Stroke constitutes a major cause of death and disability of the adult population in the industrialized world. Ischemic stroke (IS), which occurs as a result of a sudden obstruction within a cerebral artery due to an embolus or thrombus, accounts for the majority of cases. After IS, it has been observed a deactivation of the Canonical Wnt pathway. Interestingly, DKK1 levels are elevated in IS brain in patients and animals' models. DKK1 inhibits the canonical Wnt pathway by preventing Wnt ligands from binding the receptor complex formed by Frizzled (Fzd) and low-density lipoprotein receptor-related protein-5/6 (LRP5/6). Wnt ligands binding to Fzd/LRP5/6 stabilizes β-catenin in the cytosol and stimulates its subsequent translocation to the nucleus to regulate transcription of target genes implicated in a wide range of physiological processes in the brain. Our study aimed to elucidate DKK1 role following IS. For this purpose, TOPGAL-iDKK1, which induce DKK1 by doxycycline administration and C57BL/6 mice were used. C57BL/6 mice were treated intraperitoneally with a DKK1 inhibitor, WAY262611 (5 and 10 mg/kg 24h after IS and every 2 days until sacrifice at 1 week) following middle cerebral artery occlusion (MCAO) which simulate IS. WAY262611 administration had reduced infarct volume and edema compared to the control mice as well as improved sensorimotor functions in a battery of behavioral tests whereas DKK1 induction impaired them. In addition, WAY262611 attenuate neuronal degeneration in treated-mice brain whereas DKK1 induction had the opposite effect. Taken together, our data suggest that pharmacological inhibition of DKK1 could be an elegant therapeutic target after IS.

Dickkopf-1 induction impairs short- and long-term structural and functional recovery after ischemic stroke

Stroke is one of the leading causes of death and disability in the world. Unfortunately, there is still no effective therapy to treat the disease. Therapeutic angiogenesis using potent pro-angiogenic agents has already been shown to provide therapeutic benefits. However, the use of such agents is a double-edged strategy because of the increased risk of exacerbation of vascular leakage. Pericytes are specialized mural cells that play a key role in stabilizing the angiogenic vasculature and possess plastic properties, as they are able to differentiate into endothelial cells by reprogramming. Because of their angiogenic and plastic properties, pericytes are an attractive target for developing new interventions to promote neurovascular repair after stroke. Using novel pharmacological and genetic approaches to target pericytes, our results indicate that a recently discovered platelet-derived growth factor, isoform D (PDGF-D), plays an important role in promoting pericyte plasticity contributing notably to a decrease in brain atrophy and a reduction in motor impairment. Furthermore, our data demonstrate that ex vivo pre-conditioned pericytes transplanted intra-nasally migrate to the lesion site and promote its vascularization, which leads to the regression of damage. The overall results therefore suggest that pericytes are an interesting target and a new tool for the development of new therapies against stroke

Exploration of the pro-angiogenic potential of pericytes in the repair of neurovascular unity following cerebrovascular accidents

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PS-1-C -  Disorders of the Nervous System

poster

Colleagues and Friends:

I am very happy to welcome you to the 14th annual Canadian Neuroscience Meeting, and to the first virtual edition of our meeting. I want to highlight the important work the CAN meeting chair, **Roger Thompson** and co-chair, **Alyson Fournier**, did to put together the great program we are offering this year. Moving to a virtual format required a complete re-design of the program, and both Roger and Alyson did a splendid job in providing us with an appealing and well adapted program for our first virtual event. I wish to thank them for this very important effort.

Highlights of this year’s scientific meeting include invited speakers **Michael Hausser, Franck Polleux, Gwyneth Card, Magdalena Götz**and Brain Prize winner **Huda Zoghbi**. Plenary and parallel symposia, proposed by our members complete our diverse [scientific program.](https://can-acn.org/meeting-2021/program-2021/)

The 2021 Advocacy session, chaired and organized by CAN advocacy committee chair **Karun Singh**, will feature a special lecture and question period with Member of Parliament and past Science Minister **Kirsty Duncan**. This will be followed by a short overview of CAN’s advocacy activities over the last year. We invite you to participate in this session for insight from Dr. Duncan on the workings of Parliament Hill, and to learn more about what CAN has been doing to promote neuroscience research in Canada.

We are also excited to host **Lisa Willis** in the Equity Diversity and Inclusion session, organized by EDI committee chair **Jibran Khokhar**.

A special highlight of our meeting will be the lectures by award-winning young neuroscientists. We are please to host the CAN 2020 Young Investigator Award winner **Mihaela Iordanova**, and CAN 2021 Young Investigator Award winners **Aaron Phillips** and **Tabrez Siddiqui**. Highlights will also include presentation by the top three winners of the CAN-CIHR-INMHA Brain Star Award winners, **Claire Gizowski, Nuria Daviu Abant** and **Lukas Tamayo-Orrego**.

Independently organized satellite symposia complement and complete this exciting program, check them out here: https://can-acn.org/meeting-2021/2021-satellite-symposia/

Some of the most engaging sessions are always the poster sessions featuring the work of our trainees, so make sure to log in to Gather Town during the poster sessions to chat with the presenters.
We hope you enjoy this program, and look forward to welcoming you, virtually.

Shernaz Bamji

President of the Canadian Association for Neuroscience

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Dickkopf-1 induction impairs short- and long-term structural and functional recovery after ischemic stroke

Exploration of the pro-angiogenic potential of pericytes in the repair of neurovascular unity following cerebrovascular accidents

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