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Rapid degeneration of cultured human brain pericytes by amyloid beta protein.
[hereditary cerebral hemorrhage with amyloidosis]
Amyloid
beta
protein
(
A
beta
)
deposition
in
the
cerebral
arterial
and
capillary
walls
is
one
of
the
major
characteristics
of
brains
from
patients
with
Alzheimer
's
disease
and
hereditary
cerebral
hemorrhage
with
amyloidosis
-
Dutch
type
(
HCHWA-D
)
.
Vascular
A
beta
deposition
is
accompanied
by
degeneration
of
smooth
muscle
cells
and
pericytes
.
In
this
study
we
found
that
A
beta
1
-
40
carrying
the
"
Dutch
"
mutation
(
HCHWA-D
A
beta
1
-
40
)
as
well
as
wild-
type
A
beta
1
-
42
induced
degeneration
of
cultured
human
brain
pericytes
and
human
leptomeningeal
smooth
muscle
cells
,
whereas
wild-
type
A
beta
1
-
40
and
HCHWA-D
A
beta
1
-
42
were
inactive
.
Cultured
brain
pericytes
appeared
to
be
much
more
vulnerable
to
A
beta
-induced
degeneration
than
leptomeningeal
smooth
muscle
cells
,
because
in
brain
pericyte
cultures
cell
viability
already
decreased
after
2
days
of
exposure
to
HCHWA-D
A
beta
1
-
40
,
whereas
in
leptomeningeal
smooth
muscle
cell
cultures
cell
death
was
prominent
only
after
4
-
5
days
.
Moreover
,
leptomeningeal
smooth
muscle
cell
cultures
were
better
able
to
recover
than
brain
pericyte
cultures
after
short
-term
treatment
with
HCHWA-D
A
beta
1
-
40
.
Degeneration
of
either
cell
type
was
preceded
by
an
increased
production
of
cellular
amyloid
precursor
protein
.
Both
cell
death
and
amyloid
precursor
protein
production
could
be
inhibited
by
the
amyloid-binding
dye
Congo
red
,
suggesting
that
fibril
assembly
of
A
beta
is
crucial
for
initiating
its
destructive
effects
.
These
data
imply
an
important
role
for
A
beta
in
inducing
perivascular
cell
pathology
as
observed
in
the
cerebral
vasculature
of
patients
with
Alzheimer
's
disease
or
HCHWA-D
.
Diseases
Validation
Diseases presenting
"short-term treatment"
symptom
hereditary cerebral hemorrhage with amyloidosis
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