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Data from: CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer's disease


Janelidze, Shorena et al. (2019), Data from: CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer's disease, Dryad, Dataset,


Objective: To measure cerebrospinal (CSF) levels of biomarkers reflecting microglia and astrocytes activation, neuroinflammation and cerebrovascular changes and study their associations with the core biomarkers of AD pathology (amyloid &[beta] (A&[beta]) and tau), structural imaging correlates and clinical disease progression over time. Methods: The study included cognitively unimpaired elderly (n=508), patients with mild cognitive impairment (MCI, n=256), and AD dementia (n=57) from the longitudinal Swedish BioFINDER cohort. CSF samples were analyzed for YKL-40, IL-6, IL-7, IL-8, IL-15, IP-10, MCP-1, ICAM-1, VCAM-1, PlGF and Flt-1. Magnetic resonance imaging data were available from 677 study participants. Longitudinal clinical assessments were conducted in control individuals and MCI patients (mean follow-up 3 years, range 1-6 years). Results: CSF levels of YKL-40, ICAM-1, VCAM-1, IL-15 and Flt-1 were increased during the preclinical, prodromal and dementia stages of AD. High levels of these biomarkers were associated with increased CSF levels of total-tau, with the associations, especially for YKL-40, being stronger in A&[beta]-positive individuals. The results were similar for associations between phosphorylated-tau and YKL-40, ICAM-1 and VCAM-1. High levels of the biomarkers were also associated with cortical thinning (primarily in the precuneus and superior parietal regions) and with subsequent cognitive deterioration in non-demented cases as measured with MMSE (YKL-40) and CDR-SB (YKL-40, ICAM-1, VCAM-1 and IL-15). Finally, higher levels of CSF YKL-40, ICAM-1 and Flt-1 levels increased risk of development of AD dementia in non-demented cases. Conclusions: Neuroinflammation and cerebrovascular dysfunction are early events occurring already at pre-symptomatic stages of AD and contribute to disease progression.

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