"Emotionally based school avoidance" (EBSA) is a term used to describe young people who have difficulty attending school due to emotional needs. In comparison to previously favoured terms such as "school refuser", EBSA highlights the impact of unmet emotional needs over school non-attendance, which then informs the intervention offered for students struggling to attend school. This paper presents an exploratory single-case study undertaken at a specialist GCSE setting (School X) for students experiencing EBSA. The work was commissioned by the programme following three consecutive years in which all students completing their GCSEs (national curriculum) showed improvement in attendance and 85% achieved above their predicted grade. In addition, 95% of students were still in post-16 study after leaving the school. The study, therefore, aimed to explore students' views of protective factors in a setting where they have previously made progress in terms of attendance and achievement. Qualitative data were gathered using semi-structured questions with students in a group setting, delivered online using an anonymised computer software system. Quantitative data were gathered with students in a one-to-one situation using an adaption of the Q-sort technique, a self-contained "qualiquantilogical" methodology that aims to explore human subjectivity. Findings were collectively analysed using thematic analysis, which produced two over-arching themes: interconnectivity and psychological safety. Findings from this study are considered alongside research about interventions suggested to be effective for supporting students experiencing EBSA to re-engage with school and education.
Introduction: This study aims to determine whether newly introduced biomarkers Visinin-like protein-1 (VILIP-1), chitinase-3-like protein 1 (YKL-40), synaptosomal-associated protein 25 (SNAP-25), and neurogranin (NG) in cerebrospinal fluid are useful in evaluating the asymptomatic and early symptomatic stages of Alzheimer's disease (AD). It further aims to shed new insight into the differences between stable subjects and those who progress to AD by associating cerebrospinal fluid (CSF) biomarkers and specific magnetic resonance imaging (MRI) regions with disease progression, more deeply exploring how such biomarkers relate to AD pathology.
Methods: We examined baseline and longitudinal changes over a 7-year span and the longitudinal interactions between CSF and MRI biomarkers for subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI). We stratified all CSF (140) and MRI (525) cohort participants into five diagnostic groups (including converters) further dichotomized by CSF amyloid beta (Aβ) status. Linear mixed models were used to compare within-person rates of change across diagnostic groups and to evaluate the association of CSF biomarkers as predictors of magnetic resonance imaging (MRI) biomarkers. CSF biomarkers and disease-prone MRI regions are assessed for CSF proteins levels and brain structural changes.
Results: VILIP-1 and SNAP-25 displayed within-person increments in early symptomatic, amyloid-positive groups. CSF amyloid-positive (Aβ+) subjects showed elevated baseline levels of total tau (tTau), phospho-tau181 (pTau), VILIP-1, and NG. YKL-40, SNAP-25, and NG are positively intercorrelated. Aβ+ subjects showed negative MRI biomarker changes. YKL-40, tTau, pTau, and VILIP-1 are longitudinally associated with MRI biomarkers atrophy.
Discussion: Converters (CNc, MCIc) highlight the evolution of biomarkers during the disease progression. Results show that underlying amyloid pathology is associated with accelerated cognitive impairment. CSF levels of Aβ42, pTau, tTau, VILIP-1, and SNAP-25 show utility to discriminate between mild cognitive impairment (MCI) converter and control subjects (CN). Higher levels of YKL-40 in the Aβ+ group were longitudinally associated with declines in temporal pole and entorhinal thickness. Increased levels of tTau, pTau, and VILIP-1 in the Aβ+ groups were longitudinally associated with declines in hippocampal volume. These CSF biomarkers should be used in assessing the characterization of the AD progression.