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Printable Handouts
Navigable Slide Index
- Introduction
- Neurodegenerative disease (1)
- Neurodegenerative disease (2)
- Neurodegenerative disease (3)
- What causes neurodegenerative diseases?
- Misfolded aggregates deposited in the brain
- Role of protein aggregates in disease
- Research strategy
- Prion diseases
- Two conformations of the prion protein
- Brain alterations in prion diseases
- Experimental scrapie model in mice
- Sequence of events in scrapie pathogenesis
- ERp57 upregulation
- ERp57 and PrPSc correlation in the brain
- Upregulation of other ER chaperones
- ER-stress and UPR in human CJD
- The UPR pathway
- XBP-1 conditional KO did not affect prion disease
- PrP interaction with ER chaperones in brain
- PrPSc induces neuronal death in vitro
- PrPSc induces ER-stress in vitro
- Prion infection sensitizes cells to ER-stress
- Calcium release comes from the ER
- Hypothesis: Prion formation leads to ER stress
- Calcineurin properties
- Signaling pathways
- Calcineurin is implicated in PrPSc toxicity
- A novel treatment for prion diseases
- Treatment improves symptoms (behavior)
- Treatment increases animal survival
- FK506 effect on calcineurin and its targets
- Treatment decreases neuronal death
- Treatment decreases neurodegeneration
- Conclusions
- Acknowledgment
- Former lab members
Topics Covered
- Neurodegenerative disease
- Misfolded aggregates deposited in the brain
- Research strategy
- Prion diseases
- Two conformations of the prion protein
- Experimental scrapie model in mice
- Upregulation of ER chaperones
- ER-stress and UPR in human CJD
- PrP interaction with ER chaperones in brain
- PrPSc induction of ER-stress and neuronal death
- Calcineurin properties
- A novel treatment for prion diseases
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Talk Citation
Soto, C. (2012, February 2). Endoplasmic reticulum stress in neurodegenerative diseases [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 22, 2024, from https://doi.org/10.69645/KWGE4872.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Claudio Soto has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.