Sugihara Causality Analysis of Scalp EEG for Detection of Early Alzheimer\u27s Disease

Recently, Sugihara proposed an innovative causality concept, which, in contrast to statistical predictability in Granger sense, characterizes underlying deterministic causation of the system. This work exploits Sugihara causality analysis to develop novel EEG biomarkers for discriminating normal aging from mild cognitive impairment (MCI) and early Alzheimer\u27s disease (AD). The hypothesis of this work is that scalp EEG based causality measurements have different distributions for different cognitive groups and hence the causality measurements can be used to distinguish between NC, MCI, and AD participants. The current results are based on 30-channel resting EEG records from 48 age-matched participants (mean age 75.7 years) - 15 normal controls (NCs), 16 MCI, and 17 early-stage AD. First, a reconstruction model is developed for each EEG channel, which predicts the signal in the current channel using data of the other 29 channels. The reconstruction model of the target channel is trained using NC, MCI, or AD records to generate an NC-, MCI-, or AD-specific model, respectively. To avoid over fitting, the training is based on the leave-one-out principle. Sugihara causality between the channels is described by a quality score based on comparison between the reconstructed signal and the original signal. The quality scores are studied for their potential as biomarkers to distinguish between the different cognitive groups. First, the dimension of the quality scores is reduced to two principal components. Then, a three-way classification based on the principal components is conducted. Accuracies of 95.8%, 95.8%, and 97.9% are achieved for resting eyes open, counting eyes closed, and resting eyes closed protocols, respectively. This work presents a novel application of Sugihara causality analysis to capture characteristic changes in EEG activity due to cognitive deficits. The developed method has excellent potential as individualized biomarkers in the detection of pathophysiological changes in early-stage AD

Ego Identity and Relational and Social Aggression Mediated by Elaborative and Deep Processing

Abstract: In this investigation, late adolescents' (N = 629) ego identity status (e.g., identity achievement, identity diffusion, identity moratorium, and identity foreclosure), cognitive processing style, and self-reported use of relational aggression and social aggression were measured in order to assess potential relationships among these constructs. Four separate models were used to test these hypotheses, and the results showed support for some but not all the four hypotheses. In this sample, it appears that individuals with high levels of cognitive sophistication who lack social maturity by which to resolve relationship problems were more likely to use social aggression than those with lower levels of cognitive processing skills or with higher levels of emotional maturity

A Cognitive Electrophysiological Signature Differentiates Amnestic Mild Cognitive Impairment from Normal Aging

Background: Noninvasive and effective biomarkers for early detection of amnestic mild cognitive impairment (aMCI) before measurable changes in behavioral performance remain scarce. Cognitive event-related potentials (ERPs) measure synchronized synaptic neural activity associated with a cognitive event. Loss of synapses is a hallmark of the neuropathology of early Alzheimer’s disease (AD). In the present study, we tested the hypothesis that ERP responses during working memory retrieval discriminate aMCI from cognitively normal controls (NC) matched in age and education. Methods: Eighteen NC, 17 subjects with aMCI, and 13 subjects with AD performed a delayed match-to-sample task specially designed not only to be easy enough for impaired participants to complete but also to generate comparable performance between subjects with NC and those with aMCI. Scalp electroencephalography, memory accuracy, and reaction times were measured. Results: Whereas memory performance separated the AD group from the others, the performance of NC and subjects with aMCI was similar. In contrast, left frontal cognitive ERP patterns differentiated subjects with aMCI from NC. Enhanced P3 responses at left frontal sites were associated with nonmatching relative to matching stimuli during working memory tasks in patients with aMCI and AD, but not in NC. The accuracy of discriminating aMCI from NC was 85% by using left frontal match/nonmatch effect combined with nonmatch reaction time. Conclusions: The left frontal cognitive ERP indicator holds promise as a sensitive, simple, affordable, and noninvasive biomarker for detection of early cognitive impairment

A geodetic study of the 2003 January 22 Tecomán, Colima, Mexico earthquake

We use coseismic displacements and aftershock information from Global Positioning System (GPS) measurements at 27 sites in western Mexico and a 12-station local seismic network to determine the characteristics of the 2003 January 22 M_w = 7.2 subduction thrust earthquake near Tecomán, Colima, Mexico. Estimates of the earthquake moment, slip direction and best-fitting slip distribution are derived by optimizing the fit to the GPS displacements for a 3-D finite element mesh that simulates the study area. The calculated moment release is 9.1 × 10^(19) N m (M_w = 7.2) , with maximum slip of 2 m at a depth of 24 km and a maximum rupture depth of 35–40 km. The inversion indicates that coseismic rupture extended downdip from depths of 9 to 40 km along a 80 km along-strike region that is bounded by the edges of the Manzanillo Trough. The optimal solution is robust with respect to plausible changes in the subduction interface geometry and differing subsets of the data. A comparison of the cumulative post-seismic slip that can be inferred separately from earthquake aftershocks and GPS measurements within a year of the earthquake indicates that 95 per cent or more of the post-seismic deformation was aseismic. Near-term post-seismic measurements indicate that slip propagated downdip to areas of the subduction interface beneath the coastline within days following the earthquake, as also occurred after the nearby M_w = 8.0 Colima-Jalisco subduction earthquake in 1995. The similar behaviours and locations of the 1995/2003 earthquake sequence to two earthquakes in June of 1932 suggests that thrust earthquakes along the subduction interface northwest of the Manzanillo Trough may trigger earthquakes in the vicinity of the Manzanillo Trough; however, our modelling of Coulomb stress changes caused by the 1995 earthquake indicate that it induced only modest unclamping of the subduction interface in the vicinity of the Tecomán rupture. In addition, GPS measurements indicate that elastic shortening characterized areas onshore from the Tecomán rupture from mid-1997 up until the time of the rupture, consistent with progressively stronger clamping of the subduction interface during this period. This precludes any obvious triggering relationship with the 1995 earthquake. The apparent coincidence of the edge of both the 1932 and 1995/2003 rupture sequences with the edge of the Manzanillo Trough may indicate that the trough is a mechanical barrier to along-strike rupture propagation. This implies a limit to the area of potential slip and hence rupture magnitude during future large earthquakes in this region

