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Hello,
my name is Tony Schapira.
I'm going to talk to you today
about mitochondrial and lysosomal
dysfunction in the pathogenesis
of Parkinson's disease.
Parkinson's disease
is a common disorder.
Indeed, it is the second
commonest neurodegenerative
disorder after Alzheimer's disease.
It's anticipated that the total
number of people in the world
with Parkinson's disease
will double by 2030.
This is a consequence of increased
life expectancy of people,
and reflects the
increasing incidence
of Parkinson's disease with age.
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Several biochemical abnormalities
have been associated
with the pathogenesis
of Parkinson's disease,
and, of course, ultimately, with
the etiology of this disorder;
these include mitochondrial
dysfunction, oxidative stress,
intracellular calcium homeostasis,
excitotoxicity, inflammation,
protein misfolding, accumulation,
aggregation, and, of course,
now we know that this may also
include abnormal propagation
of proteins, apoptosis,
and autophagy,
which includes
mitophagy, the turnover
of mitochondria, and
lysosomal dysfunction.
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Today I'm going to focus on
mitochondrial dysfunction
and lysosomal dysfunction, as
these are two very important areas
of the pathogenesis of
Parkinson's disease,
and two which have attracted
considerable attention
over the past few years.
Let me begin with the
mitochondrial contribution
to Parkinson's disease,
and I'm first of all going to
cover some basic mitochondrial
biochemistry, so we can understand
how abnormal mitochondrial function
may contribute to the pathogenesis
of Parkinson's disease.
