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Brief description/objective

Amyotrophic lateral sclerosis is a fatal neurodegenerative disorder characterized by a progressive and selective loss of upper and lower motor neurons (MNs), causing weakness and ultimately death. Glutamate excitotoxicity has been suggested to play a major role in amyotrophic lateral sclerosis. Glutamate is acting upon ionotropic and metabotropic glutamate receptors. One of the metabotropic glutamate receptors, mGlurR5, is upregulated during progression of ALS in the SOD1 mouse model. By blocking mGluR5 in this mouse model, motor neuron degeneration slowed down and survival was slightly extended. Recently, we have been able to demonstrate upregulation of mGluR5 in post mortem brain tissue of ALS patients using the new mGluR5-specific radioligand [18F]PSS232.
Our project aims at studying mGluR5 upregulation during the course of ALS in humans, using the mGluR5-specific radioligand. If this project is successful, a biomarker would be available to visualize the progression of the disease and potentially could track the efficacy of new drugs.