Advances in Research

Datesort descending Milestone Details
July 1999

Drs Peter St George-Hyslop, David Westaway and Paul Fraser develop a robust animal model system which replicates most of the clinical features of human Alzheimer’s disease. This will expedite the discovery and testing of new diagnostics and treatments for Alzheimer’s disease.

July 2000

Drs Peter St George-Hyslop and Paul Fraser discover a new gene, Nicastrin, involved in the biochemical processes leading to Alzheimer neurodegeneration.

July 2006

Tanz Centre researchers discover that scyllo-inositol can inhibit the accumulation of Aβ into small neurotoxic aggregates (termed “oligomers”) and block many of the features of AD in mouse models of this disease. These two observations led to the initiation of human clinical trials of scyllo-inositol in patients with AD.

July 2009

Tanz Centre scientists demonstrate a common reduction in BDNF expression across multiple lines of APP-transgenic mice.

July 2011

Tanz Centre researcher creates a clinical intake tool that will be used by the five academic memory clinics associated with the University of Toronto. This tool will enable a uniform data acquisition when conducting an interview with a patient with cognitive complaints, in addition to a standard neurological exam. The standardisation of approach to the patient with cognitive complaints will facilitate research amongst the cognitive behavioral groups at UofT. This tool will also help residents rotating in our clinics learn about the different cognitive domains and how to probe for changes in personality, cognition and social cognition. This tool will initially be rolled out to the UofT memory clinics with the view of having it used across Ontario, and perhaps across Canada, so that a nationwide registry of patients with cognitive impairment could be established and queried for epidemiological research on health care necessities and outcomes.

June 1995

Dr. Peter St George-Hyslop and international colleagues announce that they have identified and cloned the defective gene (Presenilin 1) that causes the most virulent form of Alzheimer’s Disease (located on chromosome 14).

June 1997

Dr. Catherine Bergeron recognizes that involvement of the neocortex is a frequent event in progressive supranuclear palsy.

June 1998

Drs Howard Mount, Cheryl Dreyfus and Ira Black describe a molecular survival/death switch responsible for regulating the Purkinje cell fate upon exposure to nerve growth factor. This discovery challenges the orthodox notion that nerve growth factor has only positive effects on developing neurons. He and his group later go on to demonstrate the specific failure of this switch in a genetic mouse model of ataxia telangiectasia, a pediatric degenerative disease associated with massive Purkinje cell death.

June 2000

Merck Sharp Dohme & Bristol-Myers Squibb announce that they have developed compounds that bind to the presenilin proteins (first isolated at the CRND in 1995) and that inhibit the production of the neurotoxic amyloid β-peptide. Bristol-Myers Squibb compound enters Phase I trials as a novel therapeutic for Alzheimer’s disease in the US.

June 2005

Tanz researchers demonstrate that although the presenilin protein (PS1 and PS2) components of γ-secretase complexes have similar amino acid sequences, they have very different biochemical properties and different functions. This is turning out to be important for the development of drugs which selectively inhibit the role of these proteins in the generation of neurotoxic Aβ by the γ-secretase enzyme.

June 2007

Tanz Centre researchers develop the first antibody that specifically labels misfolded superoxide dismutase-1 (SOD1). Mutations in SOD1 are the only known cause of amyotrophic lateral sclerosis (ALS). The antibody has potential utility for use in biomarker studies, drug discovery and development of immunization strategies for the treatment of ALS caused by mutations in SOD1.

The researchers show that mutant SOD1 transgenic mice lack abnormalities of the TAR DNA Binding Protein (TDP-43).

They demonstrate through identification of a unique pathological epitope that superoxide dismutase-1 (SOD1) is misfolded in transgenic mice expressing mutant forms of SOD1 related to Amyotrophic Lateral Sclerosis

June 2012

Tanz Centre researcher participates in a committee to harmonize the neuropsychological assessment of patients presenting with cognitive complaints to the five academic memory clinics associated with the University of Toronto. The aim is to create a short battery that could be used by physicians and residents to assess all cognitive domains without having to wait for a full neuropsychological assessment. The tool will enable a uniform data acquisition. The standardisation of the battery will facilitate research amongst the cognitive behavioral groups at UofT. This tool will also help residents rotating in our clinics learn how to test the different cognitive domains and this information will be used to help make a diagnosis and assess functional impact.

June 2012

Tanz Centre researchers lead a large international study estimating the contribution of C9ORF72 repeat expansion in four neurodegenerative diseases. They demonstrate that the hexanucleotide expansion in C9orf72 gene is a common cause of Amyotrophic lateral sclerosis and Frontotemporal Dementia, but not of Alzheimer’s disease or Parkinson’s disease.

March 2003

Tanz Centre researchers show that there is deregulated expression of alternatively-spliced variants of the peripherin protein in ALS, and that these may play a role in the neurodegenerative process.

March 2008

Tanz Centre scientists link alterations in serotonin turnover to specific affective phenotypes in a mouse model of Williams' syndrome.

March 2009

For the first, Tanz Centre researchers address the mechanism responcible for low penetrance of a novel SOD1 deletion in the ALS family. They demonstrate that the enhanced splicing of SOD1 exon 2 acts as a natural knock-down of the mutant SOD1 allele leading to a mild disease presentation (Rogaeva)

May 1992

Drs Harry Karlinsky, Peter St George-Hyslop and Don Crapper McLachlan describe the first Canadian case of familial Alzheimer’s Disease due to a mutation in the amyloid precursor protein gene. 

May 1994

Drs Peter St George-Hyslop, Don Crapper McLachlan and others show that different genes causing susceptibility to Alzheimer’s disease interact. This interaction provides strong evidence for the existence of a multi-step metabolic pathway governing the initial stages of susceptibility to Alzheimer’s disease.

May 1997

Drs Ekaterina Rogaeva, Peter St George-Hyslop, and others provide evidence confirming the existence of a gene on chromosome 12 (the identity of which is still unknown) which causes susceptibility to late-onset Alzheimer’s disease. This work shows that, in addition to a gene on chromosome 12, there must be at least one other gene causing susceptibility to this disease which has yet to be mapped.

May 2010

Tanz Centre scientists uncover deficits in entorhinal cortical function in TgCRND8 mice and linked these to alterations in cortical BDNF expression.