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- Clinical themes
- Scientific themes
-
3. Neuroinflammation in ALS: cause or consequence?
- Prof. Philip Van Damme
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6. SOD1-related ALS: what has it told us about motor neuron degeneration? - part 1
- Prof. Dame Pamela Shaw
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7. SOD1-related ALS: what has it told us about motor neuron degeneration? - part 2
- Prof. Dame Pamela Shaw
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8. Expanding roles of RNA-binding proteins in neurodegenerative diseases
- Prof. Aaron D. Gitler
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9. Oxidative stress in amyotrophic lateral sclerosis (ALS) 1
- Prof. Dame Pamela Shaw
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10. Oxidative stress in amyotrophic lateral sclerosis (ALS) 2
- Prof. Dame Pamela Shaw
Printable Handouts
Navigable Slide Index
- Introduction
- Plan (5)
- Oxidative stress in human ALS
- Evidence that oxidative stress plays a role in non-SOD1 MND
- CSF 3-nitrotyrosine levels
- Oxidative stress induces TDP-43 proteinopathic changes
- Chronic oxidative stress induces wild type TDP-43 protein aggregates
- Oxidative stress in C9ORF72 molecular pathophysiology
- Oxidative stress at the neuromuscular junction
- Plan (6)
- 11 main pathophysiological mechanisms in ALS/MND
- Oxidative stress is a central mechanism in ALS/MND
- Links between glutamate and oxidative stress
- Oxidative stress in MND pathophysiology
- Targets damaged by ROS
- Antioxidant capacity declines and oxidative stress increases with age
- Plan (7)
- Potential mechanisms of action of anti-oxidant drugs
- Antioxidant treatment for ALS/MND Cochrane Database Systematic Review 2007
- Clinical trials of anti-oxidant therapies in ALS/MND (1)
- Clinical trials of anti-oxidant therapies in ALS/MND (2)
- Edaravone trials: key results
- Phase I copper ATSM trial
- Potential of Nrf2-ARE activators for ALS/MND
- Nuclear factor (erythroid-derived 2)-like 2: ‘NRF2’
- Conclusions
- Acknowledgments: research funding agencies
Topics Covered
- Evidence for oxidative stress in other subtypes of Motor Neuron Disease (MND)
- Causes of oxidative stress in MND
- The role of TDP-43 in MND
- Eleven main pathophysiological mechanisms in ALS/MND
- Oxidative stress as a therapeutic target in MND
- Ebselen
- Riluzole
- Edaravone, copper ATSM, and Dimethyl fumarate trials
Links
Series:
Categories:
Therapeutic Areas:
External Links
Talk Citation
Shaw, P. (2022, September 29). Oxidative stress in amyotrophic lateral sclerosis (ALS) 2 [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 5, 2024, from https://doi.org/10.69645/FMSC1814.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Dame Pamela Shaw has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Oxidative stress in amyotrophic lateral sclerosis (ALS) 2
Published on September 29, 2022
20 min
A selection of talks on Physiology & Anatomy
Transcript
Please wait while the transcript is being prepared...
0:04
What about other subtypes?
What about other genetic causes
and the 95% of
patients that don't
have a key autosomal
dominant genetic change
and have sporadic MND?
0:18
If you look in human
tissue, again,
you can find these
biochemical footprints of
free radical damage;
nitrotyrosine residues,
protein carbonyls, markers
of lipid oxidation,
markers of DNA damage.
8-hydroxy-2 deoxyguanosine
is a key marker
of oxidative damage to DNA.
You can find that in brain
and spinal cord tissue.
You can also find similar
biochemical changes
indicating the presence
of oxidative stress
in the cerebrospinal fluid,
the fluid that bathes the
brain and spinal cord,
and you can also find
biochemical evidence
of impaired antioxidant defence.
Reduced expression of the
peroxiredoxin enzyme,
reduced expression of NRF2,
and the downstream genes
controlled by that
transcription factor.
1:17
These are just some examples.
These are indices of
oxidative stress.
This is 8-hydroxy
deoxyguanosine.
You can see it's elevated in
ALS tissue compared to controls.
This is isoprostane, again,
elevated in MND patients
compared to controls.
Those oxidative stress
biomarkers are there in patients
with sporadic MND as well as
those with SOD1 mutations.