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Dr. Benedict C. Albensi

Dr. Benedict C. Albensi

Principal Investigator
Synaptic Plasticity and Cellular Memory Dysfunction Lab, Division of Neurodegenerative Disorders

Pharmacology & Therapeutics, University of Manitoba

Manitoba Dementia Research Chair

Everett Endowment Fund Chair

Research Focus

The major focus of our laboratory is to understand the biological basis of memory and to also understand what happens to memory when it is impaired. To this end, we attempt to identify molecular signaling pathways and mechanisms that could be targeted with promising therapeutics for enhancing memory and for preventing and/or reversing memory impairments, in diseases or conditions such as Alzheimer’s disease, stroke, head trauma, etc. Much of our work is centered on the signaling pathway involving the transcription factor, nuclear factor kappa B (NF-kB), which is central to not only in inflammatory processes and immune system function, but also plays a central role in basic mechanisms of memory formation and recall.

Why is this work important?

  • It provides a valuable platform for scientists to understand how brain cells and biochemical processes change at the molecular level during the formation of normal memory
  • By understanding transcriptional regulation during memory encoding, we can identify a gene (or genes) that are utilized during normal memory formation
  • Characterizing the biological basis of normal memory will lend great insight into treating age-related central nervous system diseases and/or conditions of brain injury that contribute to memory impairment
  • Our research could ultimately lead to the development of new drug targets and/or new interventions to enhance normal memory and to treat memory disorders and related neurodegenerative conditions

What techniques and equipment are used in this laboratory?

  • Brain slice electrophysiology
  • Behavioral (egs., Morris water maze, Barnes maze)
  • Cell & molecular assays (e.g.s., Western blots, gel shifts, calcium analysis, mitochondrial function assessment, etc.)
  • MRI scanning and cellular neuroimaging
  • Cell culture
  • Computational modeling of cellular function related to NF-kB signaling

For equipment list, see SBRC.CA/DND

About Dr. Benedict Albensi

Dr. Albensi’s background is diverse where he has received training in both basic and clinical research. He has also worked in both academic and in industrial sectors on several drug discovery and drug development projects. For example, prior to PhD training, he worked at NPS Pharmaceuticals in Salt Lake City, UT, USA, investigating molecular structures obtained from natural products (e.g., spider venoms) for their potential application in treating CNS disorders. Dr. Albensi continued his academic training and received a Ph.D. in Neuroscience from the University of Utah’s Medical School in 1995, where he developed novel MRI methods for characterizing neonatal hypoxic-ischemic injury. Subsequently, he was awarded a Postdoctoral Fellowship at Georgetown University in Washington, DC, USA (working with Drs. Faden and Pekar), where he further developed novel MRI methods for investigating TBI and brain cognition. Following this, he went on to work as a Postdoctoral Scholar with Dr. Mark Mattson, an internationally recognized leader in neurodegenerative research, at the Sanders-Brown Center on Aging – University of Kentucky. While working with Dr. Mattson and using electrophysiological methods, he published the ground breaking study that TNF and NF-kB play important roles in synaptic plasticity and memory (Albensi and Mattson, Synapse 2000). Subsequently, he joined the Clinical Research Department at Parke-Davis/Warner-Lambert in Ann Arbor, MI (Pfizer acquired PD-WL in 2000) to obtain additional experience in clinical trials. Following this clinical research training, he was appointed as Project Staff in the Department of Neurological Surgery – Cleveland Clinic Foundation and also as an Adjunct Assistant Professor of Biology at Case Western Reserve University in Ohio, where he conducted novel work on mechanisms of deep brain stimulation (DBS). He now has several appointments in Canada, which include serving as a Professor of Pharmacology and Therapeutics at the University of Manitoba and as a Principal Investigator at St. Boniface Hospital Research. He is also a Core Member of the Biomedical Engineering Graduate Program at the University of Manitoba. In addition, he is the new Manitoba Dementia Research Chair and the Everett Endowment Fund Chair. He is also currently a Director of the Board for MitoCanada and the Movement Ctr. of Manitoba. He previously served on the Board of the Alzheimer’s Society of Manitoba. He has reviewed grants for numerous foundations worldwide including NIH, CIHR, NSERC, US DOD, FASEB, to name a few.

