Alzheimer's disease (AD) is a complex neurodegenerative dementing illness. Over the past few years, however, remarkable advances have taken place in understanding both the genetic and molecular biology with the intracellular processing of amyloid and tau and the changes leading to the pathologic formation of extracellular amyloid plaques and the intraneuronal aggregation of hyperphosphorylated tau into neurofibrillary tangles. This progress in our understanding of the molecular pathology has set the stage for clinically meaningful advances in the development of biomarkers. Emerging diagnostic methods that are based on biochemical and imaging biomarkers of disease specific pathology hold the potential to provide effective measures of natural history (marker of disease that is predictive of outcome), biological activity (such as magnitude and frequency of response correlating with drug potency) and markers of surrogate endpoints (single or composite marker that accounts for clinical benefit of the therapy). Markers of biological activity should be also evaluated regarding their value to reflect disease progression, heterogeneity of the clinical population, for early decision making and characterization of new treatments. We focussed on the current status of core analytes which provide reasonable evidence for association with key mechanisms of pathogenesis or neurodegeneration in AD. In addition, feasibility was important, such as availability of a validated assay for the biological measure in question, with properties that included high precision and reliability of measurement, reagents and standards well described. On this basis we reviewed the body of literature that has examined CSF total tau (t-tau) and beta-amyloid 1-42 (Abeta(1-42)), phosphorylated tau (p-tau) and beta-amyloid-antibodies as diagnostic tests for AD versus clinically representative comparison groups. Measurement of t-tau and Abeta(1-42) in the CSF seems useful to discriminate early and incipient AD from age-associated memory-impairment, depression, and some secondary dementias. First studies showed that measurement of p-tau proteins significantly improves early and differential diagnosis, as well as disease prediction in subjects at risk for AD and comes closest to fulfilling proposed criteria of a biological marker for AD. However, the nature of the majority of reported findings are still preliminary and retrospective. General issues for biomarkers have to be adequately addressed, such as sensitivity of the method, frequency of assessments, stability of the method, standardization of methods and dynamic range. There is still a partial lack of comparison patient populations that must be addressed in future studies. International dementia networks have been recently established to advance the establishment of core biomarker candidates of AD as potential surrogate endpoints for clinical trials and their clinical use for predictive and diagnostic purposes.
Our actions affect the behavior of other people in predictable ways. In the present article, we describe a theoretical framework for action control in social contexts that we call sociomotor action control. This framework addresses how human agents plan and initiate movements that trigger responses from other people, and we propose that humans represent and control such actions literally in terms of the body movements they consistently evoke from observers. We review evidence for this approach and discuss commonalities and differences to related fields such as joint action, intention understanding, imitation, and interpersonal power. The sociomotor framework highlights a range of open questions pertaining to how representations of other persons' actions are linked to one's own motor activity, how specifically they contribute to action initiation, and how they affect the way we perceive the actions of others.
Motor actions are facilitated if they are foreseeably being imitated rather than counterimitated by social partners. Such beneficial effects of anticipated imitation have been explained in terms of compatibility between one's own actions and their anticipated consequences. Previous demonstrations of these effects might alternatively be explained by consistently faster partner responses for imitative than for nonimitative actions, however. This study contrasts both explanations by using virtual coactors to disentangle the contributions of anticipated action-effect compatibility and anticipated action-effect delay. The data of two experiments support previous theoretical assumptions by showing that the effects of anticipated imitation are indeed driven by compatibility rather than delay.
Sensory consequences of an agent's actions are perceived less intensely than sensory stimuli that are not caused (and thus not predicted) by the observer. This effect of sensory attenuation has been discussed as a key principle of perception, potentially mediating various crucial functions such as agency and the discrimination of self-caused sensory stimulation from stimuli caused by external factors. Precise models describe the theoretical underpinnings of this phenomenon across a variety of modalities, especially the auditory, tactile, and visual domain. Despite these strong claims, empirical evidence for sensory attenuation in the visual domain is surprisingly sparse and ambiguous. In the present article, the authors therefore aim to clarify the role of sensory attenuation for learned visual action effects. To this end, the authors present a comprehensive replication effort including 3 separate, high-powered experiments on sensory attenuation in the visual domain with 1 direct and 2 preregistered, conceptual replication attempts of an influential study on this topic (Cardoso-Leite et al., 2010). Signal detection analyses were targeted to distinguish between true visual sensitivity and response bias. Contrary to previous assumptions and despite high statistical power, however, the authors found no evidence for sensory attenuation of learned visual action effects. Bayesian analyses further supported the null hypothesis of no effect, thus constraining theories that promote sensory attenuation as an immediate and necessary consequence of voluntary actions. (PsycINFO Database Record
Deliberate rule violations have typically been addressed from a motivational perspective that asked whether or not agents decide to violate rules based on contextual factors and moral considerations. Here we complement motivational approaches by providing a cognitive perspective on the processes that operate during the act of committing an unsolicited rule violation. Participants were tested in a task that allowed for violating traffic rules by exploiting forbidden shortcuts in a virtual city maze. Results yielded evidence for sustained cognitive conflict that affected performance from right before a violation throughout actually committing the violation. These findings open up a new theoretical perspective on violation behavior that focuses on processes occurring right at the moment a rule violation takes place.
We often ask other people to carry out actions for us in order to reach our goals. However, these commanded actions may sometimes go awry, and goal attainment is hindered by errors of the following person. Here, we investigated how the commanding person processes these errors of their follower. Because such errors indicate that the original goal of the command is not met, error processing for these actions should be enhanced compared to passively observing another person's actions. Participants thus either commanded another agent to perform one of four key press responses or they passively observed the agent responding. The agent could respond correctly or commit an error in either case. We compared error processing of commanded and passively observed actions using observation-related post-error slowing (oPES) as a behavioral marker and observed-error-related negativity (oN /oERN) and observed-error positivity (oP ) as electrophysiological markers. Whereas error processing, as measured via the oERN, was similarly pronounced for commanded and observed actions, commanded actions gave rise to stronger oPES and a stronger oP . These results suggest that enhanced monitoring is an automatic by-product of commanding another person's actions.
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