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Codeposition of cystatin C with amyloid-beta protein in the brain of Alzheimer disease patients.
[hereditary cerebral hemorrhage with amyloidosis]
Immunohistochemical
analysis
of
brains
of
patients
with
Alzheimer
disease
(
AD
)
revealed
that
the
cysteine
proteinase
inhibitor
cystatin
C
colocalizes
with
amyloid
beta
-protein
(
Abeta
)
in
parenchymal
and
vascular
amyloid
deposits
.
No
evidence
of
cerebral
hemorrhage
was
observed
in
any
of
the
brains
studied
.
Immunoelectron
microscopy
demonstrated
dual
staining
of
amyloid
fibrils
with
anti-
Abeta
and
anti-
cystatin
C
antibodies
.
Cystatin
C
immunoreactivity
was
also
observed
in
amyloid
deposits
in
the
brain
of
transgenic
mice
overexpressing
human
beta
amyloid
precursor
protein
.
Massive
deposition
of
the
variant
cystatin
C
in
the
cerebral
vessels
of
patients
with
the
Icelandic
form
of
hereditary
cerebral
hemorrhage
with
amyloidosis
is
thought
to
be
responsible
for
the
pathological
processes
leading
to
stroke
.
Anti-
cystatin
C
antibodies
strongly
labeled
pyramidal
neurons
within
cortical
layers
most
prone
to
amyloid
deposition
in
the
brains
of
AD
patients
.
Immunohistochemistry
with
antibodies
against
the
carboxyl-terminus
of
Abeta
(
x-
42
)
showed
intracellular
immunoreactivity
in
the
same
neuronal
subpopulation
.
It
remains
to
be
established
whether
the
association
of
cystatin
C
to
Abeta
plays
a
primary
role
in
amyloidogenesis
of
AD
or
is
a
late
event
in
which
the
protein
is
bound
to
the
previously
formed
Abeta
amyloid
fibrils
.
Diseases
Validation
Diseases presenting
"brain of transgenic mice"
symptom
hereditary cerebral hemorrhage with amyloidosis
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