Dr. Albensi has been invited to join the Aged & Cognitively Impaired Team for ACRES, Alliance for Clinical Research Excellence and Safety.

Full CV

Dr. Albensi’s full CV is available to download.

For more information, please contact:

Dr. Benedict C. Albensi
Tel. (204) 235-3942
Cell. (204) 782-3698

(Selected Publications)
Ammonia as a Potential Neurotoxic Factor in Alzheimer’s Disease.
Adlimoghaddam A, Sabbir MG, Albensi BC.
Front Mol Neurosci. 2016 Aug 8;9:57.

Visinin-Like Protein-3 Modulates the Interaction Between Cytochrome b 5 and NADH-Cytochrome b 5 Reductase in a Ca2+-Dependent Manner.
Oikawa K, Odero GL, Nafez S, Ge N, Zhang D, Kobayashi H, Sate K, Kimura S, Tateno M, Albensi BC.
Cell Biochem Biophys. 2016 Jul 2.

Editorial: Transcriptional Regulation of Memory.
Albensi BC, Djordjevic J.
Front Mol Neurosci. 2016 Apr 19;9:24.

Protein Structural Analysis of Calbindin D28k Function and Dysregulation: Potential Competition Between Ca(2+) and Zn(2.).
Omar SI, Albensi BC, Gough KM.
Curr Alzheimer Res. 2016;13(7):777-86.

Traumatic Brain Injury as a Risk Factor for Alzheimer’s Disease: Is Inflammatory Signaling a Key Player?
Djordjevic J, Sabbir MG, Albensi BC.
Curr Alzheimer Res. 2016;13(7):730-8.

Martin M, Albensi B, Cross A, Katz-Brull R, Thiessen J, King S, Lin A.
Magn Reson Insights. 2015 Dec 15;8(Suppl 1):49-52.

Simultaneous evaluation of substrate-dependent oxygen consumption rates and mitochondrial membrane potential by TMRM and safranin in cortical mitochondria.
Chowdhury SR, Djordjevic J, Albensi BC, Fernyhough P.
Biosci Rep. 2015 Dec 8;36(1).

Morris Water Maze Training in Mice Elevates Hippocampal Levels of Transcription Factors Nuclear Factor (Erythroid-derived 2)-like 2 and Nuclear Factor Kappa B p65.
Snow WM, Pahlavan PS, Djordjevic J, McAllister D, Platt EE, Alashmali S, Bernstein MJ, Suh M, Albensi BC.
Front Mol Neurosci. 2015 Nov 18;8:70.

Mechanisms of Mitochondrial Dysfunction in Alzheimer’s Disease.
Cadonic C, Sabbir MG, Albensi BC.
Mol Neurobiol. 2015 Nov 4.

S. Nafez, K. Oikawa, G.L. Odero, M. Sproule, N. Ge, J. Schapansky, B. Abrenica, A. Hatherell, C. Cadonic, S. Zhang, X. Song, T. Kauppinen, G.W. Glazner, M. Grilli, M.P. Czubryt, D.D. Eisenstat and B.C. ALBENSI. Early Growth Response 2 (Egr-2) Expression is Triggered by NF B Activation. Molecular and Cellular Neuroscience. 64:95-103, 2015.

G.L. Odero, K. Oikawa*, K.A.C. Glazner, D. Grossman, J. Thiessen, J. Schapansky, N. Ge, M. Martin, G.W. Glazner, and B.C. ALBENSI. Evidence for the Involvement of Calbindin D28k in the Presenilin 1 Model of Alzheimer’s Disease. Neuroscience 169: 532-543, 2010. *This author is a co-first author.

K.A.C. Glazner, G. Odero*, D. Grossman, E. Anema, A. Motnenko, J. Schapansky, D. Oliver, G. Glazner and B.C. ALBENSI. Strain Specific Differences in Memory and Neuropathology in a Mouse Model of Alzheimer’s Disease. Life Sciences 86: 942-950, 2010. *This author is a co-first author.

