Aging in human cerebral arteries was associated with increased stiffness and loss of compliance due to elastin dysfunction and structural reorganization, despite preserved elastin quantity.
Cross-Sectional (n=12)
Does aging alter the functionality and biomechanical properties of elastin in human cerebral arteries?
Elastin loses its functionality in cerebral arteries with aging due to fragmentation and structural reorganization, leading to stiffer, less compliant arteries despite a constant elastin area fraction.
BACKGROUND AND PURPOSE: Aging affects elastin, a key component of the arterial wall integrity and functionality. Elastin degradation in cerebral vessels is associated with cerebrovascular disease. The goal of this study is to assess the biomechanical properties of human cerebral arteries, their composition, and their geometry, with particular focus on the functional alteration of elastin attributable to aging. METHODS: Twelve posterior cranial arteries obtained from human cadavers of 2 different age groups were compared morphologically and tested biomechanically before and after enzymatic degradation of elastin. Light, confocal, and scanning electron microscopy were used to analyze and determine structural differences, potentially attributed to aging. RESULTS: Aging affects structural morphology and the mechanical properties of intracranial arteries. In contrast to main systemic arteries, intima and media thicken while outer diameter remains relatively constant with age, leading to concentric hypertrophy. The structural morphology of elastin changed from a fiber network oriented primarily in the circumferential direction to a more heterogeneously oriented fiber mesh, especially at the intima. Biomechanically, cerebral arteries stiffen with age and lose compliance in the elastin dominated regime. Enzymatic degradation of elastin led to loss in compliance and stiffening in the young group but did not affect the structural and material properties in the older group, suggesting that elastin, though present in equal quantities in the old group, becomes dysfunctional with aging. CONCLUSIONS: Elastin loses its functionality in cerebral arteries with aging, leading to stiffer less compliant arteries. The area fraction of elastin remained, however, fairly constant. The loss of functionality may thus be attributed to fragmentation and structural reorganization of elastin occurring with age.
Fonck et al. (Fri,) conducted a cross-sectional in Aging (n=12). Aging vs. Younger age group was evaluated on Biomechanical properties, composition, and geometry of cerebral arteries. Aging in human cerebral arteries was associated with increased stiffness and loss of compliance due to elastin dysfunction and structural reorganization, despite preserved elastin quantity.