Testing perceivers' accuracy and accuracy awareness when forming personality impressions from faces

People spontaneously judge others' personality based on their facial appearance and these impressions guide many important decisions. Although the consequences of personality impressions are well documented, studies on the accuracy of personality impressions have yielded mixed results. Moreover, relatively little is known about people's accuracy awareness (i.e., whether they are aware of their judgment accuracy). Even if accuracy is generally low, awareness of accuracy would allow people to rely on their impressions in the right situations. In two studies (one preregistered), we estimated perceivers' accuracy and accuracy awareness when forming personality impressions based on facial photographs. Our studies have three crucial advantages as compared to previous studies (a) by incentivizing accuracy and accuracy awareness, (b) by relying on substantially larger samples of raters (n(Study 1)= 223, n(Study 2) = 423) and targets (k(Study 1)= 140, k(Study 2) = 1,260 unique pairs with 280 unique targets), and (c) by conducting Bayesian analyses to also quantify evidence for the null hypothesis. Our findings suggest that face-based personality impressions are not accurate, that perceivers lack insight into their (in)accuracy, and that most people overestimate their accuracy

Different electrophysiological actions of 24- and 72-hour aggregated amyloid-beta oligomers on hippocampal field population spike in both anesthetized and awake rats.

Diffusible oligomeric assemblies of the amyloid beta-protein (Abeta) could be the primary factor in the pathogenic pathway leading to Alzheimer's disease (AD). Converging lines of evidence support the notion that AD begins with subtle alterations in synaptic efficacy, prior to the occurrence of extensive neuronal degeneration. Recently, however, a shared or overlapping pathogenesis for AD and epileptic seizures occurred as aberrant neuronal hyperexcitability, as well as nonconvulsive seizure activity were found in several different APP transgenic mouse lines. This generated a renewed attention to the well-known comorbidity of AD and epilepsy and interest in how Abeta oligomers influence neuronal excitability. In this study therefore, we investigated the effect of various in vitro-aged Abeta(1-42) oligomer solutions on the perforant pathway-evoked field potentials in the ventral hippocampal dentate gyrus in vivo. Firstly, Abeta oligomer solutions (1 microl, 200 microM) which had been aggregated in vitro for 0, 24 or 72h were injected into the hippocampus of urethane-anesthetized rats, in parallel with in vitro physico-chemical characterization of Abeta oligomerization (atomic force microscopy, thioflavin-T fluorescence). We found a marked increase of hippocampal population spike (pSpike) after injection of the 24-h Abeta oligomer solution and a decrease of the pSpike amplitude after injection of the 72-h Abeta oligomer. Since urethane anesthesia affects the properties of hippocampal evoked potentials, we repeated the injection of these two Abeta oligomer solutions in awake, freely moving animals. Evoked responses to perforant pathway stimulation revealed a 70% increase of pSpike amplitude 50 min after the 24-h Abeta oligomer injection and a 55% decrease after the 72-h Abeta oligomer injection. Field potentials, that reflect synaptic potentials, were not affected by the Abeta injection. These results demonstrate that oligomeric Abeta aggregates elicit opposite electrophysiological effects on neuronal excitability which depend on their degree of oligomerization