J. Thiessen, K.A.C. Glazner, S. Nafez, A. Schellenberg, R. Buist, M. Martin, and B.C. ALBENSI. Histochemical visualization and diffusion weighted imaging in the TgCRND8 transgenic model of Alzheimer’s disease. Brain Structure and Function 215(1): 29-36, 2010.

D. Zhang, R. Buist, W. Xiong, J. Peeling, B.C. ALBENSI, F.E. Parkinson. Expression of human equilibrative nucleoside transporter 1 (hENT1) in mouse neurons regulates adenosine levels in physiological and hypoxic-ischemic conditions. Journal of Neurochemistry 118(1):4-11, 2011.

S. Kost, C. Sun, W. Xiong, K. Graham, C. E Cass, J.D. Young, B.C ALBENSI, F.E Parkinson. Behavioral effects of elevated expression of human equilibrative nucleoside transporter 1 in mice. Behavioral Brain Research 224(1):44-9, 2011.

M.Z. Kastyak-Ibrahim, M.J. Nasse, M. Rak, C. Hirschmugl, M.R. Del Bigio, B.C. ALBENSI and K.M. Gough. Biochemical label-free tissue imaging with subcellular-resolution synchrotron FTIR-FPA. NeuroImage 60: 376–383, 2012.

D. Stitt, M. Z. Kastyak-Ibrahim, C. R. Liao, J. Morrison, B.C. ALBENSI, K.M. Gough. Tissue acquisition and storage associated oxidation considerations for FTIR microspectroscopic imaging of polyunsaturated fatty acids. Vibrational Spectroscopy 60:16-22, 2012.

H. Soylu, D. Zhang, R. Buist, M. Martin, B.C. ALBENSI, F.E. Parkinson. Intracortical injection of endothelin-1 induces cortical infarcts in mice: effect of neuronal expression of an adenosine transporter. Experimental & Translational Stroke Medicine 4(1):4, 2012.

K. Oikawa, G.L. Odero, E. Platt, M. Neuendorff, A. Hatherell, M.J. Bernstein, and B.C. ALBENSI. NF-B p50 Subunit Knockout Impairs Late LTP and Alters Long Term Memory in the Mouse Hippocampus. BMC Neuroscience 13:45, 2012. Noted as “Highly Accessed” by publisher on Oct 10, 2012 (989 times).

D. Zhang, S. Chu, C. Sun, W. Xiong, B.C. ALBENSI, F. E. Parkinson. Inhibition of synaptic activity in hippocampus by ATP, hypoxia or oxygen-glucose deprivation does not require CD73. PloS One 7(6):e39772, 2012.

S. Chu, Wei Xiong, D. Zhang, H. Soylu, C. Sun, B.C. ALBENSI, F.E. Parkinson. Regulation of adenosine levels during cerebral ischemia. Acta Pharmacologica Sinica. 34(1):60-6, 2013. Invited review.

C. Liao, M. Rak, J. Lund, M. Unger, E. Platt, B.C. ALBENSI, C. Hirschmugl, K. Gough. Synchrotron FTIR reveals lipid around and within amyloid plaques in transgenic mice and Alzheimer’s Disease brain. Analyst. 138(14):3991-7, 2013.

M.Z. Kastyak-Ibrahim, D.L. Di Curzio, R. Buist, S. Herrera, S. Feng, J. Kong, X.M. Li, B.C. ALBENSI, M.R. Del Bigio, M. Martin. Neurofibrillary tangles and plaques are not accompanied by white matter pathology in aged triple transgenic-Alzheimer disease mice. Magnetic Resonance Imaging. Nov;31(9):1515-21, 2014.

W.M. Snow, B.M. Stoesz, D. Kelly and B.C. ALBENSI. Roles for NF-kB and Gene Targets of NF-kB in Synaptic Plasticity, Memory, and Spatial Orientation. Molecular Neurobiology. Apr;49(2):757-7, 2014.

C. Cadonic and B.C. ALBENSI. Oscillations and NMDA receptors: their interplay create memories. Aims Neuroscience. 1(1):52-64, 2014. Invited Review.

