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Hyaluronan (HA), a multifunctional, high molecular weight glycosaminoglycan, is a component of the majority of extracellular matrices. HA is synthesised in a unique manner by a family of hyaluronan synthases, degraded by hyaluronidases and exerts a biological effect by binding to families of cellular receptors, the hyaladhedrins. Receptor binding activates signal pathways in endothelial cells leading to proliferation, migration and differentiation collectively termed angiogenesis. HA and associated enzymes are implicated in the aetiology of cardiovascular disease and cancer and manipulation of HA expression offers a therapeutic target. HA microspheres have been developed as drug delivery agents to deliver HA to sites of disease and also in diagnosis. In this review we discuss some of the recent therapeutic applications of hyaluronan in tissue repair, as a drug delivery system and the synthesis, application and delivery of hyaluronan nanoparticles to target drugs to sites of disease.

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Background and Method: We investigated the progression of cognitive and cerebral changes in 30 patients with a first-ever lacunar infarct (LI): 15 with vascular mild cognitive impairment (MCI-V) and 15 without cognitive impairment. All cases were followed up 18 ± 6 months after the stroke and underwent neurological, neuropsychological and MRI assessments at baseline and longitudinally. Results: Differences in the changes in cognitive function over time were observed between the 2 groups, with the MCI-V patients showing slight memory improvements and frontal-lobe-related test impairments from baseline to follow-up evaluations. At baseline, the 2 groups presented similar white matter hyperintensity (WMH) ratings and whole brain gray matter (GM) volumes, and at the follow-up evaluations, both groups had increased WMH lesions and decreased GM volumes; no statistical differences between groups were found. In contrast, a voxel-based morphometry analysis revealed that only MCI-V patients presented clear regional GM volume losses between the first and the second evaluations in cortical (frontal and temporal) and subcortical (pons, cerebellum and caudate) regions. Conclusion: Frontal lobe dysfunction and regional cortical and subcortical GM atrophy best differentiate the clinical course of LI patients with and without cognitive impairment.