Hello, my name is Karl Herholz.
I'm a professor in Clinical Neuroscience at the University of Manchester.
This presentation is about molecular brain imaging
with PET in diseases that may lead to dementia.
It is mainly based on studies done at
the Max-Planck Institute for Neurological Research in Cologne,
Germany, where I have been working for many years before moving to Manchester.
Let me start with an explanation of positron emission tomography,
which is usually abbreviated as PET.
It is based on short living positron emitting isotopes which are produced by a cyclotron.
Commonly used isotopes are carbon-11 and fluorine-18.
They are coupled to various small amounts typically
micrograms of biomolecules for production of radiopharmaceuticals.
These are briefly called radiotracers or simply tracers.
They can be applied to humans,
usually by intravenous injection.
They act like contrast agent,
but the amounts are so small that they have
no pharmacological actions and side effects are extremely rare.
They emit positrons which annihilate with electrons.
Imaging by a PET scanner is then based on the resulting gamma radiation.
It represents quantitatively the in
vivo distribution of the tracer in the body or in our case,
especially in the brain.
From that distribution, local metabolic rates or
receptor binding potentials can be calculated using physiological modeling.
The scope of brain PET imaging is enormous.
It allows imaging of neuronal function and of specific neurotransmitters and receptors.
In addition, at the logical proteins and cellular markers can also be displayed.
Thus, PET provides images of brain function as well of underlying molecular mechanisms.
Let's start with images of brain function.