[Article Review] Unveiling the Secrets of CORD7 Mutation: A Pathway to Enhanced Cognitive Abilities

Reference

Paul, M. M., Dannhäuser, S., Morris, L., Mrestani, A., Hübsch, M., Gehring, J., ... & Langenhan, T. (2022). The human cognition-enhancing CORD7 mutation increases active zone number and synaptic release. Brain, 145(11), 3787-3802. https://doi.org/10.1093/brain/awac011

Review

In a recent study published in Brain, Paul et al. (2022) delved into the enigmatic CORD7 mutation, which is associated with increased verbal IQ and working memory in humans. The autosomal dominant syndrome results from the R844H exchange in the C2A domain of RIMS1/RIM1, a vital component of presynaptic active zones. Until now, the impact of the CORD7 mutation on synaptic function remained unclear.

Using Drosophila melanogaster as a disease model, the researchers employed protein expression and X-ray crystallography to resolve the molecular structure of the fly's C2A domain. They found that the location of the CORD7 mutation is structurally conserved in fly RIM. CRISPR/Cas9-assisted genomic engineering was then utilized to generate rim alleles encoding the R915H CORD7 exchange or R915E, R916E substitutions to investigate their effects on synaptic transmission.

Electrophysiological characterization revealed that the CORD7 mutation exerted a semi-dominant effect on synaptic transmission, resulting in the faster, more efficient synaptic release, increased size of the readily releasable pool, and decreased sensitivity for the fast calcium chelator BAPTA. Additionally, the rim CORD7 allele increased the number of presynaptic active zones without altering their nanoscopic organization, as demonstrated by super-resolution microscopy of the presynaptic scaffold protein Bruchpilot/ELKS/CAST.

These findings suggest that the CORD7 mutation enhances synaptic transmission efficiency by promoting tighter release coupling, an increased readily releasable pool size, and more release sites. The authors conclude that similar mechanisms may underlie the CORD7 disease phenotype in patients and contribute to their heightened cognitive abilities. This study not only provides valuable insights into the molecular underpinnings of the CORD7 mutation but also paves the way for further research into potential therapeutic applications.

[Article Review] Unraveling the Impact of Digital Media on Children's Intelligence: A Comprehensive Study

Reference

Sauce, B., Liebherr, M., Judd, N., & Klingberg, T. (2022). The impact of digital media on children’s intelligence while controlling for genetic differences in cognition and socioeconomic background. Scientific Reports, 12(1), 7720. https://doi.org/10.1038/s41598-022-11341-2

Review

In their article, Sauce, Liebherr, Judd, and Klingberg (2022) explore the cognitive effects of digital media on children, addressing the ongoing debate surrounding this topic. The authors advocate for the inclusion of genetic data in such studies to clarify causal claims and account for typically unaddressed genetic predispositions. The study analyzed 9,855 children in the United States, part of the ABCD dataset, with intelligence measurements taken at ages 9-10 and after two years.

The authors discovered that time spent watching (r = -0.12) and socializing (r = -0.10) was negatively correlated with intelligence at baseline, while gaming showed no correlation. However, after two years, gaming had a positive impact on intelligence (standardized β = +0.17), which aligns with experimental studies on video gaming's cognitive benefits. Socializing, on the other hand, had no effect.

Interestingly, watching videos also benefited intelligence (standardized β = +0.12), which contradicts prior research on the impact of watching TV. A post hoc analysis, though, revealed that this was not significant when controlling for parental education instead of SES. Overall, the results support research on cognitive abilities' malleability from environmental factors, such as cognitive training and the Flynn effect.

The study by Sauce et al. (2022) provides valuable insights into the cognitive impact of digital media on children while addressing potential confounding factors. The findings contribute to a more nuanced understanding of the relationship between screen time and children's intelligence, offering implications for future research and educational policy.

[Article Review] Unraveling Cognitive Deficits in Post-Acute COVID-19 Patients: A Comprehensive Study

Reference

Hampshire, A., Chatfield, D.A., Manktelow, A.M., Jolly, A., Trender, W., Hellyer, P.J., ... & Menon, D.K. (2022). Multivariate profile and acute-phase correlates of cognitive deficits in a COVID-19 hospitalized cohort. eClinicalMedicine, 47, 101417. https://doi.org/10.1016/j.eclinm.2022.101417

Review

This study by Hampshire et al. (2022) aimed to confirm the association between severe COVID-19 and persistent cognitive deficits, determine whether cognitive deficits relate to acute-phase clinical features or mental health status at the assessment point, and quantify the rate of recovery. The researchers conducted a comprehensive computerized cognitive assessment of 46 individuals who received critical care for COVID-19 at Addenbrooke's Hospital between March 10th, 2020, and July 31st, 2020, and compared their results with matched controls (N = 460) using normative datasets (N = 66,008).

The results showed that COVID-19 survivors were less accurate and slower in their responses than their matched controls. Acute illness severity, but not chronic mental health, significantly predicted cognitive deviation from expected scores. The most prominent task associations with COVID-19 were for higher cognition and processing speed, which was qualitatively distinct from the profiles of normal aging and dementia and similar in magnitude to the effects of aging between 50 and 70 years of age. The trend towards reduced deficits with time from illness did not reach statistical significance.

The study concluded that cognitive deficits after severe COVID-19 are most strongly related to acute illness severity, persist long into the chronic phase, and recover slowly, if at all, with a characteristic profile highlighting higher cognitive functions and processing speed. The research was supported by funding from the National Institute for Health Research (NIHR), Cambridge Biomedical Research Centre (BRC), NIHR Cambridge Clinical Research Facility (BRC-1215-20014), Addenbrooke’s Charities Trust, and NIHR COVID-19 BioResource RG9402.