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Toxicity of Dutch (E22Q) and Flemish (A21G) mutant amyloid beta proteins to human cerebral microvessel and aortic smooth muscle cells.
[hereditary cerebral hemorrhage with amyloidosis]
Cerebral
amyloid
angiopathy
(
CAA
)
is
characterized
by
the
deposition
of
amyloid
beta
protein
(
Abeta
)
in
cortical
and
leptomeningeal
vessels
of
patients
with
Alzheimer
's
disease
and
hereditary
cerebral
hemorrhage
with
amyloidosis
,
Dutch
type
.
Smooth
muscle
cells
(
SMC
)
from
cerebral
microvessels
(
MV
)
are
of
particular
interest
as
a
site
of
Abeta-related
injury
because
CAA
is
much
more
pronounced
in
the
tunica
media
of
cortical
arterioles
than
meningeal
arteries
.
Patients
carrying
point
mutations
at
residues
22
(
E
22
Q
)
and
21
(
A
21
G
)
of
Abeta
show
severe
CAA
with
various
degrees
of
brain
parenchymal
Abeta
deposition
.
The
purpose
of
this
study
was
to
investigate
the
effects
of
2
mutant
E
22
Q
-
and
A
21
G-Abeta
peptides
on
MV
and
aortic
SMC
.
MERHODS
:
SMC
were
isolated
from
human
cerebral
MV
and
aorta
.
Cell
morphology
,
viability
,
and
proliferation
as
parameters
of
Abeta
toxicity
were
investigated
after
3
days
of
peptide
treatment
by
trypan
blue
exclusion
and
[
(
3
)
H
]
thymidine
incorporation
.
E
22
Q-Abeta
induced
significant
decreased
cellular
proliferation
and
viability
,
as
well
as
obvious
degeneration
of
both
MV
and
aortic
SMC
.
A
21
G-Abeta
and
wild-
type
Abeta
did
not
cause
significant
toxicity
,
as
judged
by
cell
morphology
,
viability
,
or
cell
proliferation
,
on
either
type
of
SMC
.
E
22
Q-Abeta
induced
greater
toxicity
in
all
parameters
than
A
21
G-Abeta
and
wild-
type
Abeta
with
respect
to
both
MV
and
aortic
SMC
.
A
21
G-Abeta
did
not
show
a
significant
toxic
effect
on
MV
and
aortic
SMC
.
This
differential
effect
may
be
linked
to
cell
type
-
specific
processing
and
metabolism
of
mutant
forms
of
Abeta
.
Mutations
in
amyloid
precursor
protein
may
lead
to
CAA
by
different
pathogenetic
mechanisms
or
share
an
unknown
property
that
distinguishes
them
from
wild-
type
Abeta
.
Diseases
Validation
Diseases presenting
"metabolism of mutant forms of abeta"
symptom
hereditary cerebral hemorrhage with amyloidosis
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