This study represents one of the largest and most clinically diverse investigations of the ACE-III. Our results demonstrate that the ACE-III is an acceptable alternative to the ACE-R. In addition, ACE-III performance has broader clinical implications in that it relates to carer reports of functional impairment in most common dementias. (JINS, 2018, 24, 854-863).

Normative word frequency has played a key role in the study of human memory, but there is little agreement as to the mechanism responsible for its effects. To determine whether word frequency affects binding probability or memory precision, we examined working memory for spatial positions of words. Each of three experiments included 300 trials in which five words were presented sequentially around an invisible circle followed by one of those words shown in the middle of the circle as a probe to test its location. Participants had to click on the associated location and the degree of error around the circle was the dependent measure. Across experiments we varied word frequency, presentation rate and the proportion of low frequency words on each trial. A mixture model dissociated memory precision, binding failure and guessing rates from the continuous distribution of errors. On trials that contained only low- or high-frequency words, low-frequency words lead to a greater degree of error in recalling the associated location. This was due to a higher word-location binding failure and not due to differences in memory precision or guessing rates. Slowing down the presentation rate eliminated the word frequency effect by reducing binding failures for low-frequency words. Mixing frequencies in a single trial hurt high-frequency and helped low-frequency words, but frequency composition and presentation rate did not interact. These findings support the idea that low-frequency words require more resources for binding and that the binding fails when these resources are insufficient.

Normative word frequency has played a key role in the study of human memory, but there is little agreement as to the mechanism responsible for its effects. To determine whether word frequency affects binding probability or memory precision, we used a continuous reproduction task to examine working memory for spatial positions of words. In three experiments, after studying a list of five words, participants had to report the spatial location of one of them on a circle. Across experiments we varied word frequency, presentation rate and the proportion of low frequency words on each trial. A mixture model dissociated memory precision, binding failure and guessing rate parameters from the continuous distribution of errors. On trials that contained only low-or only high-frequency words, low-frequency words lead to a greater degree of error in recalling the associated location. This was due to a higher word-location binding failure and not due to differences in memory precision or guessing rates. Slowing down the presentation rate eliminated the word frequency effect by reducing binding failures for low-frequency words.Mixing frequencies in a single trial hurt high-frequency and helped low-frequency words. These findings support the idea that word frequency can lead to both positive and negative mnemonic effects depending on a trade-off between a HF encoding advantage and a LF retrieval cue advantage. We suggest that 1) low-frequency words require more resources for binding, 2) that these resources recover gradually over time, and that 3) binding fails when these resources are insufficient.

Some individuals do not return to baseline health following SARS-CoV-2 infection, leading to a condition known as long COVID. The underlying pathophysiology of long COVID remains unknown. Given that autoantibodies have been found to play a role in severity of SARS-CoV-2 infection and certain other post-COVID sequelae, their potential role in long COVID is important to investigate. Here, we apply a well-established, unbiased, proteome-wide autoantibody detection technology (T7 phage-display assay with immunoprecipitation and next-generation sequencing, PhIP-Seq) to a robustly phenotyped cohort of 121 individuals with long COVID, 64 individuals with prior COVID-19 who reported full recovery, and 57 pre-COVID controls. While a distinct autoreactive signature was detected that separated individuals with prior SARS-CoV-2 infection from those never exposed to SARS-CoV-2, we did not detect patterns of autoreactivity that separated individuals with long COVID from individuals fully recovered from COVID-19. These data suggest that there are robust alterations in autoreactive antibody profiles due to infection; however, no association of autoreactive antibodies and long COVID was apparent by this assay.