Advances in Research

Datesort ascending Milestone Details
September 2007

Tanz Centre scientists demonstrate that the SPRN gene encodes a CNS expressed protein “shadoo” with biochemical resemblance to PrP. In functional assays in cerebellar neurons the protein has PrP-like protective activity against delta PrP or the Doppel protein. Most remarkably, steady state levels of the shadoo protein are markedly reduced in prion-infected animals. A simple hypothesis is that clinical target areas in prion disease reflect loss of shadoo’s protective action.

September 1999

Using a novel imaging method called atomic force microscopy, Drs Paul Fraser, JoAnne McLaurin and Christopher Yip discover a sequence of events that mediates the neurotoxicity of amyloid in Alzheimer’s disease.

September 1995

Drs Howard Mount, Cheryl Dreyfus and Ira Black discover glial cell-line-derived neurotrophic factor (GDNF) to be the most potent survival and development-promoting factor for Purkinje cells. Purkinje cells are output neurons of the cerebellum and are targeted for degeneration in a broad range of disorders, including hypothyroidism, autism, hereditary ataxias, certain forms of cancer and drug toxicity. This discovery led to trials of GDNF in animal models of Purkinje cell degeneration.

September 1994

A mutation in CuZnSOD, an enzyme linked to familial ALS, is discovered. Analysis of the biochemistry and function of this enzyme in the brain at the CRND by Drs William Tatton, Peter St George-Hyslop and Don Crapper McLachlan clarifies the cause and propagation of ALS.

September 1993

The Apolipoprotein e 4 variant is found to be a risk factor for Alzheimer’s disease by a collaborative team led by Dr. A.D. Roses of Duke University that included Dr. Peter St George-Hyslop at the Tanz Centre.

September 1990

Drs Peter St George-Hyslop, Don Crapper McLachlan and others show that Alzheimer’s Disease is a complex disorder with multiple etiologies, some of which are genetic.  This discovery causes a significant shift in experimental paradigms used by all Alzheimer’s Disease researchers because it had previously been assumed that Alzheimer’s Disease was a single disease.

October 2011

Tanz CRND celebrates its 20th anniversary.

October 2011

Tanz Centre scientists contribute to the discovery of novel hexanucleotide (GGGGCC) repeat expansion in the C9orf72 gene, which is responsible for two common neurodegenerative disorders: amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). This mutation explains 46% familial and 21% sporadic ALS in the Finnish population; and also presents in ~30% familial ALS and ~20% familial FTD cases of outbred European descent, making it the most common genetic cause of these fatal neurodegenerative diseases.

Tanz Centre scientists identify RNA targets of the TAR-DNA Binding Protein (TDP-43) and show that some of these are deregulated in Amyotrophic Lateral Sclerosis.

Tanz Centre scientists discover that heterogeneity of neuropatholgical changes in athletes with multiple concussions- not all is chronic traumatic encephalopathy.

Tanz Centre scientists participate in a consortium identifying Common variants that affect risk for the tauopathy in Progressive Supranuclear Palsy.
 

October 2009

Tanz Centre researchers lead a large collaborative study demonstrating that GBA gene (known to be responsible for Gaucher’s Disease) is among the most significant Parkinson’s disease risk factors indentified to date. They reveal that clinically, subjects with a GBA mutation presented earlier, and were more likely to have affected relatives and atypical manifestations.

October 2006

Tanz Centre researchers identify regulation of α-synuclein solubility in neurons by specific brain proteins, a process that is disrupted by PD-linked mutations in α-synuclein. Identification of these factors has implications for understanding PD pathogenesis.

October 2006

Tanz Centre scientists generate a robust transgenic mouse model of disorders such as FTD, AD, and PSP, in which the tau protein accumulates inside brain cells, and leads to neurodegeneration. The tau protein is the principal component of neurofibrillary tangles. This mouse model will help scientists understand why the tau protein aggregates into neurotoxic intracellular inclusions, and how this causes neurodegeneration.

October 2005

Tanz Centre scientists identify the protective role of PINK1 protein to suppress neuronal death and loss-of-function effects induced by PD-linked mutations.

October 1999

Dr. David Westaway clones the Doppel gene, which provides new insights into the biology of the PrP protein involved in human Creutzfeldt-Jakob Disease and into scrapie and bovine spongiform encephalopathy (Mad Cow Disease) in animals.

November 2009

the Centre for Drug Research and Development and MaRS Innovation announces a new collaboration on projects of mutual interest with a goal to advance and commercialize early-stage health-related discoveries. The first project funded under the arrangement saw Prof. Paul Fraser working with the University of British Columbia's Dr. Bruce Verchere, to investigate amyloid aggregation inhibitors as a novel approach to address the treatment of diabetes.

November 2006

Tanz Centre scientists discover that Corticobasal Degeneration can be caused by mutations in the progranulin gene.

November 1999

Using a number of biophysical approaches, Drs Paul Fraser, Christopher Yip and Avi Chakrabartty identify a potentially key element that may mediate the assembly of intracellular amyloid, which is thought to play a central role in neurodegeneration.

May 2011

Tanz Centre scientists contribute to the discovery of several novel genes associated with late-onset Alzheimer's disease: MS4A4/MS4A6E, CD2AP, CD33 and EPHA1.

May 2010

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

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 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.

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