S. Nafez, K. Oikawa, G.L. Odero, M. Sproule, N. Ge, J. Schapansky, B. Abrenica, A. Hatherell, C. Cadonic, S. Zhang, X. Song, T. Kauppinen, G.W. Glazner, M. Grilli, M.P. Czubryt, D.D. Eisenstat and B.C. ALBENSI. Early Growth Response 2 (Egr-2) Expression is Triggered by NF kB Activation. Molecular and Cellular Neuroscience. Submitted (MCN-13-103R1).

K. Oikawa, G.L. Odero, S. Nafez, N. Ging, D. Zhang, H. Kobayashi, K. Sato, S. Kimura, M. Tateno and B.C. ALBENSI. Visinin-like protein-3 modulates the interaction between cytochrome b5 and NADH-cytochrome b5-reductase in a Ca++ dependent manner. Cell Biochemistry and Biophysics. Submitted (CBBI-D-14-00066).

S.I. Omar, B.C. ALBENSI, K. Gough. Modelling the binding of Ca2+ and Zn2+ to Calbindin D28k and understanding their competition through protein structural analysis. Journal of Molecular Graphics and Modelling. Submitted.


B.C. ALBENSI (editor). Transcription Factors NF-B and CREB: Involvement in Synaptic Plasticity and Memory Formation (senior authors: Albensi, Barger, Romano, Mariagrazia, Murphy, Josselyn, Rodríguez). Released, Jan. 2012. Pub. Bentham Science.

Book Chapters

2. B.C. ALBENSI. V. Plasticity and Epileptogenesis, D. Electrical Stimulation Protocols for Seizure Attenuation, in, Encyclopedia of Basic Epilepsy Research, Edited by Philip A. Schwartzkronin. Academic Press, Elsevier Sci. Publishers, Invited submission – 2009.

3. B.C. ALBENSI. Brain stimulation for seizure control: Considerations and potential mechanisms, in Epilepsy / Book 1, Edited by Humberto Foyaca-Sibat. InTech Publishers, ISBN 979-953-307-011-6, Invited Submission –2011.

4. G. Odero, W. Snow, K. Vadakkan, B.C. ALBENSI. Chapter 4, Roles for NF-B in Regulating Gene Expression in Synaptic Plasticity and Memory in Transcription Factors NF-B and CREB: Involvement in Synaptic Plasticity and Memory Formation. Edited by Ben Albensi. Bentham Science Publishers, 2012.

5. C. Cadonic and B.C. ALBENSI. Memory Deficits and Transcription Factor Activity Following Traumatic Brain Injury, in Traumatic Brain Injury. Edited by Farid Sadaka and Tanya Quinn. InTech Publishers. ISBN 980-953-307-1139-4. Invited Submission. 2014.

View on Mendeley


View on Scopus


Academic Awards

  • Weston Brain Institute Outstanding Achievement Award 2016 Nominee
  • March 2013 Sanofi BioGENEius Challenge Canada Mentor Award, Wpg., MB
  • Sept. 2012 Richard Hoeschen Award, $1000-B.Sc.(Med) Student Supervisors, MMSF/SBGHRC, Wpg., MB
  • 2011 to current. Everett Endowment Fund Chair
  • April 2007 Sanofi-Aventis Biotech Challenge Award of Appreciation, Wpg., MB
  • 1998 U. of Kentucky Med. Ctr., Spring Neurosci. Day, 1st Prize-Best Poster (cash award)
  • 1996 – 1997 Georgetown University Medical Center Research Fellowship
  • 1994 William D. Carey Science Award – American Association for the Advancement of Science
  • 1994 Medical Imaging Res. Lab Symp., Oral Finalist, Sundance, UT
  • 1993 Graduate Research Fellowship Award, $5,000, Univ. of Utah


2015 Manitoba Dementia Research Chair for 5 years. $500,000 over 5 yrs.

2014– 2019. Mitochondrial Function, Neural Plasticity, and Memory. Natural Sciences and Engineering Research Council of Canada (NSERC), Discovery Grant. Principal Investigator. $130,000 total, $26,000/year.

2014-2017. Endowment – Everett family (Douglas Everett, former Canadian Senator and owner of the DOMO gasoline chain, etc.). Principal Investigator/Chair. Year 1, $42,697.


