Increased peripheral benzodiazepine binding sites in the brain of patients with Huntington's disease.

Huntington's disease (HD) is a hereditary disorder associated with the development of dyskinesias and dementia, characterised by profound atrophy of the striatum and, to a lesser extent, other brain areas. A relative gliosis has been described. One marker for such inflammatory gliosis is an elevation of peripheral type benzodiazepine binding sites (PTBBS); these have also been shown to be increased following acute experimental and chronic degenerative neuronal damage. The present study investigates [3H]PK11195 binding to PTBBS in three brain areas of HD patients. We found a highly significant increase in PTBBS density in the putamen, a moderate but significant increase in the frontal cortex of HD patients and no significant change in the temporal cortex. Comparing these results to findings in other neurodegenerative diseases, e.g. Alzheimer's disease, where inflammation is discussed as a possible primary as well as a secondary pathological mechanism, our observations point to a possible involvement of inflammation in the neurodegenerative process in HD.