Adler, Charles H.

Abnormal expression of genes for energy regulation in Parkinson’s disease patients identifies a master regulator as a possible therapeutic target for early intervention.

PurposeCorticomuscular electroencephalographic-electromyographic (EEG-EMG) coherence elicited by speech and nonspeech oromotor tasks in healthy participants and those with Parkinson’s disease (PD) was examined. Hypotheses were the following: (a) corticomuscular coherence is demonstrable between orbicularis oris (OO) muscles' EMG and scalp EEG recording; (b) the presence, location, and magnitude of coherence is task specific; (c) differences in corticomuscular coherence patterns exist between healthy and PD participants; and (d) differences will manifest as either increased or decreased coherence values in certain frequency bands, with EEG localization at primary sensorimotor cortex and/or supplementary motor area (SMA).MethodSimultaneous EEG, EMG (OO), and speech samples were recorded on 20 healthy and 20 PD participants during speech and nonspeech tasks. Fast Fourier transform and coherence analysis was performed with Neuroscan software on 1,000 randomly generated epochs per task per group. Corticomuscular coherence was analyzed between each EEG electrode and right and left superior and inferior OO muscles up to 200 Hz. Significant coherence peaks exceeded 95% confidence limits (.003).ResultsCorticomuscular coherence existed for both groups and for all tasks, but to varying degrees in primary sensorimotor cortex and SMA.ConclusionsResults support task specificity for both groups and, in PD, a diminished modulation flexibility linked to the sensorimotor area and reduced corticomuscular coherence at the SMA.

BackgroundWe evaluated the amounts of amyloid beta (Aβ)) peptides in the central nervous system (CNS) and in reservoirs outside the CNS and their potential impact on Aβ plasma levels and Alzheimer's disease (AD) pathology.MethodsAmyloid β levels were measured in (1) the plasma of AD and nondemented (ND) controls in a longitudinal study, (2) the plasma of a cohort of AD patients receiving a cholinesterase inhibitor, and (3) the skeletal muscle, liver, aorta, platelets, leptomeningeal arteries, and in gray and white matter of AD and ND control subjects.ResultsPlasma Aβ levels fluctuated over time and among individuals, suggesting continuous contributions from brain and peripheral tissues and associations with reactive circulating proteins. Arteries with atherosclerosis had larger amounts of Aβ40 than disease‐free vessels. Inactivated platelets contained more Aβ peptides than activated ones. Substantially more Aβ was present in liver samples from ND patients. Overall, AD brain and skeletal muscle contained increased levels of Aβ.ConclusionsEfforts to use plasma levels of Aβ peptides as AD biomarkers or disease‐staging scales have failed. Peripheral tissues might contribute to both the circulating amyloid pool and AD pathology within the brain and its vasculature. The wide spread of plasma Aβ values is also due in part to the ability of Aβ to bind to a variety of plasma and membrane proteins. Sources outside the CNS must be accounted for because pharmacologic interventions to reduce cerebral amyloid are assessed by monitoring Aβ plasma levels. Furthermore, the long‐range impact of Aβ immunotherapy on peripheral Aβ sources should also be considered.