Iron Accumulation in Multiple Sclerosis

[Ironjustic]

<<snip>> accumulation of iron in the deep gray matter in
patients with MS <<snip>>

AJNR Am J Neuroradiol. 2007 Sep 24; [Epub ahead of print]
Quantitative Assessment of Iron Accumulation in the Deep Gray
Matter of Multiple Sclerosis by Magnetic Field Correlation
Imaging. Ge Y, Jensen JH, Lu H, Helpern JA, Miles L, Inglese
M, Babb JS, Herbert J, Grossman RI. Center for Biomedical
Imaging, Department of Radiology, New York University Medical
Center, New York, NY; and the Department of Neurology, MS Care
Center, Hospital for Joint Diseases, New York University
School of Medicine, New York, NY.

BACKGROUND AND PURPOSE: Deposition of iron has been recognized
recently as an important factor of pathophysiologic change
including neurodegenerative processes in multiple sclerosis
(MS). We propose that there is an excess accumulation of iron
in the deep gray matter in patients with MS that can be
measured with a newly developed quantitative MR technique-
magnetic field correlation (MFC) imaging. MATERIALS AND
METHODS: With a 3T MR system, we studied 17 patients with
relapsing-remitting MS and 14 age-matched healthy control
subjects. We acquired MFC imaging using an asymmetric
single-shot echo-planar imaging sequence. Regions of interest
were selected in both deep gray matter and white matter
regions, and the mean MFC values were compared between
patients and controls. We also correlated the MFC data with
lesion load and neuropsychologic tests in the patients.
RESULTS: MFC measured in the deep gray matter in patients with
MS was significantly higher than that in the healthy controls
(P </= .03), with an average increase of 24% in the globus
pallidus, 39.5% in the putamen, and 30.6% in the thalamus. The
increased iron deposition measured with MFC in the deep gray
matter in the patients correlated positively with the total
number of MS lesions (thalamus: r = 0.61, P
= .01; globus pallidus: r = 0.52, P = .02). A moderate but
= significant
correlation between the MFC value in the deep gray matter and
the neuropsychologic tests was also found. CONCLUSION:
Quantitative measurements of iron content with MFC demonstrate
increased accumulation of iron in the deep gray matter in
patients with MS, which may be associated with the disrupted
iron outflow pathway by lesions. Such abnormal accumulation of
iron may contribute to neuropsychologic impairment and have
implications for neurodegenerative processes in MS.

PMID: 17893225 [PubMed - as supplied by publisher]

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[Ron Peters]

http://www.nhfw.info/multiple-sclerosis.html states:

One study noted that hospital patients with MS had low levels
of both zinc and iron.

--
Ron

[Ironjustic]

>> On Sep 26, 5:48 am, Ron Peterson
>> <r...@shell.core.com> wrote:
http://www.nhfw.info/multiple-sclerosis.htmlstates:

One study noted that hospital patients with MS had low levels
of both zinc and iron. <<

Well seeing they have ONLY .. just .. discovered .. they have
been NOT been able to test the available iron in the body ..
CORRECTLY .. with any kind of confidence .. then the fact zinc
is depleted by iron .. either through increased red blood cell
production or directly at absorption .. leaves one with ..
STILL .. the iron in the brain.

Increased red blood cell production strips zinc .. increased
red blood cell production induces .. anemia / commonly
recognized by stupid people as iron deficiency .. and it
causes / associated CLOSELY with ataxia.

IN the mouse model of increased red blood cell production the
brain leaks .. blood .. therefore .. iron.

Lysophosphatidylcholine seems to be kinda .. interesting ..

It seems this lysophosphatidylcholine is simply oxidized ..
phosphatidylcholine / lecithin .. and it paralyzes ya / lack
of remyelination ..

