphoton in vivo imaging, AD mouse models
Diseases studied Alzheimer's disease
Selected publications

NCBI PubMed link - Arbel-Ornath
NCBI PubMed link - Arbel-Ornath

  1. Wu, H., Hudry, E., Hashimoto, T., Kuchibhotla, KV, Rozkalne, A., Fan, Z., Spires-Jones, T., Xie, H., Arbel-Ornath, M., Grosskreutz, CL.,  Bacskai, BJ.,Hyman, BT,  2010. Calcineurin (CaN)/NFAT Activation Mediates the Amyloid Beta (Ab)-induced Morphological Neurodegenerative Triad of Spine Loss, Dendritic Simplification, and Neuritic Dystrophies. Journal Neurosci 30(7):2636-49.
  2. Arbel-Ornath, M., Becker, M.,Rabinovich-Toidman, P., Gartner, M. and Solomon, B. 2010. APP β-site antibody alleviates Aβ related pathology in Alzhiomer’s disease mice model. J Alzheimers Dis. 22(2):469-82.
  3. Hudry E, Wu HY, Arbel-Ornath M, Hashimoto T, Matsouaka R, Fan Z, Spires-Jones TL, Betensky RA, Bacskai BJ, Hyman BT. 2012. Inhibition of the NFAT pathway alleviates amyloid β neurotoxicity in a mouse model of Alzheimer's disease. J Neurosci. 32(9):3176-92.
  4. Gregory JL, Prada CM, Fine SJ, Garcia-Alloza M, Betensky RA, Arbel-Ornath M, Greenberg SM, Bacskai BJ, Frosch MP. 2012. Reducing available soluble β-amyloid prevents progression of cerebral amyloid angiopathy in transgenic  mice. J NeuropatholExp Neurol.  71(11):1009-17.
  5. Arbel-Ornath M, Hudry E, Eikermann-Haerter K, Hou S, Gregory JL, Zhao L, Betensky RA, Frosch MP, Greenberg SM, Bacskai BJ (2013) Interstitial fluid drainage is impaired in ischemic stroke and Alzheimer's disease mouse models. Acta neuropathologica 126: 353-364 Doi 10.1007/s00401-013-1145-2
Lab mailing address MassGeneral Institute for Neurodegenerative Disease
Room 2001
114 16th Street
Charlestown MA 02129

 

 

Updated 9/27/2013