Journal
BRAIN PATHOLOGY
Volume 19, Issue 4, Pages 573-585Publisher
WILEY
DOI: 10.1111/j.1750-3639.2008.00195.x
Keywords
ECM; neurodegeneration; CNS
Categories
Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [S10RR014772] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH064921, K24MH001717, R01MH071151] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R21AG025829] Funding Source: NIH RePORTER
- NCRR NIH HHS [S10 RR014772-018202] Funding Source: Medline
- NIA NIH HHS [R21 AG025829-02, R21 AG025829-01, R21 AG025829] Funding Source: Medline
- NIMH NIH HHS [K24 MH001717, R01 MH071151-04S1, R01 MH064921, R01 MH071151, K24 MH001717-09, R01 MH064921-03] Funding Source: Medline
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The role of extracellular matrix (ECM) in neurological development, function and degeneration has evolved from a simplistic physical adhesion to a system of intricate cellular signaling. While most cells require ECM adhesion to survive, it is now clear that differentiated function is intimately dependent upon cellular interaction with the ECM. Therefore, it is not surprising that the ECM is increasingly found to be involved in the enigmatic process of neurodegeneration. Descriptive studies of human neurodegenerative disorders and experimental studies of animal models of neurodegeneration have begun to define potential mechanisms of ECM disruption that can lead to synaptic and neuronal loss.
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