Journal
NEUROBIOLOGY OF DISEASE
Volume 15, Issue 3, Pages 601-609Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2003.12.012
Keywords
amyotrophic lateral sclerosis; motor neuron disease; microglia; PK11195; positron emission tomography
Categories
Funding
- Medical Research Council [G0000749] Funding Source: Medline
- MRC [G0000749] Funding Source: UKRI
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Microglial activation is implicated in the pathogenesis of ALS and can be detected in animal models of the disease that demonstrate increased survival when treated with anti-inflammatory drugs. PK11195 is a ligand for the peripheral benzodiazepine binding site expressed by activated microglia. Ten ALS patients and 14 healthy controls underwent [C-11](R)-PK11195 PET of the brain. Volumes of interest were defined to obtain [C-11](R)-PK11195 regional binding potential values for motor and extra-motor regions. Significantly increased binding was found in motor cortex (P = 0.003), pons (P = 0.004), dorsolateral prefrontal cortex (P = 0.010) and thalamus (P = 0.005) in the ALS patients, with significant correlation between binding in the motor cortex and the burden of upper motor neuron signs clinically (r = 0.73, P = 0.009). These findings indicate that cerebral microglial activation can be detected in vivo during the evolution of ALS, and support the previous observations that cerebral pathology is widespread. They also argue for the development of therapeutic strategies aimed at inflammatory pathways. (C) 2004 Elsevier Inc. All rights reserved.
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