Salinity and temperature balances at the SPURS central mooring during fall and winter

Author Posting. © The Oceanography Society, 2015. This article is posted here by permission of The Oceanography Society for personal use, not for redistribution. The definitive version was published in Oceanography 28, no. 1 (2015): 56-65, doi:10.5670/oceanog.2015.06.One part of the Salinity Processes in the Upper-ocean Regional Study (SPURS) field campaign focused on understanding the physical processes affecting the evolution of upper-ocean salinity in the region of climatological maximum sea surface salinity in the subtropical North Atlantic (SPURS-1). An upper-ocean salinity budget provides a useful framework for increasing this understanding. The SPURS-1 program included a central heavily instrumented mooring for making accurate measurements of air-sea surface fluxes, as well as other moorings, Argo floats, and gliders that together formed a dense observational array. Data from this array are used to estimate terms in the upper-ocean salinity and heat budgets during the SPURS-1 campaign, with a focus on the first several months (October 2012 to February 2013) when the surface mixed layer was becoming deeper, fresher, and cooler. Specifically, we examine the salinity and temperature balances for an upper-ocean mixed layer, defined as the layer where the density is within 0.4 kg m–3 of its surface value. The gross features of the evolution of upper-ocean salinity and temperature during this fall/winter season are explained by a combination of evaporation and precipitation at the sea surface, horizontal transport of heat and salt by mixed-layer currents, and vertical entrainment of fresher, cooler fluid into the layer as it deepened. While all of these processes were important in the observed seasonal (fall) freshening at this location in the salinity-maximum region, the variability of salinity on monthly-to-intraseasonal time scales resulted primarily from horizontal advection.J.T. Farrar, A.J. Plueddemann, J.B. Edson, and the deployment of the central mooring were supported by NASA grant NNX11AE84G. L. Rainville, C. Lee, C. Eriksen, and the Seaglider program were supported by NASA grant NNX11AE78G. R. Schmitt was supported by NSF grant OCE-1129646. B. Hodges and D. Fratantoni were supported by NASA grant NNX11AE82G. The Prawler moorings were funded by PMEL. The data analysis was also supported by NASA grant NNX14AH38G

Distinct Clinicopathologic Clusters of Persons with TDP-43 Proteinopathy

To better understand clinical and neuropathological features of TDP-43 proteinopathies, data were analyzed from autopsied research volunteers who were followed in the National Alzheimer’s Coordinating Center (NACC) data set. All subjects (n = 495) had autopsy-proven TDP-43 proteinopathy as an inclusion criterion. Subjects underwent comprehensive longitudinal clinical evaluations yearly for 6.9 years before death on average. We tested whether an unsupervised clustering algorithm could detect coherent groups of TDP-43 immunopositive cases based on age at death and extensive neuropathologic data. Although many of the brains had mixed pathologies, four discernible clusters were identified. Key differentiating features were age at death and the severity of comorbid Alzheimer’s disease neuropathologic changes (ADNC), particularly neuritic amyloid plaque densities. Cluster 1 contained mostly cases with a pathologic diagnosis of frontotemporal lobar degeneration (FTLD-TDP), consistent with enrichment of frontotemporal dementia clinical phenotypes including appetite/eating problems, disinhibition and primary progressive aphasia (PPA). Cluster 2 consisted of elderly limbic-predominant age-related TDP-43 encephalopathy (LATE-NC) subjects without severe neuritic amyloid plaques. Subjects in Cluster 2 had a relatively slow cognitive decline. Subjects in both Clusters 3 and 4 had severe ADNC + LATE-NC; however, Cluster 4 was distinguished by earlier disease onset, swifter disease course, more Lewy body pathology, less neocortical TDP-43 proteinopathy, and a suggestive trend in a subgroup analysis (n = 114) for increased C9orf72 risk SNP rs3849942 T allele (Fisher’s exact test p value = 0.095). Overall, clusters enriched with neocortical TDP-43 proteinopathy (Clusters 1 and 2) tended to have lower levels of neuritic amyloid plaques, and those dying older (Clusters 2 and 3) had far less PPA or disinhibition, but more apathy. Indeed, 98% of subjects dying past age 85 years lacked clinical features of the frontotemporal dementia syndrome. Our study revealed discernible subtypes of LATE-NC and underscored the importance of age of death for differentiating FTLD-TDP and LATE-NC