2011-2014. Endowment – Everett family (Douglas Everett, former Canadian Senator and owner of the DOMO gasoline chain, etc.). Principal Investigator./Chair. Year 1, $43,000; Year 2, $24,466; Year 3, $35,000.

2009 – 2014. The Role of p50 NF-B and Egr-2 in Long Term Potentiation and Memory. Natural Sciences and Engineering Research Council of Canada (NSERC), Discovery Grant. Principal Investigator. $125,000 total, $25,000/year.

2008 – 2013. Regulation of Brain Adenosine Levels by Ecto-enzymes and Membrane Transporters. Canadian Inst. of Health Research (CIHR), Operating Grant. Co-Principal Investigator, $599,205 total, ~$119,841/year.

2010 – 2012 Stroke Injury in Genetic Mouse Models. Heart and Stroke Foundation of Canada (HSFC), Renewal, Co-Principal Investigator, $100,000 total, $50,000/year.

2008 – 2010. Hippocampal Gene Expression Profiling and the Possible Involvement of Homer1 in Alzheimer’s Disease. Alzheimer’s Society of Canada. Principle Applicant, $130,000 total, $65,000/year.

2009-2010. Memory-Associated Gene-Expression Profiling During Aging. University of Manitoba’s Centre on Aging, Operating Grant, Principal Investigator, $10,000 total over 1 year.

2009. CFI-Partnering Grant. St Boniface Hospital and Research Foundation, Open Grants Competition, Principal Investigator, $6,500 total over one year.

2008 – 2010. Stroke Injury in Genetic Mouse Models. Heart and Stroke Foundation of Canada (HSFC),
Co-Principal Investigator, $90,000 total, $45,000/year.

2005 – 2010. Multidisciplinary 2-Photon Imaging of Calcium and Mitochondrial Dysregulation in Intact Tissues. Canada Foundation for Innovation (CFI) – Equipment Grant, Co-Principal Investigator, $1,004,835.

2007 – 2009. Regulation of Adenosine Levels. Canadian Inst. of Health Research (CIHR), Operating Grant (funded by RPP – MHRC). Co-Applicant, $182,184 total, $91,092/year.

2006 – 2009. The Role of sAPP and NF-B in Alzheimer’s Disease, Scottish Rite Charitable Foundation of Canada, Principal Investigator, $105,000 total, $35,000/year.

2006 – 2009. Roles for PS1 Mutations, Calcium Overload, and NF-B Activation in Synaptic and Cognitive Dysfunction, MHRC, Establishment grant. Principal Investigator, $100,000 total, ~$33,333/year.

2007 – 2008. Regulation of GABAergic Interneuron Migration and Differentiation in the Vertebrate Forebrain by DLX Transcription Factors. Manitoba Inst. of Child Health (MICH), Operating Grant.
Co-Applicant, $45,000 total, $22,500/year.

2007. Programmable Stimulus Generator and Multielectrode Array to Investigate New Electrical Stimulation Protocols for Relief from Seizure-Like Activity, Natural Sciences & Research Council of Canada (NSERC), Research Tools & Instruments Grant. Co-Applicant $79,835 total over one year.

2007. Diffusion-Weighted Imaging for Identifying Markers Associated with Brain Injury Leading to Alzheimer’s Disease. Manitoba Medical Service Foundation (MMSF), Principal Invest., $35,000 total 1 year.

2006 – 2007. Multidisciplinary 2-Photon Imaging of Calcium and Mitochondrial Dysregulation in Intact Tissues. Canada Foundation for Innovation (CFI) – Infrastructure Support, Co-Principal Investigator, $119,000.

2006 – 2008. Roles of PS1 Mutations and NF-B in Synaptic Plasticity and Alzheimer’s Disease, Manitoba Health Research Council (MHRC), Operating grant. Principal Investigator, $100,000 total, $50,000/year.

2006 – 2007. Novel Electrical Stimulation Protocols for Relief From Epileptic Seizure-Like Activity, Dr. Paul H.T. Thorlakson Foundation Fund, Co-Investigator, $29,500.

