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Printable Handouts
Navigable Slide Index
- Introduction
- Parkinson’s disease (PD)
- Loci, genes and susceptibility factors
- PD molecular pathways
- Functional roles of mitochondria
- Parkin
- Parkin is recruited on impaired mitochondria
- PINK1 - PTEN-induced putative kinase 1
- PINK1 deficiency and mitochondrial dysfunction
- Modelling pathogenesis
- PINK1-Parkin interaction in drosophila
- Mitochondrial quality control by mitophagy
- The PINK1-Parkin mitophagy pathway
- PINK1 protein levels regulation
- Mitophagy - degradation of defective mitochondria
- The PINK1-Parkin mitophagy pathway (2)
- PD molecular pathways - Fbxo7
- Fbxo7 - background
- Role of Fbxo7 in the PINK1-Parkin mitophagy
- Fbxo7 interacts with Parkin
- Fbxo7 is recruited to damaged mitochondria
- Fbxo7 recruits Parkin to damaged mitochondria
- Fbxo7 rescues Parkin knockout in drosophila
- Fbxo7 is required for Mfn1 ubiquitination
- Fbxo7 is required for mitophagy
- Role of Fbxo7 in the PINK1-Parkin mitophagy (2)
- PINK1-Parkin mitophagy pathway-other players
- PINK1-Parkin mitophagy pathway-other players (2)
- PINK1 deficiency and mitochondrial dysfunction (2)
- Valosin Containing Protein (VCP)
- Degradation of defective mitochondria - mitophagy
- Modelling pathogenesis (2)
- Mitochondrial dysfunction and VCP deficiency
- VCP deficiency & mitochondrial depolarisation (1)
- VCP deficiency & mitochondrial depolarisation (2)
- VCP deficiency & mitochondrial depolarisation (3)
- Mitochondrial quality control by mitophagy (2)
- Mitochondrial dysfunction vs. mitophagy defect
- Perspectives
Topics Covered
- Parkinson's disease (PD) and mitophagy
- Pathogenic mutations in the genes associated with autosomal recessive PD interfere with the mitophagy pathway
- Mitophagy is the selective degradation of damaged mitochondria by autophagy
- Mitophagy allows optimal cellular energy production while it avoids toxic accumulation of damaged mitochondria in neurons.
Links
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Therapeutic Areas:
Talk Citation
Plun-Favreau, H. (2014, July 1). Autosomal recessive Parkinson’s disease and mitophagy [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 14, 2024, from https://doi.org/10.69645/CELG6674.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Helene Plun-Favreau has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Genetics & Epigenetics
Transcript
Please wait while the transcript is being prepared...
0:00
My name is Helene Plun-Favreau
and I am a Senior Lecturer at
UCL Institute of Neurology.
So my lab is interested
in mitophagy and autosomal
recessive Parkinson's disease.
0:13
Parkinson's disease is a progressive
neurodegenerative movement
disorder.
It affects about 1%
of the population
above the age of 65 years old.
The clinical features
of Parkinson's disease
are resting tremor, rigidity and
slowness in movement, as well as
the characteristic
postural instability.
Parkinson's disease can be
induced by toxins that poison
the mitochondria such as
neurotoxins and pesticides.
It is characterized by the slow
and progressive degeneration
of dopaminergic neurons in the
substantia nigra.
On the left, you can see a normal
brain where dopaminergic neurons
are stained with neuromelanin,
a natural dark pigment.
And on the right, a
Parkinson's diseased brain.
You can see that most of the
dopaminergic neurons are lost.
Parkinson's disease
is also characterized
by some characteristic cytoplasmic
inclusions called Lewy bodies.
Although Parkinson's
disease was long considered
as a non-genetic disorder of
sporadic origin, 5% to 10%
of the patients are now known to
have genetic forms of the disease.
1:22
In fact, the research in
Parkinson's disease genetics
has been extremely prolific
over the past 15 years.
The first gene discovered was
alpha-synuclein encoded by SNCA.
Alpha-synuclein is the main
constituent of the Lewy bodies
together with ubiquitin.
Since then, a number of loci
and genes have been identified.
This table is about a year old and
most probably out of date already.