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Daniela M. Menichella

Researcher at Northwestern University

Publications -  29
Citations -  1302

Daniela M. Menichella is an academic researcher from Northwestern University. The author has contributed to research in topics: Schwann cell & Myelin. The author has an hindex of 14, co-authored 24 publications receiving 1113 citations. Previous affiliations of Daniela M. Menichella include Wayne State University & Harvard University.

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Journal ArticleDOI

Connexins Are Critical for Normal Myelination in the CNS

TL;DR: Evidence is provided that gap-junction communication is crucial for normal central myelination in oligodendrocytes and that animals lacking both connexins die by postnatal week 6 from profound abnormalities in central myelin.
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Subcutaneous immunoglobulin for maintenance treatment in chronic inflammatory demyelinating polyneuropathy (PATH): a randomised, double-blind, placebo-controlled, phase 3 trial

Ivo N. van Schaik, +149 more
- 01 Jan 2018 - 
TL;DR: This study, which is to the authors' knowledge, the largest trial of CIDP to date and the first to study two administrations of immunoglobulins and two doses, showed that both doses of SCIg IgPro20 were efficacious and well tolerated, suggesting thatSCIg can be used as a maintenance treatment for C IDP.
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Genetic and physiological evidence that oligodendrocyte gap junctions contribute to spatial buffering of potassium released during neuronal activity.

TL;DR: Examination of the effect of neuronal activity on the appearance of vacuoles and genetic complementation implicate oligodendrocytes and their connexins as having critical roles in the buffering of K+ released during neuronal activity.
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Heterozygous P0 knockout mice develop a peripheral neuropathy that resembles chronic inflammatory demyelinating polyneuropathy (CIDP).

TL;DR: It is found that heterozygous P0 knockout mice develop a neuropathy that resembles CIDP, and morphological analysis of affected nerves reveals severe and selective demyelination of motor fibers, focal regions of demyElination, and inflammatory cells, which suggest that immune-mediated mechanisms may contribute to the pathogenesis of the neuropathy in P0+/- mice.
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MicroRNA-Deficient Schwann Cells Display Congenital Hypomyelination

TL;DR: A model wherein microRNAs are critical for downregulation of antecedent programs of gene expression is posited in SC differentiation, particularly relevant in the key developmental transition from a promyelinating to myelinating SC.