Rev Neurol (Paris). 2007 Apr;163(4):448-54. Links
[Oligodendroglial defect and insufficiency of remyelination
during MS: anatomoclinical and experimental comparative
study][Article in French]

Fressinaud C. D=E9partement de Neurologie, UPRES EA 3143,
C.H.U., Angers, France. Catherine.fressinaud@univ-angers.fr

INTRODUCTION: The mechanisms responsible for the failure of
remyelination during MS are poorly understood. We have
analyzed in which way oligodendrocytes (OL) could be involved.
METHODS: The number of remyelinated fiber per OL has been
determined in 18 chronic MS lesions and compared to normal
appearing white matter (NAWM), as well as in the center of
lysophosphatidyl choline (LPC)- induced lesions in adult rats
in which remyelination was accelerated by microinjection of
neurotrophin-3 (NT-3). RESULTS: In chronic MS lesions and in
LPC-induced lesions the number of myelinated fibers per OL was
strongly decreased compared to NAWM and to animals treated
with NT-3 respectively. CONCLUSION: Our results suggest that
the capacity of OL to remyelinate axons could be impaired, due
to successive relapses, during MS.

PMID: 17452946 [PubMed - indexed for MEDLINE]

J=2E Clin. Invest. 0021-9738/96/06/2736/09 $2.00 Volume 97,
Number 12, June 1996, 2736-2744

Role of Lysophosphatidylcholine in the Inhibition of
Endothelial Cell Motility by Oxidized Low Density Lipoprotein
Gurunathan Murugesan, and Paul L. Fox

Department of Cell Biology, Cleveland Clinic Research
Institute, Cleveland, Ohio 44195

Endothelial cell (EC) movement is required for the development
and repair of blood vessels. We have previously shown that LDL
oxidized by transition metals almost completely suppressed the
wound-healing migratory response of vascular EC in vitro. We
now report that lysophosphatidylcholine (lysoPC), a lipid
component of oxidized LDL, has an important role in the
antimigratory activity of the lipoprotein. Purified
1-palmitoyl lysoPC inhibited movement with a half-maximal
activity at 12-15 =B5M, and near complete inhibition at 20
=B5M; the inhibitory concentration of lysoPC was consistent
with its abundance in oxidized LDL. The inhibition was not due
to cytotoxicity since protein synthesis was unaffected and
since EC movement was restored after removal of lysoPC.
Lysophospholipid activity was dependent on lipid structure.
LysoPC's containing 1-position C16 or C18 saturated fatty
acids were antimigratory, but those containing C14 saturated
fatty acids or polyunsaturated fatty acids were not. The
activity of 1-palmitoyl lysolipids with various head groups
was examined. Lysophosphatidylinositol was more antimigratory
than lysophosphatidylglycerol and lysophosphatidylcholine,
which were more potent than lysophosphatidylserine and
lysophosphatidylethanolamine. Monoglyceride was inactive while
lysophosphatidate had promigratory activity. These results are
consistent with head group size rather than charge as a
critical determinant of activity. To show that
lysophospholipids within an intact lipoprotein were active,
LDL was treated with bee venom phospholipase A2 (PLA2). The
modified lipoprotein inhibited EC movement to the same extent
as iron-oxidized LDL and antimigratory activity correlated
with the amount of lysoPC formed. To determine antimigratory
activity of lysoPC present in oxidized LDL, lipid extracts
from oxidized LDL were fractionated by normal phase HPLC. The
fraction comigrating with lysoPC had nearly the same activity
as the total extract confirming that lysoPC (or a co- eluting
lipid) was a major antimigratory molecule in oxidized LDL.
These studies demonstrate that lysoPC in oxidized LDL limit EC
wound healing responses in vitro, and suggest a possible role
for lysolipids in limiting endothelial regeneration after a
denuding injury in vivo.
(J. Clin. Invest. 1996. 97:2736- 2744.)

Key words: atherosclerosis; cell migration; endothelial cells;
lysophospholipids; oxidized low density lipoprotein

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