Amyloid clue to Parkinson’s dementia

By Eleanor McDermid, Senior medwireNews Reporter

Study findings link amyloid (A)β burden to future cognitive decline in patients with Parkinson's disease (PD).

However, Aβ burden, as assessed by Pittsburgh compound B (PiB) retention on positron emission tomography, did not distinguish between patients with normal cognitive function and mild cognitive impairment (MCI) at baseline.

John Growdon (Massachusetts General Hospital, Boston, USA) and team studied 35 PD patients with normal cognition and 11 with MCI, finding that the average cortical PiB uptake in these groups was 1.14 and 1.13, respectively. Both groups had uptake well below that commonly seen in patients with Alzheimer's disease (AD), and the team notes that nearly a third of cognitively normal people without AD or PD reportedly have "substantial" PiB uptake.

"The significance of elevated PiB retention in cognitively normal individuals is uncertain, and it is an open research question whether their amyloidosis represents a disease process that will progress to dementia on some timescale or whether it represents a risk factor," they write in Neurology.

Nevertheless, high PiB retention in people with MCI is a strong predictor for a later diagnosis of AD and Growdon et al found this to be the case in the PD patients in their study.

Eight of the patients with normal cognition developed MCI during up to 5 years of follow up, and one developed dementia, while five of those with MCI at baseline progressed to dementia. Patients with MCI at baseline had a faster cognitive decline than those with normal cognition, but PiB retention had an additional impact, with each unit increase at baseline raising the risk for patients transitioning to a more severe cognitive diagnosis 8.78-fold.

When divided according to the median PiB retention, patients with higher retention progressed to a more severe diagnosis faster than those with lower levels, despite having similar cognitive function at baseline.

PiB retention was strongly related to decline in executive function and weakly to visuospatial function. "These results are tantalizing, as frontal lobe functions and visuospatial skills are prominently affected in PD," says the team.

Growdon et al note that a number of drugs to combat Aβ are in development for AD. Should any prove effective, "similar treatments will become immediately relevant for treating PD with the expectation of preventing dementia, or at least slowing progression of cognitive impairments," they say.

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