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Primary over-expression of AβPP in muscle does not lead to the development of inclusion body myositis in a new lineage of the MCK-AβPP transgenic mouse.
[inclusion body myositis]
The
aim
of
this
study
is
to
determine
whether
primary
over-expression
of
AβPP
in
skeletal
muscle
results
in
the
development
of
features
of
inclusion
body
myositis
(
IBM
)
in
a
new
lineage
of
the
MCK-AβPP
transgenic
mouse
.
Quantitative
histological
,
immunohistochemical
and
western
blotting
studies
were
performed
on
muscles
from
3
to
18
month
old
transgenic
and
wild-
type
C
5
7
BL
6
/
SJL
mice
.
Electron
microscopy
was
also
performed
on
muscle
sections
from
selected
animals
.
Although
western
blotting
confirmed
that
there
was
over-expression
of
full
length
AβPP
in
transgenic
mouse
muscles
,
deposition
of
amyloid-β
and
fibrillar
amyloid
could
not
be
demonstrated
histochemically
or
with
electron
microscopy
.
Additionally
,
other
changes
typical
of
IBM
such
as
rimmed
vacuoles
,
cytochrome
C
oxidase-
deficient
fibres
,
upregulation
of
MHC
antigens
,
lymphocytic
inflammatory
infiltration
and
T
cell
fibre
invasion
were
absent
.
The
most
prominent
finding
in
both
transgenic
and
wild-
type
animals
was
the
presence
of
tubular
aggregates
which
was
age-related
and
largely
restricted
to
male
animals
.
Expression
of
full
length
AβPP
in
this
MCK-AβPP
mouse
lineage
did
not
reach
the
levels
required
for
immunodetection
or
deposition
of
amyloid-β
as
in
the
original
transgenic
strains
,
and
was
not
associated
with
the
development
of
pathological
features
of
IBM
.
These
negative
results
emphasise
the
potential
pitfalls
of
re
-deriving
transgenic
mouse
strains
in
different
laboratories
.
Diseases
Validation
Diseases presenting
"and was not associated with the development of pathological features of ibm"
symptom
inclusion body myositis
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