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Printable Handouts
Navigable Slide Index
- Autophagy and neurodegeneration
- Lecture outline
- Can we enhance clearance of mutant protein?
- Autophagy-lysosome pathway
- Autophagy substrates – cells, flies, mice
- Autophagy induction in other proteinopathies
- mTOR-independent autophagy-inducing drugs
- Autophagy signalling: mTOR & VPS35
- Canonical autophagy signalling
- Non-canonical autophagy signalling– new targets
- Neurodegenerative diseases impairing autophagy
- Endocytic trafficking & autophagosome biogenesis
- VPS35 PD mutation affects ATG9 trafficking
- CALM; an AD risk locus
- PolyQ diseases
- Exploring pathogenic mechanism
- Interesting considerations
- Wild-type Ataxin 3 regulates autophagy
- Wild-type Ataxin 3 regulates PI3P levels
- Ataxin 3 protects Beclin 1 from degradation
- Model
- Ataxin 3 polyQ interacts with Beclin 1
- Impaired autophagy in various models
- Results
- Autophagy and neurodegeneration
- Acknowledgements
Topics Covered
- Autophagy-lysosome pathway
- Autophagy signaling (canonical & non-canonical)
- Neurodegenerative diseases impairing autophagy
- Exploring pathogenic mechanism
- Ataxin 3 & autophagy
- Autophagy and neurodegeneration
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Rubinsztein, D.C. (2018, October 31). Autophagy and neurodegeneration [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 5, 2024, from https://doi.org/10.69645/PLMA7989.Export Citation (RIS)
Publication History
Financial Disclosures
- No conflicts of interest for this talk.
Other Talks in the Series: Autophagy and Lysosomal Storage Diseases
Transcript
Please wait while the transcript is being prepared...
0:00
I'm David Rubinsztein from the Cambridge Institute for Medical Research.
Today, I will give an overview of the links between autophagy and neurodegeneration.
While these will be primarily illustrated with examples from my lab,
I want to stress that many others have made important contributions to this area.
0:20
I'm going to structure my talk in three components.
First, I will give an overview of some older work
that describes key relationships between autophagy and neurodegeneration.
I'm then going to move on to more recent studies illustrating
how we searched for new signals that regulate the autophagy process,
and in the third part of the talk,
I'm going to focus on trying to understand how the process of
autophagy might be compromised in various neurodegenerative diseases.
0:54
Most of the neurodegenerative diseases that afflict man manifest with
the intracellular accumulation of aggregate-prone proteins in inclusions.
So, on this slide,
you can see in boxes A and D
panels from Huntington's disease brains showing such inclusions.
B and E show Parkinson's, and tau in Alzheimer's disease in E,
and C and F show extracellular inclusions in Alzheimer's disease.
Today we're primarily concerned with
the inclusions that form within the cells in the cytoplasm.
In these cases, for instance in Huntington's disease and
Parkinson's disease and tau,
there is extensive genetic and transgenic data arguing that these proteins are
toxic for the cells and manifest toxicity by gain-of-function mechanisms.
Therefore, a key objective we've had in my lab for many years,
is to see if we can enhance the clearance of
such mutant proteins relative to their wild-type counterparts.