Distracted Attention, Temporal Switches, and the Consolations of Performing

Distraction is frequently blamed for interfering with the ergonomic production of capital, for encouraging substandard performance. Indeed, it is frequently configured as an impediment to timekeeping, a thorn in the side of consciousness, a drag on intentional action, and a brake on decision-making. Reality, however, is complex. While distraction can interfere with timing, anxiety, memory, error, and fatigue, it can also be exploited under controlled conditions to enhance performance by helping the performer to maintain an open cognitive and physical responsiveness to the world and a pragmatic mode of engagement with the task at hand. Indeed, distraction ensures that the performer is in close contact cognitively and socially with the full phenomenological plenitude of sound, thereby contributing to performance’s transformative value as a way of accumulating social capital in everyday life.

Neuroprotective Effect of Clobenpropit against Lipopolysaccharide-Induced Cognitive Deficits via Attenuating Neuroinflammation and Enhancing Mitochondrial Functions in Mice

Clobenpropit (CLO), an antagonist on histamine H3 receptors (HH3R), has been shown to protect NMDA-induced neuronal necrosis in cortical neuronal cell culture from rats. In this work, we explored its potential on lipopolysaccharide (LPS)-induced memory deficits, neuroinflammation, and mitochondrial dysfunction in mice. CLO (1 and 3 mg/kg, p.o.) was treated continually for 30 days, and neurotoxicity was induced by four doses of LPS (250 µg/kg, i.p.). The radial arm maze (RAM) was used to access memory behaviors. After the REM test, brain tissue was collected from each mouse to estimate pro-inflammatory cytokines (TNFα and IL6), anti-inflammatory cytokines (TGF-β1 and IL-10), cyclooxygenase-2 (COX 2), and mitochondrial respiratory chain complex (MRCC- I, II and IV) enzymes. CLO treatment reversed the LPS-induced behavioral deficits by a significant reduction in time taken to consume all five bites (TTB), working memory error (WME), and reference memory error (REM) in the REM test. Regarding neuroinflammation, it attenuated the release of COX, TNF-α, and IL-6, and augmented TGF-β1 and IL-10 levels in the brain. Reversal of LPS-induced brain MRCC (I, II, and IV) levels also resulted with CLO treatment. From these findings, CLO promises neuroprotection against LPS-induced cognitive deficits by ameliorating neuroinflammation and restoring the MRCC enzymes in mice.

The Visual Mandela Effect as evidence for shared and specific false memories across people

The Visual Mandela Effect (VME) is a pop internet phenomenon describing shared and consistent false memories for specific images; for example, the Monopoly Man is falsely remembered with a monocle. However, it has not been empirically tested whether certain images trigger the same false memory across observers. Here, across three experiments, we characterize images from popular iconography that elicit consistent and specific false memories. Using a method analogous to eye-tracking, we find that there are no clear attentional or low-level differences that drive this false memory phenomenon. Furthermore, a drawing experiment reveals that VME-errors can occur during recall. These results demonstrate for the first time that there are certain images for which people consistently make the same false memory error, despite only having seen the veridical image. A closer examination of the nature of these errors can inform us about shared processes in how we represent information for memory.