@JoelWattsLab

Associate Professor at the Tanz Centre for Research in Neurodegenerative Diseases/Department of Biochemistry, University of Toronto

 Toronto, Ontario
joelwattslab.org
Joined September 2018
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  • Following173
  • Followers352
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Our most recent work on amyloid beta strains is finally available here: doi.org/10.1186/s40478-026-0… We show that de novo formation of strains relevant to familial Alzheimer's disease occurs only in the human brain #Alzheimer #amyloidbeta #neurodegeneration

De novo formation of familial Alzheimer’s disease-relevant Aβ strains occurs exclusively in the...

Acta Neuropathologica Communications - In familial Alzheimer’s disease (FAD), mutations in the amyloid precursor protein gene (APP) accelerate the aggregation of Aβ peptide, leading to...

link.springer.com
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Joel Watts retweeted
Simon Mead@smead2Apr 17
Nice paper from colleagues emphasising prion-like mechanisms in dementia and inclusion of CJD in funding mechanisms for dementia disorders. Surprising resistance to prion-like mechanisms in dementia communities which imo often stems from poor understanding sciencedirect.com/science/ar…
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Online now in Neuron, the final published version of @xsakuraphie's PhD work on α-synuclein strain generation: Stochastic misfolding drives the emergence of distinct α-synuclein strains: Neuron cell.com/neuron/fulltext/S08…
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One of Raphie's most interesting findings was that α-synuclein PFFs that mimic the seeding behavior of Parkinson's disease brain extract can be generated in vitro, but we only obtained the specific "PD-like" PFF polymorph once from 35 independent PFF preparations.
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Perhaps the most important take home message from her work is that there is intrinsic structural variability between individual preparations of α-synuclein PFFs generated under identical conditions, which needs to be accounted for when designing and interpreting experiments.
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I'm pleased to announce that our latest prion-related work is now available as a preprint: biorxiv.org/content/10.64898… Dr. Genki Amano looked at whether P4HB, a protein disufide isomerase often identified in PrPC interactome screens, affects PrPC biosynthesis and prion replication.

The Protein Disulfide Isomerase P4HB/PDIA1 Modulates PrPC Levels and Prion Replication

Prions are misfolded, self-propagating versions of the cellular prion protein (PrPC) that cause invariably fatal transmissible neurodegenerative diseases in humans and animals. Little is known about...

biorxiv.org
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Genki's results support a model in which P4HB helps to stabilizes PrPC levels but also directly enhances the conversion of PrPC into PrPSc. Although much work remains to be done, targeting P4HB may constitute a new strategy for modulating prion replication.
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The Protein Disulfide Isomerase P4HB/PDIA1 Modulates PrPC Levels and Prion Replication biorxiv.org/content/10.64898… #biorxiv_neursci

The Protein Disulfide Isomerase P4HB/PDIA1 Modulates PrPC Levels and Prion Replication

Prions are misfolded, self-propagating versions of the cellular prion protein (PrPC) that cause invariably fatal transmissible neurodegenerative diseases in humans and animals. Little is known about...

biorxiv.org
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A huge congratulations to Dr. Raphaella So (@xsakuraphie) on a wildly successful PhD defense today. Also, a big thanks to @lvolpic for serving as the external examiner.
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Mount Pilatus in Lucerne, Switzerland. Amazing scenery and a fun luge-like ride down the hill.
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It is my great pleasure to share our most recent work on α-synuclein strains: biorxiv.org/content/10.1101/…. This study was led by @xsakuraphie and represents an amazing collaboration with Gunnar Schröder's lab.

Stochastic Misfolding Drives the Emergence of Distinct α-Synuclein Strains

The existence of α-synuclein conformational strains provides a potential explanation for the clinical and pathological differences among synucleinopathies such as Parkinson’s disease and multiple...

biorxiv.org
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Furthermore, our work reveals that stochastic misfolding results in considerable prep-to-prep variability among PFFs, which can influence downstream phenotypes. Thus, the inherent variability of α-synuclein PFFs needs to be accounted for when designing/interpreting experiments.
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Congratulations to all involved in this study (including @speedyerica), and a special thanks to Benedikt Frieg and José Camino for performing the cryo-EM experiments.
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Joel Watts retweeted
Raphie@xsakuraphie19 Nov 2024
Lab field trip! It’s rare to have so many lab members at a conference together (since we usually travel in packs of 2-3, max) Thanks TRIDENT for having us :) Excited to be learning here in the beautiful town of London, ON @JoelWattsLab @SurabhiMehra5
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Today is #CJDAwarenessDay. #Prions cause devastating neurological diseases such as CJD in humans. No cures are available, but promising research recently presented at the #Prion2024 conference. More about prion diseases and support here: cjdfoundation.org/

Home - CJD Foundation

The mission of the Creutzfeldt-Jakob Disease Foundation is to support families affected by Prion Disease, raise awareness, and support medical education and research.Learn MoreCommunity Statement...

cjdfoundation.org
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Joel Watts retweeted
Simon Mead@smead212 Nov 2024
Today is #CJDAwarenessDay. Check out this lovely collaborative video from the CJD International Support Alliance: cjdisa.com/video-globally… Help us spread the word to raise awareness and hope. #cjdawareness #priondiseaseawareness
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