Journal
BRAIN PATHOLOGY
Volume 22, Issue 4, Pages 547-561Publisher
WILEY
DOI: 10.1111/j.1750-3639.2011.00557.x
Keywords
aggrecan; astrocytes; ss-amyloid; brevican; chondroitin sulphate proteoglycan; microglia; neuroprotection; plaque
Categories
Funding
- NIA [P30 AG19610]
- Arizona Department of Health Services [211002]
- Arizona Biomedical Research Commission [4001, 0011, 05-901, 1001]
- Michael J. Fox Foundation for Parkinson's Research
- German Research Foundation GRK [1097]
- EU [223077]
- COST Action [BM1001]
- Alzheimer Forschungsinitiative e.V. (AFI) [11861]
- Universitat Leipzig
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Brain extracellular matrix (ECM) is organized in specific patterns assumed to mirror local features of neuronal activity and synaptic plasticity. Aggrecan-based perineuronal nets (PNs) and brevican-based perisynaptic axonal coats (ACs) form major structural phenotypes of ECM contributing to the laminar characteristics of cortical areas. In Alzheimer's disease (AD), the deposition of amyloid proteins and processes related to neurofibrillary degeneration may affect the integrity of the ECM scaffold. In this study we investigate ECM organization in primary sensory, secondary and associative areas of the temporal and occipital lobe. By detecting all major PN components we show that the distribution, structure and molecular properties of PNs remain unchanged in AD. Intact PNs occurred in close proximity to amyloid plaques and were even located within their territory. Counting of PNs revealed no significant alteration in AD. Moreover, neurofibrillary tangles never occurred in neurons associated with PNs. ACs were only lost in the core of amyloid plaques in parallel with the loss of synaptic profiles. In contrast, hyaluronan was enriched in the majority of plaques. We conclude that the loss of brevican is associated with the loss of synapses, whereas PNs and related matrix components resist disintegration and may protect neurons from degeneration.
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