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 signalling 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 centred on the signalling 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.)
- PET/MRI scanning and cellular neuroimaging
- Cell culture
- Computational modelling of cellular function
For the equipment list, seehttps://www.sbrc.ca/dnd/dnd-research-equipment/.
About Dr. Benedict Albensi
Dr. Benedict C. Albensi, Ph.D., BCMAS, CRQM is a Professor of Pharmacology and Therapeutics at the Max Rady College of Medicine – University of Manitoba and a Principal Investigator and the Everett Endowment Fund Chair for Alzheimer’s Research at the St. Boniface Hospital Research Centre (since 2005). He is best known for his work with factors involved in ageing, cognition, and Alzheimer’s disease (AD), such as nuclear factor kappa B (NF-kB), a mediator of inflammation and a required molecule for memory. He obtained his Ph.D. in Neuroscience from the University of Utah’s Medical School in 1995. He was awarded a Postdoctoral Fellowship at Georgetown University in Washington, DC, working with Drs. Faden and Pekar, where he developed MRI methods for investigating head trauma and cognition. He then 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 where he was the first to show NF-kB is required for synaptic plasticity in mammals. Other appointments have included the Cleveland Clinic, NPS Pharmaceuticals, Pfizer, Case Western Reserve University. Over the last few years, his work has been largely focused on mitochondrial dysfunction in AD. Recently, the Albensi lab has shown very early deficits and sex-based differences in mitochondrial function before the appearance of plaques and tangles, the classic hallmarks of AD. He has been ranked in the top 1% worldwide by Expertscape.com for his number of publications from 2010-2020 in 7 areas including Alzheimer Disease (0.48%), neurocognitive disorders (0.76%), tauopathies (0.98%), dementia (0.85%), NF-kappa B (0.42%), memory (68%) & energy metabolism (0.68%).
Dr. Albensi’sfull CV is available to download:Download CV (PDF)
For more information, please contact:
Benedict C. Albensi,
Synaptic Plasticity and Cellular Memory Dysfunction Lab, Division of Neurodegenerative Disorders
Everett Endowment Fund Chair
Manitoba Dementia Research Chair
Department of Pharmacology & Therapeutics, College of Medicine, Faculty of Health Sciences,University of Manitoba
(204) 235-3942 (office)
(204) 235-3941 (lab)
(204) 782-3698 (cell)
(204) 235-3939 (DND administrative manager)
(204) 237-4092 (fax)
St. Boniface Hospital Albrechtsen Research Centre
351 Taché Ave./Lab 4050
Winnipeg, Manitoba R2H 2A6
2019-2022 – Effects of dietary flaxseed on memory and cognition. Canadian Agricultural Partnership (CAP). $430,746 total over 3 years.
2019-2024Canadian Institutes of Health Research.Sex-based differences associated with mitochondrial dysfunction in Alzheimer’s disease.$725,985
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
Several 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
Alzheimer’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.
Currently, 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.