Putative neuropathological interactions in MSA: focus in the rostral ventrolateral medulla.
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.
Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA, benarroch.eduardo@mayo.edu.
E E
EE
Benarroch
A M
AM
Schmeichel
J E
JE
Parisi
P A
PA
Low
D000368:Aged; D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D000071186:Beclin-1; D001933:Brain Stem / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D016022:Case-Control Studies; D027682:Cation Transport Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008875:Middle Aged; D019578:Multiple System Atrophy / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology; D009836:Oligodendroglia / Q000378:metabolism / Q000473:pathology; D051844:alpha-Synuclein / Q000378:metabolism; D000098742:Ferroportin
D051017:Apoptosis Regulatory Proteins; C491997:BECN1 protein, human; D000071186:Beclin-1; D027682:Cation Transport Proteins; D008565:Membrane Proteins; D051844:alpha-Synuclein; D000098742:Ferroportin