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Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
Published on: July 31, 2017
Meningioangiomatosis: an immunocytochemical study
J J Goates1, D W Dickson, D S Horoupian
1Department of Pathology/Neuropathology, Stanford University School of Medicine, CA 94305-5324.
Abstract:
Meningioangiomatosis (MA) is a rare malformative lesion of the central nervous system. It has generally been thought that the main cells forming this lesion are derived from arachnoidal cap cells. We report a case of MA in which histochemical, immunoperoxidase and electron microscopic studies did not support a meningothelial origin of this lesion. Rather, the lesion in this case appears to be a vascular malformation with the dominant cells being fibroblastic, derived from vessel walls; however, their origin from arachnoid cap cells that differentiated into fibroblast-like cells could not be totally ruled out. Residual neurons within the lesion contained neurofibrillary tangles with ultrastructural and immunostaining properties identical to those seen in Alzheimer's disease except for the absence of A4 amyloid.
Insights
Meningioangiomatosis (MA) is a rare CNS lesion. This case suggests MA may be a vascular malformation, not solely of arachnoid cap cell origin, with potential links to Alzheimer's disease pathology.
Area of Science:
- Neuroscience
- Pathology
- Vascular Malformations
Background:
- Meningioangiomatosis (MA) is a rare central nervous system (CNS) lesion.
- MA is typically attributed to arachnoidal cap cells.
Observation:
- This case report details a meningioangiomatosis lesion.
- Histochemical, immunoperoxidase, and electron microscopic studies were performed.
Findings:
- The lesion's cellular origin was investigated.
- Findings did not support a meningothelial origin.
- The lesion appears to be a vascular malformation with fibroblastic cells from vessel walls, though arachnoid cap cell origin cannot be excluded.
- Neurons within the lesion showed Alzheimer's-like neurofibrillary tangles without A4 amyloid.
Implications:
- Challenges the traditional understanding of meningioangiomatosis cellular origins.
- Suggests a potential vascular malformation component in MA.
- Highlights potential, albeit atypical, links between MA and Alzheimer's disease neuropathology.
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