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Tauroursodeoxycholic acid prevents E22Q Alzheimer's Abeta toxicity in human cerebral endothelial cells.
[hereditary cerebral hemorrhage with amyloidosis]
The
vasculotropic
E
22
Q
mutant
of
the
amyloid-
beta
(
Abeta
)
peptide
is
associated
with
hereditary
cerebral
hemorrhage
with
amyloidosis
Dutch
type
.
The
cellular
mechanism
(
s
)
of
toxicity
and
nature
of
the
AbetaE
22
Q
toxic
assemblies
are
not
completely
understood
.
Comparative
assessment
of
structural
parameters
and
cell
death
mechanisms
elicited
in
primary
human
cerebral
endothelial
cells
by
AbetaE
22
Q
and
wild-
type
Abeta
revealed
that
only
AbetaE
22
Q
triggered
the
Bax
mitochondrial
pathway
of
apoptosis
.
AbetaE
22
Q
neither
matched
the
fast
oligomerization
kinetics
of
Abeta
42
nor
reached
its
predominant
beta
-sheet
structure
,
achieving
a
modest
degree
of
oligomerization
with
a
secondary
structure
that
remained
a
mixture
of
beta
and
random
conformations
.
The
endogenous
molecule
tauroursodeoxycholic
acid
(
TUDCA
)
was
a
strong
modulator
of
AbetaE
22
Q
-
triggered
apoptosis
but
did
not
significantly
change
the
secondary
structures
and
fibrillogenic
propensities
of
Abeta
peptides
.
These
data
dissociate
the
pro-apoptotic
properties
of
Abeta
peptides
from
their
distinct
mechanisms
of
aggregation
/
fibrillization
in
vitro
,
providing
new
perspectives
for
modulation
of
amyloid
toxicity
.
Diseases
Validation
Diseases presenting
"primary human cerebral endothelial cells"
symptom
hereditary cerebral hemorrhage with amyloidosis
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