The association of parent-reported executive functioning, reading, and math is explained by nature, not nurture

According to the hybrid model (van Bergen, van der Leij, & de Jong, 2014), the significant association among executive functioning (EF), reading, and math may be partially explained by parent-reported EF's role as a common risk and/or protective factor in reading and math (dis)abilities. The current study used a sample of 434 twin pairs (Mage = 12.12) from Florida to conduct genetically sensitive modeling on children's parent-reported EF, reading, and math skills to determine the common and unique etiological influences among the three domains. EF was measured through parent report and reading and math were measured with standardized test scores drawn from Florida's Progress Monitoring and Reporting Network as well as standardized parent-administered assessments collected by mail. Our trivariate Cholesky modeling showed that no matter which parent-reported EF component was modeled, the overlap of parent-reported EF with reading and math was explained by common genetic influences. Supplemental analysis suggested that this might in part be due to general parent report of problem behaviors. Additionally, significant environmental influences, with higher shared environmental overlap than previous work, were also found for reading and math. Findings indicate that poor parent-reported EF is a common cognitive risk factor for reading and math disabilities, which is driven by a shared genetic basis among all three domains. (PsycInfo Database Record (c) 2020 APA, all rights reserved)

Socioeconomic status and response to a reading intervention: A quantile regression approach

In response to inadequate response to instruction in reading, interventions are often implemented to address deficiencies in component skills associated with reading performance. However, there are factors that influence how children respond to these interventions. Specifically, socioeconomic status (SES) is a well-known correlate of academic achievement, and we hypothesized that family-SES would be associated with response to reading intervention. We explored the estimated associations between SES (free and reduced lunch status) and the distribution of response to intervention (residualized gain scores on the decoding and expressive vocabulary subtests of the Woodcock-Johnson Tests of Achievement) using the quantile regression approach in a diverse sample of elementary students (N = 1,651). Results indicated that higher family-SES was more strongly associated with greater responsiveness to intervention for both the decoding and expressive vocabulary skills measured. We conclude with a call to more thoroughly consider predictors of individual differences in response to intervention

N-acetyl cysteine mitigates the acute effects of cocaine-induced toxicity in astroglia-like cells.

Cocaine has a short half-life of only about an hour but its effects, predominantly on the central nervous system (CNS), are fairly long-lasting. Of all cells within the CNS, astrocytes may be the first to display cocaine toxicity owing to their relative abundance in the brain. Cocaine entry could trigger several early response changes that adversely affect their survival, and inhibiting these changes could conversely increase their rate of survival. In order to identify these changes and the minimal concentrations of cocaine that can elicit them in vitro, rat C6 astroglia-like cells were treated with cocaine (2-4 mM for 1h) and assayed for alterations in gross cell morphology, cytoplasmic vacuolation, viability, reactive oxygen species (ROS) generation, glutathione (GSH) levels, cell membrane integrity, F-actin cytoskeleton, and histone methylation. We report here that all of the above identified features are significantly altered by cocaine, and may collectively represent the key pathology underlying acute toxicity-mediated death of astroglia-like cells. Pretreatment of the cells with the clinically available antioxidant N-acetyl cysteine (NAC, 5 mM for 30 min) inhibited these changes during subsequent application of cocaine and mitigated cocaine-induced toxicity. Despite repeated cocaine exposure, NAC pretreated cells remained highly viable and post NAC treatment also increased viability of cocaine treated cells to a smaller yet significant level. We show further that this alleviation by NAC is mediated through an increase in GSH levels in the cells. These findings, coupled with the fact that astrocytes maintain neuronal integrity, suggest that compounds which target and mitigate these early toxic changes in astrocytes could have a potentially broad therapeutic role in cocaine-induced CNS damage

NAC mitigates cocaine-induced toxicity.

<p>Measurements of cell viability with NAC pretreatment (<i>n</i> = 12, <b>A</b>) or post NAC exposure (<i>n</i> = 16, <b>B</b>) and total GSH levels (<i>n</i> = 8–12, <b>C</b>) with NAC pretreatment (5 mM, 30 min) followed by exposure to the indicated concentrations of cocaine for 1h. Data represent mean ± S.E.M. (<i>n</i> = number of assays), *<i>P</i><0.05, **<i>P</i><0.01–0.001 significance of comparison with corresponding control; ^##<i>P</i><0.001 significance of comparison between cocaine alone and cocaine + NAC.</p

Detection of glial fibrillary acidic protein marker in <i>C6</i> astroglia-like cells.

<p>Cells were incubated with rabbit-anti-rat GFAP 1° antibody and then with goat anti-rabbit Alexa Fluor 488 conjugate for 2 h. Samples were counterstained for nuclei with PI and photomicrographed using an inverted microscope with a 40x objective.</p

Gross morphological features of astroglia-like cells in culture during acute exposure to cocaine.

<p>Cells were treated with PBS (control) (<b>A</b>) and 2–4 mM cocaine (<b>B-D</b>) for 1h. Optical images are of crystal violet stained cells taken with an inverted phase contrast IX-70 Olympus microscope with a 40x objective. Note the conspicuous cocaine-induced vacuoles in the cytoplasm (<b>B</b>-<b>D</b>). Scale bar: 50 μm.</p

Measurement of the acute effects of cocaine exposure in astroglia-like cells on <i>cell viability</i> (A), <i>ROS production</i> (B), <i>total GSH levels</i> (C), and <i>LDH release</i> (D).

<p>Cells were treated with the indicated concentrations of cocaine for 1h. Cell viability was assessed using the crystal violet dye (0.1%) uptake protocol (<i>n</i> = 9). <i>ROS production</i> was assessed by loading cells with a H₂DCFDA dye (10 μM, 30 min), followed by cocaine exposure in phenol red–free media. Dichlorodihydrofluorescein (DCF) was measured on a micro plate fluorometer with the excitation and emission filters set at 485 and 530 nm respectively (<i>n</i> = 4). Depletion in <i>GSH levels</i> were quantified on a plate reader following exposure to cocaine (<i>n</i> = 6). For measurements of <i>LDH release</i>, cells in phenol red–free media were treated with cocaine following which they were incubated in equal volumes of media and substrate from the assay kit (50 μl, 30 min) before being read on a micro plate reader (<i>n</i> = 12). Data for all measures are represented as mean ± S.E.M. (<i>n</i> = number of assays), *<i>P</i><0.05; **<i>P</i><0.001–0.01 w.r.t to control.</p

Histone methylation with acute cocaine treatment.

<p>Standard curve of methylated H3-K27 (<b>A</b>). Cells were pretreated with NAC (5 mM, 30 min; n = 6) followed by exposure to the indicated concentrations of cocaine for 1h (<b>B</b>). Data represent mean ± S.E.M. (<i>n</i> = number of assays), *<i>P</i><0.05, significance of comparison with corresponding control; ^#<i>P</i><0.05, significance of comparison between cocaine alone and cocaine + NAC.</p

Schematic representation of NAC protection against cocaine toxicity.

<p>The acute effects of cocaine (<i>black</i>) on astroglia-like cells and the mode of protection rendered by NAC (<i>red</i>) through measured (<i>solid</i>) and/or inferred (<i>broken</i>) increases (<i>up arrows</i>) or decreases (<i>down arrows</i>) in levels of the indicated parameters.</p