Welcome to this
Henry Stewart lecture
on cellular pathways linked to
dominant Parkinson's disease.
My name is Patrick Lewis, and
I am an associate professor
in the School of Pharmacy at
the University of Reading.
I will be covering our current
understanding of the biology
autosomal dominant Mendelian
forms of Parkinson's disease,
discussing how research
into this area is helping us
understand Parkinson's and develop
new therapies for this disorder.
Before I start, I
want to briefly put
the genetic forms of Parkinson's
into the context of the disease
as a whole, and in particular the
clinical and pathological nature
of this disorder.
Parkinson's as a recognized disease
entity has been around for well
over 100 years, with its origins
in this seminal monograph
from James Parkinson back in 1817.
The photo on the right is a
patient seen by Jean-Martin Charcot
in Paris in the 1870s and
displays the stooped posture that
is very typical of
Our concept of Parkinson's has
evolved over the past century.
However, the key symptoms
are well established.
The age of onset is
usually over the age of 60
with a disease duration
of around 12 years.
Resting tremor, bradykinesia
or slowed movement,
and akinesia, an inability
to initiate movement,
are the key movement phenotypes.
It is now well recognized that a
large proportion of Parkinson's
patients go on to develop dementia
in the later stages of the disease,
indicating a clinical overlap with
Dementia with Lewy Bodies, or DLB,
and that here are a range
of psychiatric symptoms
associated with the disease as well.
disease is characterized by loss
neurons in the midbrain
and in particular the substantia
nigra pars compacta, the region
displaying a dark coloring
in the upper right panel here
and absent due to cell
death in the panel below.