Putative neuropathological interactions in MSA: Focus in the rostral ventrolateral medulla

E. E. Benarroch; A. M. Schmeichel; J. E. Parisi; P. A. Low

doi:10.1007/s10286-015-0273-2

Putative neuropathological interactions in MSA: Focus in the rostral ventrolateral medulla

E. E. Benarroch, A. M. Schmeichel, J. E. Parisi, P. A. Low

Research output: Contribution to journal › Letter › peer-review

4 Scopus citations

Abstract

We used double immunocytochemistry for α-synuclein and markers of sympathoexcitatory neurons, oligodendrocytes, iron metabolism, and autophagy to study putative neuropathological interactions in multiple system atrophy. We focused in the rostral ventrolateral medulla as a prototype vulnerable region. We found that loss of C1 neurons and oligodendrocytes related to glial cytoplasmic inclusion accumulation, downregulation of iron transport, and upregulation of autophagy and ferritin expression in these area.

Original language	English (US)
Pages (from-to)	77-80
Number of pages	4
Journal	Clinical Autonomic Research
Volume	25
Issue number	1
DOIs	https://doi.org/10.1007/s10286-015-0273-2
State	Published - Feb 1 2015

Keywords

Alpha-synuclein
Beclin-1
Ferroportin
Multiple system atrophy

ASJC Scopus subject areas

Endocrine and Autonomic Systems
Clinical Neurology

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10.1007/s10286-015-0273-2

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title = "Putative neuropathological interactions in MSA: Focus in the rostral ventrolateral medulla",

abstract = "We used double immunocytochemistry for α-synuclein and markers of sympathoexcitatory neurons, oligodendrocytes, iron metabolism, and autophagy to study putative neuropathological interactions in multiple system atrophy. We focused in the rostral ventrolateral medulla as a prototype vulnerable region. We found that loss of C1 neurons and oligodendrocytes related to glial cytoplasmic inclusion accumulation, downregulation of iron transport, and upregulation of autophagy and ferritin expression in these area.",

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T2 - Focus in the rostral ventrolateral medulla

AU - Benarroch, E. E.

AU - Schmeichel, A. M.

AU - Parisi, J. E.

AU - Low, P. A.

PY - 2015/2/1

Y1 - 2015/2/1

N2 - We used double immunocytochemistry for α-synuclein and markers of sympathoexcitatory neurons, oligodendrocytes, iron metabolism, and autophagy to study putative neuropathological interactions in multiple system atrophy. We focused in the rostral ventrolateral medulla as a prototype vulnerable region. We found that loss of C1 neurons and oligodendrocytes related to glial cytoplasmic inclusion accumulation, downregulation of iron transport, and upregulation of autophagy and ferritin expression in these area.

AB - We used double immunocytochemistry for α-synuclein and markers of sympathoexcitatory neurons, oligodendrocytes, iron metabolism, and autophagy to study putative neuropathological interactions in multiple system atrophy. We focused in the rostral ventrolateral medulla as a prototype vulnerable region. We found that loss of C1 neurons and oligodendrocytes related to glial cytoplasmic inclusion accumulation, downregulation of iron transport, and upregulation of autophagy and ferritin expression in these area.

KW - Alpha-synuclein

KW - Beclin-1

KW - Ferroportin

KW - Multiple system atrophy

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Putative neuropathological interactions in MSA: Focus in the rostral ventrolateral medulla

Abstract

Keywords

ASJC Scopus subject areas

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