Seminar with David J. Brooks, MD, DSc, FRCP, FMedSci
“Recent Advances in Imaging Alzheimer’s and Parkinson’s Diseases”
Wednesday, May 2nd, 2007
McGovern Institute for Brain Research

David J. Brooks, MD, DSc, FRCP, FMedSci
Hartnett Professor of Neurology, Imperial College London

Recent Advances in Imaging Alzheimer’s and Parkinson’s Diseases

Dr. Brooks presented how molecular tracers for PET imaging can detect changes that contribute to the cognitive decline in Alzheimer’s and Parkinson’s diseases. (He noted that in early dementia associated with Parkinson’s much is in fact Alzheimer’s.) PET studies of people with mild cognitive impairment (MCI) who progress to Alzheimer’s disease show that one of the earliest detectable changes, a reduction in glucose metabolism, occurs in the back of the brain, where tau tangles inside neurons also appear, while amyloid plaques accumulate in both the forebrain and the back of the brain. One ligand, 11C-PIB PET, detects amyloid in 90% of clinically probable Alzheimer patients and 50% of MCI cases, which go on to develop AD. Longitudinal studies show that the plaques may have already accumulated before clinical symptoms occur and do not continue to accumulate as symptoms worsen. What then explains the cognitive decline? Brooks is examining the role of microglia, the scavenger immune cells in the brain that become activated in AD and PD-related dementia, to see if their activity supports the theory that inflammation triggers neural damage. He uses the ligand, 11C-PK11195 PET that detects widespread microglial activation in both forms of dementia. Early clinical studies of drug molecules are underway to see if switching off the microglia’s activity can impact the course of cognitive decline.