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Molecular brain imaging (PET) in diseases with dementia

Published on December 31, 2025   24 min

A selection of talks on Neuroscience

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0:00
Hello. My name is Karl Herholz. I'm a Professor Emeritus at the University of Manchester. This presentation is about molecular imaging with PET in diseases that may lead to dementia. It is mainly based on studies that I have done at the Max Planck Institute for Neurological Research in Cologne, Germany, where I have been working for many years before becoming a professor in clinical neuroscience at the University of Manchester.
0:30
Let me start with an explanation of positron-emission tomography, which is usually abbreviated as PET. It is based on short-lived positron-emitting isotopes, which are produced by a cyclotron. Commonly used isotopes are Carbon-11 and Fluorine-18. They are coupled to very small amounts, typically micrograms of biomolecules, for the production of radiopharmaceuticals. These are briefly called radio tracers or simply traces. They can be applied to humans usually by intravenous injection. They act like a contrast agent. But the amounts are so small that they have no pharmacological actions, and side effects are extremely rare. They emit positrons, which immediately react with electrons and tissue. Positrons and electrons annihilate each other and generate gamma radiation. Imaging by a PET camera is then based on a tomographic reconstruction of that camera's radiation. The scans show the in vivo distribution of the trace in the body, or in our case, especially in the brain. Ultimately, local metabolic rates or receptor binding potentials can be calculated from the tracer distribution using physiological modeling. The scope of brain PET imaging is enormous.

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Molecular brain imaging (PET) in diseases with dementia

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