Published January 1, 2014 | Version v1
Book chapter Restricted

PET tracers for amyloid and other proteinopathies

Authors/Creators

  • 1. Karolinska Institutet, Alzheimer Neurobiology Center, Department of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden

Description

The recent rapid development of molecular imaging techniques has provided us with great possibilities to follow disease processes in brain in neurodegenerative diseases. Molecular imaging with positron emission tomography (PET) has so far to have been quite important for the further understanding of the role of various proteinpathies in dementia disorders. For Alzheimer´s disease (AD) several PET beta amyloid (Aß) tracers have been developed. These include the most investigated 11C-Pittsburgh compound B (11C-PIB), but also several 18F-labelled tracers as 18F-florbetapir, 18F-florbetaben, 18F-flutemetamol, 18F-NAV-4694 with longer half-life and therefore more suitable for clinical use. Fibrillar brain Aß is detected by PET very early in the progression of AD and precedes with several years the decline in cerebral glucose metabolism which is more closely are related to cognitive impairment. PET Aß imaging allows discrimination between AD and other non-Aß disease including FTLD. However other dementia disorders including DLB and Parkinson´s disease with dementia (PDD) and cortical basal dementia may also express Aß in brain. Most importantly there is presently a development of different PET tau tracers which will provide a further important insight and understanding of the complex pathophysiology processes in various neurodegenerative diseases.

Files

Restricted

The record is publicly accessible, but files are restricted. Log in to check if you have access.

Additional details

Funding

European Commission
INMIND - Imaging of Neuroinflammation in Neurodegenerative Diseases 278850