13
amyloid specific
endoplasmic
reticulum
associated
protein
that promotes
damage
of cell
membranes and
the stimulation
of active oxygen radicals
,
resulting in the
death of these
cells
[Yan SD
et al.,
1997
].
In addition
,
-amyloid
and special
senile plaques
deposited
in the cerebral vessels
.
In this case,
partially
penetrate the
senile plaques
in
the vascular
wall
,
and
-amyloid
cylindrically
surrounds
the vessel
,
narrowing
the lumen
[Uchihara T.
et al.,
1997
].
In Alzheimer's disease
patients
exhibit
elevated levels of
apolipoprotein
E,
which indicates the
proximity
of such a
pathology
with
"vas
cular dementia» [
Marin
DB
et
al.,
1988
].
There is a large
role
of activation
of the complement
proteins
produced by
cells of
the microglia
,
astrocytes
and
pyramidal
neurons
[Terai K.
et al.,
1997
].
Perlecan
enhances this
process
- a specific
heparan
sulfate proteoglycan
that accumulates in the
-amyloid fibrils
[Castillo G.
et al.,
1997
].
The structure of
amyloid deposits
include not
only
amyloid
,
but other
so-called
amyloid-associated proteins composed of
complement
regulatory factors
and
proteolytic
enzymes
,
apolipoprotein
E and other
components
[Aizawa Y.
et al.,
1997
].
The predecessor of
-amyloid
(
-APP)
is a multifunctional
protein that
is widely
represented
in the nervous system
.
This
prekruisor
(
-APP)
is transported
along the
axons
and accumulates
in presynaptic
terminals and
"points of
growth".
-amyloid
,
is
released enzymatically from
-APP, has a tendency to form fibrils, damaging neurons
and increases their vulnerability. This mechanism involves the generation of oxygen
radicals
and damage to
membrane transport
systems
[Mattson MP,
1997
].
There are
signs of
permeability of
blood-brain
barrier
facilitating
penetration
as
amyloid proteins
in brain tissue
,
and
the reverse transition of
neurospecific
protein
into
the systemic circulation
,
where they
fall into the "field of vision"
of the immune system
and stimulate
the formation of autoantibodies
to
affect not only
against these
proteins
but
similar
protein
structures of the central
nervous system.
Among pathogenetic factors
of
Alzheimer
we detected
the role
of oxidative stress
and
the accumulation
of free radical
molecules
,
affecting
not only
the structure of
the
brain
,
but also
the peripheral
cells
,
including
lymphocytes
[Mecocci P.
et al.,
1998
].
Causes and
treatment of this serious
disease
of the brain
are unknown, but
the
above facts
indicate that
the autoimmune
nature
of the disease
of "accumulation"
and
unequivocally
put a question on
the possibility of using
methods
of efferent therapy
,
at
least
to slow the progression
of this
severe illness with a
bleak prognosis and in recent
years some have described the successful experience of plasma exchange with
replacement of removed plasma with albumin [Boada M. et al., 2009; Boada-Rovira M.,
2010; Roca I., Cuberas-Borros G., 2010]. This is based on the fact that 90% of the
circulating beta amyloid associated with albumin and after plasmapheresis the donor
albumin mobilizes of brain amyloid, thereby contributing to the improvement
of cognitive
functions in these
patients
[Anaya F.,
2010]
.
Possible is the development of
autoimmune
dementia
,
where
hormone therapy
,
including plasmapheresis,
has a positive effect
[Flanagan EP
et al.,
2010]
.