Beta Amyloid Deposition Is Not Associated With Cognitive Impairment in Parkinson's Disease

The extent to which Alzheimer neuropathology, particularly the accumulation of misfolded beta-amyloid, contributes to cognitive decline and dementia in Parkinson's disease (PD) is unresolved. Here, we used Florbetaben PET imaging to test for any association between cerebral amyloid deposition and cognitive impairment in PD, in a sample enriched for cases with mild cognitive impairment. This cross-sectional study used Movement Disorders Society level II criteria to classify 115 participants with PD as having normal cognition (PDN, n = 23), mild cognitive impairment (PD-MCI, n = 76), or dementia (PDD, n = 16). We acquired 18F-Florbetaben (FBB) amyloid PET and structural MRI. Amyloid deposition was assessed between the three cognitive groups, and also across the whole sample using continuous measures of both global cognitive status and average performance in memory domain tests. Outcomes were cortical FBB uptake, expressed in centiloids and as standardized uptake value ratios (SUVR) using the Centiloid Project whole cerebellum region as a reference, and regional SUVR measurements. FBB binding was higher in PDD, but this difference did not survive adjustment for the older age of the PDD group. We established a suitable centiloid cut-off for amyloid positivity in Parkinson's disease (31.3), but there was no association of FBB binding with global cognitive or memory scores. The failure to find an association between PET amyloid deposition and cognitive impairment in a moderately large sample, particularly given that it was enriched with PD-MCI patients at risk of dementia, suggests that amyloid pathology is not the primary driver of cognitive impairment and dementia in most patients with PD

“Pervasive ocular tremor of Parkinson’s” is not pervasive, ocular, or uniquely parkinsonian

A putative tremulous oscillation of the eyes has been proposed to provide the long-sought objective, sensitive and specific diagnostic sign for Parkinson’s disease . Vigorous debate has ensued as to whether this “ocular tremor” is a real phenomenon or an artefact secondary to head motion. Contradictory arguments have centred on the capabilities of magnetic movement measurement technologies, with small numbers of illustrative cases presented to bolster either side. A large, definitive study able to either confirm or reject the original finding on a purely oculographic basis was required. We examined 681 oculomotor recordings from a longitudinal study of 188 Parkinson’s patients and 66 controls. Fourier analysis was used to detect oscilla- tions not only in their raw pupil motion data but also in corneal reflection signals, which can correct for head motion. We replicated the original authors’ findings inasmuch as we detected oscillations in raw pupil position data that often occurred in their reported frequency range of 5.7 ± 3 Hz. They were not, however, present universally in patients and the frequency (if not power) distribution was similar in controls. Crucially, oscillations in that frequency range were abolished when corneal reflection correction was applied to compensate for head-motion. The oscillations in the uncorrected data were strongly related to clinical ratings of somatomotor tremor severity. We found strong evidence that the postulated purely ocular tremor of Parkin- son’s does not exist, other than as an artefact arising from head motion secondary to somatic tremor

Accelerated atrophy in PD.

<p>Blue-green indicates areas where PD showed a higher rate of GM atrophy than controls over one year, overlaid on the MNI152_T1_brain image (slices displayed: z = -18, -14, 0, 12 mm; TFCE-corrected p<0.05; radiological convention).</p

Level I PD-MCI Using Global Cognitive Tests and the Risk for Parkinson's Disease Dementia

BackgroundThe criteria for PD-MCI allow the use of global cognitive tests. Their predictive value for conversion from PD-MCI to PDD, especially compared to comprehensive neuropsychological assessment, is unknown.MethodsThe MDS PD-MCI Study Group combined four datasets containing global cognitive tests as well as a comprehensive neuropsychological assessment to define PD-MCI (n&nbsp;=&nbsp;467). Risk for developing PDD was examined using a Cox model. Global cognitive tests were compared to neuropsychological test batteries (Level I&amp;II) in determining risk for PDD.ResultsPD-MCI based on a global cognitive test (MMSE or MoCA) increases the hazard for developing PDD (respectively HR&nbsp;=&nbsp;2.57, P&nbsp;=&nbsp;0.001; HR&nbsp;=&nbsp;4.14, P&nbsp;=&nbsp;&lt;0.001). The C-statistics for MMSE (0.72) and MoCA (0.70) were lower than those based on neuropsychological tests (Level I&nbsp;=&nbsp;0.82; Level II&nbsp;=&nbsp;0.81). Sensitivity, specificity and diagnostic accuracy balance was best in Level II.ConclusionMMSE and MoCA predict conversion to PDD. However, Level II neuropsychological assessment seems the preferred assessment for PD-MCI