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Neuroinflammation in plaque and vascular beta-amyloid disorders: clinical and therapeutic implications.
[hereditary cerebral hemorrhage with amyloidosis]
The
cerebral
beta
-amyloid
(
Abeta
)
disorders
show
a
great
variability
in
the
distribution
of
parenchymal
and
vascular
amyloid
deposits
.
To
study
the
relationship
between
amyloid
deposition
and
inflammatory
responses
in
three
distinct
subtypes
of
cerebral
Abeta
disorders
.
The
distribution
of
inflammatory
proteins
and
cells
in
vascular
and
plaque
amyloid
deposits
was
evaluated
in
postmortem
brain
tissue
using
immunohistochemistry
.
The
effects
of
a
mixture
of
Abeta
peptides
and
inflammation
-related
Abeta-associated
proteins
were
studied
in
postmortem
obtained
human
microglia
cell
cultures
.
T
he
chronic
inflammatory
response
is
associated
with
amyloid
plaques
(
but
not
with
amyloid
in
the
walls
of
larger
vessels
)
in
Alzheimer
's
disease
(
AD
)
,
with
amyloid
in
cerebral
arteries
in
hereditary
cerebral
hemorrhage
with
amyloidosis
-
Dutch
type
and
with
amyloid
microangiopathy
in
the
vascular
variant
of
AD
.
Abeta
(
1
-
42
)
fibrils
complexed
with
complement
factor
C
1
q
and
serum
amyloid
P
component
(
the
relevant
amyloid-associated
proteins
)
stimulate
the
production
of
proinflammatory
cytokines
in
human
microglia
cell
cultures
and
this
production
is
attenuated
by
minocycline
.
The
pattern
of
the
chronic
inflammatory
response
associated
with
fibrillar
Abeta
is
strikingly
different
in
the
three
studied
types
of
Abeta
disorders
.
The
site
of
the
fibrillar
Abeta-induced
chronic
inflammatory
response
is
closely
related
to
clinical
symptoms
.
Minocycline
is
a
drug
of
interest
to
inhibit
microglia-mediated
neuroinflammatory
response
in
Abeta
brain
disorders
.
