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This Thematic Minireview Series of Matrix Biology focused on elastin, from structure to disease celebrates the memory of Ladislas Robert, a pioneer in Matrix Biology in France and Europe. Since his first publication on elastin and elastases in 1957, the huge development in matrix biology led to major findings on elastic fibers and their component proteins including elastin architecture, the role of fibrillins and microfibril-binding proteins on elastin assembly, the effects of sequence variants of human tropoelastin on its assembly, structure and functions, the role of elastin peptides in health and diseases, the identification of neuraminidase-1 as a member of the elastin receptor complex, and the fate of elastic fibers upon aging, which are reviewed in this series. Two other reviews, focused on the design and use of elastin-like recombinamers as biomaterials, and on the circadian rhythms in skin and other elastic tissues, complete this series. • This Thematic Minireview Series of Matrix Biology focused on Elastin celebrates the memory of Ladislas Robert. • He was a pioneer in Matrix Biology in France and Europe. • He published his first paper on elastin and elastases in 1957. • Since then, the huge development in matrix biology led to major findings on elastic fibers and its component proteins. • The more recent data are detailed in the ten chapters of this series. [ABSTRACT FROM AUTHOR]

Background: Multimorbidity (the co-occurrence of multiple chronic conditions) is increasingly common, especially among people with dementia. Few neuroimaging studies have explored amyloid biomarkers in people with multimorbidity.Objective: We aimed to conduct the first study of the association between multimorbidity and cerebrospinal fluid amyloid-β42 (CSF Aβ).Method: The European Prevention of Alzheimer's Dementia (EPAD) Longitudinal Cohort Study V500.0 dataset includes volunteers aged ≥50 years from 12 sites. Participants undergo detailed phenotyping, including CSF measures and a self-reported medical history. Using logistic and linear regression analyses, we explored the association between multimorbidity and continuous chronic condition count with CSF Aβ positivity (Aβ42 <1000pg/ml) and continuous CSF Aβ concentration. All models were adjusted for age, sex, APOE status, education, and family history of dementia.Results: Among 447 eligible participants without dementia, the mean (SD) age was 66.6 (6.6) years, 234 (52.3%) were women, and 157 (35.1%) were amyloid positive. With chronic conditions regarded as pseudo-continuous, each additional condition carried a decreased likelihood of amyloid positivity (OR = 0.82, 95% CI: 0.68-0.97; p = 0.026). With CSF Aβ as a continuous variable, each additional condition was associated with an increase of 54.2 pg/ml (95% CI: 9.9-98.5, p = 0.017). Having ≥2 conditions was inversely associated with amyloid positivity (OR 0.59, 95% CI: 0.37-0.95, p = 0.030) compared to one or none.Conclusion: Our findings suggest that the established association between multimorbidity and dementia may be due to a pathway other than amyloid. However, this cross-sectional study does not allow us to make causal inferences. Longitudinal work is required to confirm the inverse association found. [ABSTRACT FROM AUTHOR]