The challenge of causal inference
β Scribed by Olaf Dammann; Alan Leviton
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 292 KB
- Volume
- 68
- Category
- Article
- ISSN
- 0364-5134
No coin nor oath required. For personal study only.
β¦ Synopsis
We have read with great interest the article by Henderson and colleagues 1 in a recent issue of the Annals, in which the authors describe early loss of oligodendrocytes, without concomitant T-cell and B-cell infiltration or macrophage activity in tissue that borders a small selection of acute multiple sclerosis (MS) lesions. Neighboring areas with degenerate myelin were found to be infiltrated with macrophages, and fully demyelinated white matter areas contained lipid-laden macrophages, T-cells and B-cells, and immunoglobulin G deposits. These results are certainly interesting and thought-provoking. The authors' findings further strengthen the notion that MS is not so much, as has classically been argued, a primary autoimmune disease, but rather a disease starting within the central nervous system, with responses of the immune system only in later stages.
The atypical character of the cases and of the hyperacute lesions that were selected for this study may be insightful as a model for the (rapid) expansion of demyelination in the brain.
π SIMILAR VOLUMES
## THE DIRECTION OF CAUSATION MODEL My comments here are stimulated by the interesting lead articles on the "Direction of Causation" (DOC) model by Neale et al. [I9921 and by Duffy and Martin [1992]. In this paradigm, MZ and DZ twin paris are measured on at least two variables (X and Y ) , and a v