Skip Navigation
Search Menu
Find an Expert

 


Shaida A Andrabi, M.Sc., Ph.D.

Syed Shaida Ahmad Andrabi, M.Sc., Ph.D.

Photo of Dr. Shaida A Andrabi, M.Sc., Ph.D.

Assistant Professor of Neurology

Expertise: Brain Injury, Stroke

Research Interests: Neuroregeneration; Parkinsons disease; Molecular pathways of cell death and pathogenesis of stroke

Contact for Research Inquiries

Wilmer Building
600 N. Wolfe Street
Phone: 443-287-0171
Fax: 410-614-9568

Email me

Background

Shaida Andrabi, Ph.D., is an Assistant Professor in the Department of Neurology. Dr. Andrabi has extensive experience in mitochondrial biology, bioenergetics, and glucose metabolism. His research investigates the molecular mechanisms of mitochondrial and metabolic alteration in neurodegeneration.

Dr. Andrabi has demonstrated an excellence in collaborating and working with other investigators while excelling at his own studies. He provides a major support for the Bioenergetics Core B due to his considerable knowledge in mitochondrial biology and bioenergetics. He supervises the daily activities of the Bioenergetics Core B while working closely with other investigators of the Udall Center.

...read more

Titles

  • Assistant Professor of Neurology

Departments / Divisions

Education

Degrees

  • M.Sc., Hamdard University (India) (1999)
  • Ph.D., Otto Von Guerick University - Magdeburg (East Germany) (2004)

Research & Publications

Research Summary

Stroke is a leading cause of death and disability with no effective treatment available. There is a critical need to understand the molecular pathways of cell death in stroke so that important therapeutic targets can be identified. Defects in glucose metabolism, bioenergetic failure, mitochondrial damage and redox imbalance are all major hallmarks in the pathogenesis of stroke. The Andrabi lab studies molecular pathways of bioenergetic, redox and mitochondrial alterations in stroke. Their research employs advanced imaging technology, metabolic flux analysis and molecular biology in mouse and cell culture models of stroke. Ongoing research has identified several post-stroke modifications of glucose metabolizing enzymes in stroke. These pathological modifications cause defects in glucose metabolism and alter mitochondrial function. They are also studying how astrocyte glycogen stores can be utilized as alternative sources of energy to salvage brain tissue after stroke. This is critically important as deprivation of glucose and oxygen to the affected brain areas is the main cause of cell death in stroke. Andrabi’s goal is to identify molecular targets suitable for effective treatment in stroke and related brain injury.

The research group is also establishing induced pluripotent stem cell therapy in stroke. They are using combinations of live animal imaging and functional assessments to characterize the long-term safety and effectiveness of stem-cell therapy in stroke.

Technology Expertise Keywords

Parkinsons, stroke, cell death, neuroregeneration

Selected Publications

View all on Pubmed

  1. Iduna is a poly(ADP-ribose) (PAR)-dependent E3 ubiquitin ligase that regulates DNA damage. Kang HC, Lee YI, Shin JH, Andrabi SA, Chi Z, Gagné JP, Lee Y, Ko HS, Lee BD, Poirier GG, Dawson VL, Dawson TM. Proc Natl Acad Sci U S A. 2011 Aug 23;108(34):14103-8. doi: 10.1073/pnas.1108799108. Epub 2011 Aug 8. PMID: 21825151
  2. Iduna protects the brain from glutamate excitotoxicity and stroke by interfering with poly(ADP-ribose) polymer-induced cell death. Andrabi SA, Kang HC, Haince JF, Lee YI, Zhang J, Chi Z, West AB, Koehler RC, Poirier GG, Dawson TM, Dawson VL. Nat Med. 2011 Jun;17(6):692-9. doi: 10.1038/nm.2387. Epub 2011 May 22. PMID: 21602803
  3. Poly(ADP-ribose) (PAR) binding to apoptosis-inducing factor is critical for PAR polymerase-1-dependent cell death (parthanatos). Wang Y, Kim NS, Haince JF, Kang HC, David KK, Andrabi SA, Poirier GG, Dawson VL, Dawson TM. Sci Signal. 2011 Apr 5;4(167):ra20. doi: 10.1126/scisignal.2000902. PMID: 21467298
  4. Resistance to MPTP-neurotoxicity in α-synuclein knockout mice is complemented by human α-synuclein and associated with increased β-synuclein and Akt activation. Thomas B, Mandir AS, West N, Liu Y, Andrabi SA, Stirling W, Dawson VL, Dawson TM, Lee MK. PLoS One. 2011 Jan 31;6(1):e16706. doi: 10.1371/journal.pone.0016706. Erratum in: PLoS One. 2012;7(3). doi: 10.1371/annotation/f743434e-a6bf-4c6c-a836-ae5af66035a4. PMID: 21304957
  5. Contributions of poly(ADP-ribose) polymerase-1 and -2 to nuclear translocation of apoptosis-inducing factor and injury from focal cerebral ischemia. Li X, Klaus JA, Zhang J, Xu Z, Kibler KK, Andrabi SA, Rao K, Yang ZJ, Dawson TM, Dawson VL, Koehler RC. J Neurochem. 2010 May;113(4):1012-22. doi: 10.1111/j.1471-4159.2010.06667.x. Epub 2010 Mar 4. PMID: 20236222

Videos & Media

Lectures and Presentations

  • Bioenergetic Alterations in Stroke
    Zayed 2117 Arcade Conference Room (01/13/2014)
  • Bioenergetic Alterations in Stroke
    Baltimore, MD (01/13/2014)
    Johns Hopkins University

Recent News Articles and Media Coverage

Is this you? Edit Profile