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Glial reactions and the clearance of amyloid beta protein in the brains of patients with hereditary cerebral hemorrhage with amyloidosis-Dutch type.
[hereditary cerebral hemorrhage with amyloidosis]
Although
the
amyloid
beta
protein
(
Abeta
)
E
693
Q
mutation
enhances
Abeta
fibrillization
in
vitro
and
cerebral
amyloid
angiopathy
(
CAA
)
in
vivo
,
brain
parenchymal
Abeta
deposition
and
tau
pathology
in
hereditary
cerebral
hemorrhage
with
amyloidosis
-
Dutch
type
(
HCHWA-D
)
are
limited
.
To
evaluate
whether
clearance
of
Abeta
by
glial
cells
may
play
a
role
in
this
regard
,
this
immunohistochemical
study
of
frontal
cortex
of
14
HCHWA-D
autopsy
brains
was
performed
using
double
staining
with
glial
markers
and
end-
specific
antibodies
to
Abetax-
42
(
Abeta
42
)
and
Abetax-
40
(
Abeta
40
)
.
Tau
pathology
was
also
assessed
.
Numerous
microglia
and
/
or
astrocytes
carrying
cytoplasmic
Abeta
42
(
+
)
40
(
-
)
granules
were
scattered
among
non-fibrillar
(
Congo
red
-negative
)
Abeta
deposits
,
i
.
e
.
,
clouds
,
fine
diffuse
plaques
,
and
Abeta
42
(
+
)
40
(
-
)
dense
diffuse
plaques
.
On
the
other
hand
,
activated
microglia
and
reactive
astrocytes
associated
with
fibrillar
(
Congo
red
-
positive
)
Abeta
deposition
,
i
.
e
.
,
Abeta
42
(
+
)
40
(
+
)
dense
diffuse
plaques
and
CAA
invading
the
parenchyma
,
were
virtually
devoid
of
Abeta
granules
.
Tau
pathology
was
scant
and
most
frequently
associated
with
CAA
.
These
results
suggest
that
relatively
non-fibrillar
parenchymal
Abeta
deposits
may
be
liable
to
glial
clearance
.
Abeta
sequestration
by
glial
cells
may
be
a
factor
limiting
the
levels
of
neurotoxic
soluble
Abeta
oligomers
in
HCHWA-D
brain
.
Diseases
Validation
Diseases presenting
"specific antibodies"
symptom
benign recurrent intrahepatic cholestasis
congenital toxoplasmosis
cutaneous mastocytosis
hereditary cerebral hemorrhage with amyloidosis
inclusion body myositis
omenn syndrome
scrub typhus
typhoid
x-linked adrenoleukodystrophy
zellweger syndrome
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