Cognitive Status Doesn’t Impact Cortical Aβ, Tau in Parkinson’sLast Updated: December 12, 2017. Patterns of cortical β-amyloid and tau are not different for patients with Parkinson's disease who are cognitively normal or with mild cognitive impairment and for healthy adults, according to a study published online Dec. 11 in JAMA Neurology.
TUESDAY, Dec. 12, 2017 (HealthDay News) -- Patterns of cortical β-amyloid (Aβ) and tau are not different for patients with Parkinson's disease (PD) who are cognitively normal (PD-CN) or with mild cognitive impairment (MCI) and for healthy adults, according to a study published online Dec. 11 in JAMA Neurology.
Joseph R. Winer, from the University of California in Berkeley, and colleagues conducted a cross-sectional study involving 29 patients with PD (15 with PD-CN and 14 with PD-MCI) and 49 healthy controls to compare tau positron emission tomographic (PET) measurements.
The researchers found that six PD patients were Aβ-positive, of whom one had PD-MCI, and 23 patients were Aβ-negative. There were no significant differences in voxel-wise contrasts of whole-brain tau PET uptake between patients with PD-CN and PD-MCI, or for all patients with PD versus Aβ-negative controls. There were no differences in tau PET binding between patients with PD-MCI and PC-CN in brain regions reflecting Alzheimer's disease Braak stages 1/2, 3/4, or 5/6, nor was there any difference from Aβ-negative healthy older adults. In Aβ-positive patients with PD there was significantly elevated tau PET binding relative to Aβ-negative patients with PD within brain regions reflecting Alzheimer's disease Braak stage 3/4 and Braak stage 5/6.
"Age, Aβ, and tau do not differentiate patients with PD-CN and PD-MCI," the authors write. "Cognitive deficits in people with PD without dementia do not appear to reflect measureable Alzheimer disease."
Two authors disclosed financial ties to the pharmaceutical industry; Avid Radiopharmaceuticals enabled use of the [18F] AV-1451 tracer.
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