On Oct 2, 9:25 pm, ironjustice <teamtan...@hotmail.com> wrote: Their
research has also shown that this association was particularly
strong in females compared to males. <<

I think I .. if I remember correctly .. was questioned .. "why then
smartass do women have such a high rate of MS as opposed to
men !!??" ..

"Iron may play a role in neurodegenerative disease."

ScienceDaily (Mar. 14, 2008) — A team of scientists, led by Professor
Jon Dobson, of Keele University in Staffordshire, UK, have found, for
the first time, raised levels of magnetic iron oxides in the part of
the brain affected by Alzheimer's Disease (AD).
Their research has also shown that this association was particularly
strong in females compared to males. The group speculates that this
may be a result of gender differences in the way the body handles and
stores iron.

Though the results are based on a small number of samples, they give
an indication that iron accumulation associated with Alzheimer's
appears to involve the formation of strongly magnetic iron compounds.
As these compounds have a strong effect on MRI signal intensity, with
further study, it may be possible to use this as a biomarker for the
development of an MRI-based Alzheimer's diagnostic technique.

The research team also included Quentin Pankhurst, London Centre for
Nanotechnology and Department of Physics & Astronomy, University
College, London; Dimitri Hautot, Institute of Science and Technology
in Medicine, Keele University, and Nadeem Khan, Department of
Neuropathology, Institute of Psychiatry, King's College London.

The study looked at brain tissue from 11 Alzheimer's Disease and 11
age-matched control subjects. It showed, for the first time, that the
total concentration of biogenic magnetite is generally higher in the
Alzheimer brain (in some cases as much as 15 times greater than
controls) and that there are gender-based differences, with
Alzheimer's Disease with female subjects having significantly higher
concentrations than all other groups.

Professor Dobson said: "Iron accumulation and dysregulation of iron
transport and storage has been found to be associated with many other
neurodegenerative conditions, such as Parkinson's disease,
Huntington's disease (HD), multiple sclerosis and Amyotrophic Lateral
Sclerosis. In recent years, a hereditary neurodegenerative disease,
neuroferritinopathy, has been linked to a mutation in the gene
encoding for the ferritn light polypeptide. This direct link between
neurodegeneration in the basal ganglia and ferritin, the body's
primary iron storage protein, results in the accumulation of iron in
the brain and symptoms similar to HD.

"There is still little known about the chemical form of iron
associated with these diseases, its role in neurodegeneration (if
any)
and its origin. Investigations of brain iron based on histochemical
staining techniques have generally ignored its chemical state."

This study shows a clear correlation in the concentration and the
size
of the biogenic magnetite in both the Alzheimer disease and control
groups. It is also notable that the largest magnetite concentrations
and smallest particles are all from Alzheimer disease subjects, and
that the data from the control subjects follow the same trend. This
implies that the genesis of the biogenic magnetite may be the same in
all cases, but that in Alzheimer Disease it may be more indicative of
an accelerated process.

Professor Dobson added: "We speculate that magnetite formation within
the ferritin core may occur generally in the brain, perhaps
associated
with aging, and that the process may become abnormal and uncontrolled
in the Alzheimer brain. At this stage, this should be considered a
working hypothesis and needs to be examined in larger studies. It
appears, however, that elevated levels of magnetic iron oxides, which
include reactive Fe2+, are present in AD tissue, a finding that lends
weight to the suggestion that redox-active iron may play a role in
neurodegenerative disease."

A paper on the study, Increased Levels of Magnetic Compunds in
Alzheimer's Disease, is scheduled for publication in the January 2008
issue of the Journal of Alzheimer's Disease (Volume 13:1). This work
was supported by the UK Medical Research Council and National
Institutes of Health.

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Adapted from materials provided by IOS Press.

Who loves ya.
Tom

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