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Structural and Functional Remodeling of the Extracellular Matrix during Brain Development and Aging

Journal

TRENDS IN GLYCOSCIENCE AND GLYCOTECHNOLOGY
Volume 33, Issue 194, Pages E79-E84

Publisher

GAKUSHIN PUBL CO
DOI: 10.4052/tigg.2003.1E

Keywords

extracellular matrix; perineuronal net; hyaluronan; chondroitin sulfate proteoglycan

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The extracellular matrix of the central nervous system primarily consists of hyaluronan and chondroitin sulfate proteoglycans. Recent advances in understanding the molecular mechanisms underlying ECM organization and remodeling during CNS development, maturation, and aging have been reviewed. Different stages of ECM play crucial roles in neural developmental processes and the transition from juvenile to adult neural circuits, with evidence suggesting that age-dependent degradation of ECM molecules may contribute to decline in brain function.
The extracellular matrix (ECM) of the central nervous system (CNS) primarily consists of hyaluronan (HA) and chondroitin sulfate proteoglycans (CSPGs). HA polymer serves as the backbone of the ECM and binds multiple CSPGs, forming a macromolecular complex in the extracellular space. Recent advances in our understanding of the molecular mechanisms underlying the organization and remodeling of the ECM during the development, maturation, and aging of the CNS are reviewed herein. A juvenile-type ECM, which shows a relatively loose and diffuse structure, plays crucial roles in neural developmental processes, such as neurogenesis, neuronal migration, and neurite outgrowth. During late postnatal development, the juvenile-type ECM is replaced by an adulttype mature ECM, which drives the transition from more plastic, juvenile neural circuits to a more stable adult circuit. Perineuronal nets ( PNNs), a prominent example of the adult- type ECM, are mesh-like insoluble aggregates that form around subpopulations of neurons and promote memory retention and consolidation in the adult brain. Furthermore, emerging evidence indicates that the degradation of ECM molecules during aging may contribute to an age-dependent decline in brain function.

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