On Sunday, April 20th 2025, starting 8:30am GMT, there will be maintenance work that will involve the website being unavailable during parts of the day. We apologize for any inconvenience this may cause and appreciate your understanding.
We noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Amyotrophic lateral sclerosis
- ALS - classification
- Death of motor neurons
- Gene discovery in ALS
- ALS – SOD1 mutations overview
- Abundance of ALS models: mice/rats/flys/fish
- The mechanisms of neuron/glial toxicity
- Astroglial cells contribute to ALS pathogenesis
- Evidence for astroglial dysfunction in ALS
- Astroglial defect in ALS
- ALS is disorder of oligodendroglial function
- Neural/glial stem cell lineages
- An enigmatic population of glial cells in CNS
- NG2+ cells in the adult spinal cord
- Gliosis in the spinal cord of ALS mice
- Enhanced proliferation of NG2+ cells in ALS mice
- PDGFalphaR-CreER BAC transgenic mice
- Enhanced cell proliferation in ALS mice
- NG2+ cells remain lineage restricted
- Human cortical ALS NG2 altered morphology
- Myelin protein(s) in motor cortex of ALS patients
- Human ALS: cortical demyelination
- ALS spinal cord ventral gray demyelination
- Loss of myelin basic protein (MBP)
- MTR abnormalities in human ALS
- Is there evidence for oligo injury in ALS?
- Oligodendroglia metabolically support axons
- Astrocyte-oligodendrocyte-neuron lactate shuttle
- Topology of MCT1
- MCT1 is widely expressed in oligodendroglia
- MCT1-TdTom is not expressed by astroglia
- Immunolocalization confirms MCT1 to Oligo
- MCT1 is present only in oligodendrocytes
- Loss of MCT1 leads to MN degeneration
- Lactate rescues MCT1i mediated neuronal toxicity
- Lactate also rescues neuronal toxicity in vivo
- MCT1 het mice show axonal degeneration
- MCT1 knockdown leads to axonal degeneration
- Hypothesis
- MCT1 in affected areas of ALS patients
- MCT1 expression in ALS gray matter oligos
- Oligodendroglia: metabolic stabilizers of axons
- C14-lactate uptake and block by MCTi
- More questions should be explored…
- Acknowledgements
Topics Covered
- The variety of cellular pathways causing Amyotrophic Lateral Sclerosis (ALS)
- A new ALS-causing cellular pathway implicating oligodendroglia and their newly discovered property of metabolic support neurons via lactate transport
- Unexpected major cellular injury in ALS gray matter and the relationship to newly discovered ALS-causing pathway – Current and future targets for therapeutic intervention in ALS
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Rothstein, J.D. (2013, August 19). Oligodendroglia/MCT1 are an unexpected contributor to CNS toxicity/neurodegeneration [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 15, 2025, from https://doi.org/10.69645/NOCT4579.Export Citation (RIS)
Publication History
- Published on August 19, 2013
Financial Disclosures
- Prof. Jeffrey D. Rothstein has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Oligodendroglia/MCT1 are an unexpected contributor to CNS toxicity/neurodegeneration
Published on August 19, 2013
38 min
A selection of talks on Neuroscience
Hide