2002. A Model of the Human Blood Brain Barrier Using Human Endothelial and Glial Cells. Berkeley Citizens Commission/Bayer Pharmaceutical Division, Principal Investigator, $25,000 USD.

1997 – 1998. MRI of Brain Injury in TNF Double Knock-Out Mice. Univ. of Kentucky, MRI Center Pilot Project Grant Award (during postdoc. appointment), Principal Investigator, $1,125 USD.

1993 – 1994. MRI of Hypoxic-Ischemic Injury in Neonatal Mice. Univ. of Utah Graduate Research Fellowship Grant (during PhD studies), Principal Investigator, $5,000 USD.

Dr. Wanda Snow

Dr. Wanda SnowSeveral transcription factors, key regulators of gene expression, have been implicated in Alzheimer’s disease. The transcription factor nuclear factor kappa B (NF-κB) is best known for its role in inflammation, but more recent studies implicate this factor in synaptic plasticity, learning, and memory. In Alzheimer’s disease, characterized by severe memory deficits, levels of this important gene regulator are altered. Creatine, an endogenous amino acid that regulates cellular energy, has been shown to activate NF-κB in neurons. Supplementation with creatine has been shown to enhance brain function and memory in healthy individuals and has been studied in clinical trials of neurodegenerative diseases, such as Parkinson’s disease. It has not, however, been investigated as a potential therapy for Alzheimer’s disease. As a postdoctoral fellow in Dr. Albensi’s lab, I am currently carrying out several projects looking at the effects of creatine, including its effects on energy and transcriptional regulation in isolated neurons and its effects on memory and brain bioenergetics in healthy mice and in a mouse model of Alzheimer’s disease in the hopes of understanding if NF-κB signaling mediates the neurobeneficial effects of creatine. In addition, I am investigating plasticity-induced expression of the transcription factor early growth response-2 , also implicated in memory and a gene target of NF-κB, in the normal and AD-like mouse hippocampus using long-term potentiation. These studies are aimed at determining which transcriptional networks are affected in Alzheimer’s disease in efforts to uncover how memory becomes compromised in the disease and how best to treat or prevent memory impairments. This work was generously supported by a postdoctoral fellowship from Research Manitoba.

Dr. Jelena Djordjevic

Dr. Jelena DordevicAlzheimer’s disease (AD) is a late-onset, progressive, neurodegenerative disorder, characterized by cognitive and memory decline, speech loss and personality changes, affecting almost 1 million elderly in Canada alone. Besides plaques and tangles, a cascade of other pathological events ranging from synaptic dysfunction, oxidative stress, mitochondrial dysfunction, and neuroinflammation, are routinely detected in patients. Some scientists suspect that brain metabolism and mitochondrial function become altered early in AD, and these alterations, which include deficits in ATP generation, may be gender dependent. The focus of my research is centered on the mitochondrial bioenergetics in animal models engineered to mimic the brain pathology seen in Alzheimer’s disease (3xTg and CRND8 mice), since mitochondria play active roles in synaptogenesis and morphological and functional responses to synaptic activity. The goal is to characterize the mitochondrial impairments at different points in disease progression, to address sex differences in mitochondrial dysfunction in AD, and to establish the connection with inflammatory signaling, which is known to affect brain energy metabolism. This work was generously supported by a postdoctoral fellowship from Research Manitoba.

Dr. Aida Adlimoghaddam

Dr. Aida AdlimoghaddamCurrently, as a postdoctoral fellow, I am working on two main projects:

First project: How memory is impaired by Alzheimer’s disease (AD; most common form of dementia) and vascular dementia (VD; second most common form of dementia). To discriminate these different type of dementia, I am using both in vitro and in vivo mouse models of AD and VD in conjunction with pathological/inflammatory markers, cell and molecular techniques, electrophysiological methods, and neuroimaging.

Second project: The characterization of an altered ammonia transport system that contributes to AD. My focus is to investigate the effects of ammonia exposure on the brain nitrogen transport system and brain mitochondrial function using an in vitro mouse model of AD. I am a recipient of a Research Manitoba Fellowship to investigate the second project.

My long-term goal for both projects is to develop new treatments for improving memory as a result of the mentioned diseases/conditions.


Life In the Lab