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Inclusion body myositis: from immunopathology and degenerative mechanisms to treatment perspectives.
[inclusion body myositis]
Inclusion
body
myositis
is
the
most
common
inflammatory
myopathy
above
the
age
of
50
.
It
becomes
clinically
apparent
around
the
fourth
decade
and
leads
to
a
slowly
,
but
relentlessly
progressive
decline
in
muscular
wasting
and
weakness
.
The
pathology
consists
of
a
complex
network
of
inflammatory
and
degenerative
mechanisms
,
which
lead
to
an
attack
of
muscle
fibers
by
auto-reactive
T
cells
and
possibly
antibodies
.
At
the
same
time
,
various
aberrant
proteins
accumulate
within
the
muscle
fibers
,
including
β-amyloid
,
tau
and
α-synuclein
.
Several
key
components
of
proinflammatory
cell
stress
mechanisms
such
as
nitric
oxide
production
and
macroautophagic
processing
contribute
to
the
muscle
fiber
damage
.
So
far
,
none
of
the
anti-
inflammatory
or
immunomodulatory
treatment
efforts
have
been
able
to
halt
the
disease
progression
and
help
the
patients
.
In
this
summary
,
the
current
concept
of
the
complex
disease
pathology
of
IBM
is
reviewed
with
a
focus
on
recent
findings
as
well
as
future
treatment
perspectives
.
Diseases
Validation
Diseases presenting
"weakness"
symptom
achondroplasia
adrenomyeloneuropathy
alexander disease
aniridia
aromatase deficiency
coats disease
congenital toxoplasmosis
epidermolysis bullosa simplex
esophageal adenocarcinoma
familial hypocalciuric hypercalcemia
familial mediterranean fever
focal myositis
gm1 gangliosidosis
hydrocephalus with stenosis of the aqueduct of sylvius
inclusion body myositis
locked-in syndrome
lymphangioleiomyomatosis
malignant atrophic papulosis
neuralgic amyotrophy
pendred syndrome
pleomorphic liposarcoma
pyomyositis
pyruvate dehydrogenase deficiency
sneddon syndrome
systemic capillary leak syndrome
thoracic outlet syndrome
triple a syndrome
typhoid
von hippel-lindau disease
waldenström macroglobulinemia
werner syndrome
x-linked adrenoleukodystrophy
This symptom has already been validated