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Printable Handouts
Navigable Slide Index
- Introduction
- First description of ALS
- Amyotrophic lateral sclerosis/MN disease
- Plan of lecture
- The normal human motor system
- Normal vs. affected human spinal cord
- Characteristics of affected motor neurons
- TDP-43 protein in affected neurons
- Motor neuron disease: clinical consequences
- Spared motor neuron groups
- Motor neuron disease prognosis
- MNs: features underlying selective vulnerability
- ALS/MND: a complex and multifactorial disease
- Genetic factors in MND - Mendelian
- Cu/Zn SOD1 product and its related gene
- Cu/Zn SOD1 gene structure
- SOD1 mutations
- SOD1 mutations: loss of function?
- SOD1 mutations: toxic gain of function
- Potential mechanisms of neuronal oxidative stress
- Causes of oxidative stress
- Sources of intracellular oxidative stress
- Mitochondria: energy generators of the cell
- Mitochondrial free radical production
- The mitochondrial electron transport chain
- Intracellular reactive oxygen species (ROS)
- Targets damaged by ROS
- Anti-oxidant defence mechanisms
- Mitochondrial anti-oxidant defence
- Evidence for oxidative stress role in ALS/MND
- NSC34 cell model
- Use of NSC34 cell model
- Mitochondrial morphology in NSC34 MN cells
- Mitochondrial complex activity
- Alteration in the mitochondrial proteome
- Main altered proteins
- Dichlorofluorescein assay
- Oxidative stress measured by DCF in NSC34 cells
- DCF assay validation
- Protective effect of Ebselen on oxidative stress
- Affymetrix GeneChips
- Affymetrix system
- Differential gene expression in MN cell line (1)
- Differential gene expression in MN cell line (2)
- Key transcriptome changes in MN cell line
- Anti-oxidant related genes and pathways
- The Nrf2-ARE signalling pathway
- SOD1 G93A transgenic mouse model of ALS
- Disease progression in mutant transgenic mice
- Evidence for oxidative damage in transgenic mice
- Oxidative stress in human ALS
- CSF 3-nitrotyrosine levels
- Isolating motor neurons from tissue sections
- Peroxiredoxin 3 levels in human ALS
- Causes of oxidative stress in ALS/MND
- Major pathogenetic factors in ALS/MND
- Consequences of SOD1 gain of function mutation
- SOD1 chemistry
- How does mutant SOD1 exert neurotoxic effect?
- Glutamate-mediated injury to nerve cells
- Glutamate-mediated injury of motor neurons
- Normal glutamate neurotransmission
- Excitotoxicity and ALS
- Links between glutamate and oxidative stress
- Oxidative stress and links with excitotoxicity
- Mitochondria as targets for injury in ALS/MND
- Mitochondrial dysfunction in motor neuron injury
- Mitochondrial alterations in ALS/MND model cells
- Mitochondrial dysfunction in mutant SOD1 mice
- Evidence for mitochondrial dysfunction in humans
- COX and SDH mitochondrial enzyme activities
- Oxidative stress as a therapeutic target in ALS
- Mechanisms of action of anti-oxidant drugs
- Antioxidant treatment for ALS/MND
- Clinical trials of anti-oxidant therapies in ALS
- Ongoing trials of anti-oxidant therapies in ALS
- Preclinical testing in SOD1 mutant mouse
- Conclusions
Topics Covered
- Key facts
- The normal human motor system
- Motor neurone disease: clinical consequences
- Spared motor neurone groups
- Prognosis
- Features of motor neurones which may underlie selective vulnerability
- Complex and multifactorial disease
- Genetic factors
- SOD1 mutations
- Potential mechanisms of neuronal oxidative stress
- Sources of intracellular oxidative stress
- Mitochondrial free radical production
- ROS
- Evidence for the role of oxidative stress in ALS
- NSC34 cell model
- G93A mutant SOD1
- Oxidative stress in human ALS
- Major pathogenetic factors
- Glutamate
- Excitotoxicity
- Mitochondrial dysfunction
- Potential mechanisms of action of antioxidant drugs
- Clinical trials
Links
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Talk Citation
Shaw, P. (2007, November 1). Oxidative stress in ALS [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 26, 2024, from https://doi.org/10.69645/OCXQ3852.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.