#dc-system-status
for updates. The development team can be contacted at datacentre@scilifelab.se
if you have any question.Akinci M, Peña-Gómez C, Operto G, Fuentes-Julian S, Deulofeu C, Sánchez-Benavides G, Milà-Alomà M, Grau-Rivera O, Gramunt N, Navarro A, Minguillón C, Fauria K, Suridjan I, Kollmorgen G, Bayfield A, Blennow K, Zetterberg H, Molinuevo JL, Suárez-Calvet M, Gispert JD, Arenaza-Urquijo EM
Neurology - (-) - [2022-08-02; online 2022-08-02]
Increased anxious-depressive symptomatology is observed in the preclinical stage of Alzheimer's disease (AD), which may accelerate disease progression. We investigated whether amyloid-β, , neuroinflammation and sociodemographic factors were associated with cortical thickness in medial temporal lobe structures anxious-depressive symptoms during the COVID-19 confinement.greater This retrospective observational study included cognitively unimpaired older adults from the ALFA (Alzheimer and FAmilies) cohort, the majority with a family history of sporadic AD. Participants performed the Hospital Anxiety and Depression Scale (HADS) during the COVID-19 confinement. A subset had available retrospective (on average: 2.4 years before) HADS assessment, amyloid [18F] flutemetamol PET and structural MRI scans and CSF markers of neuroinflammation (interleukin-6 [IL-6], triggering receptor expressed on myeloid cells 2 and glial fibrillary acidic protein levels). We performed multivariable regression models to investigate the associations of linear biomarkers and sociodemographic factors with HADS scores during the confinementpre-pandemic AD-related. . Finally, we explored the role of stress and lifestyle changes (sleep patterns, eating, drinking, smoking habits, and medication use) on the tested associations and performed sex-stratified analyses.We further performed an analysis of covariance in order to adjust by participants' pre-pandemic anxiety-depression levels We included 921 (254 with AD biomarkers) participants. Amyloid-β positivity (B=3.73; 95%CI=1.1 to 6.36; p=.006), caregiving (B=1.37; 95%CI=0.24 to 2.5; p=.018), sex (women: B=1.95; 95%CI=1.1 to 2.79; p<.001), younger age (B=-0.12; 95%CI=-0.18 to -0.052; p<.001) and lower education (B=-0.16; 95%CI=-0.28 to -0.042; p=.008) were associated with greater anxious-depressive symptoms during the confinement. Considering pre-pandemic anxiety-depression levels, we further observed an association between (B=-5.11; 95%CI=-10.1 to -0.13; lower levels of CSF IL-6p=.044) and HADS scores. The results were independent of stress-related variables and lifestyle changes. Stratified analysis revealed that the associations were mainly driven by women.greater Our results link AD-related pathophysiology and neuroinflammation with anxious-depressive symptomatology during the COVID-19-related confinement, notably in women. AD pathophysiology may increase neuropsychiatric symptomatology in response to stressors. This association may imply a worse clinical prognosis in people at risk for AD after the pandemic, and thus deserves to be considered by clinicians.greater ClinicalTrials.gov Identifier NCT02485730.
PubMed 35918160
DOI 10.1212/WNL.0000000000200948
Crossref 10.1212/WNL.0000000000200948
pii: WNL.0000000000200948
ClinicalTrials.gov: NCT02485730