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MicroRNAs as the cause of schizophrenia in 22q11.2 deletion carriers, and possible implications for idiopathic disease: a mini-review.
[22q11.2 deletion syndrome]
The
22
q
11
.
2
deletion
is
the
strongest
known
genetic
risk
factor
for
schizophrenia
.
Research
has
implicated
microRNA-mediated
dysregulation
in
22
q
11
.
2
deletion
syndrome
(
22
q
11
.
2
DS
)
schizophrenia
-risk
.
Primary
candidate
genes
are
DGCR
8
(
DiGeorge
syndrome
critical
region
gene
8
)
,
which
encodes
a
component
of
the
microprocessor
complex
essential
for
microRNA
biogenesis
,
and
MIR
185
,
which
encodes
microRNA
185
.
Mouse
models
of
22
q
11
.
2
DS
have
demonstrated
alterations
in
brain
microRNA
biogenesis
,
and
that
DGCR
8
haploinsufficiency
may
contribute
to
these
alterations
,
e
.
g
.
,
via
down-regulation
of
a
specific
microRNA
subset
.
miR-
185
was
the
top-scoring
down-regulated
microRNA
in
both
the
prefrontal
cortex
and
the
hippocampus
,
brain
areas
which
are
the
key
foci
of
schizophrenia
research
.
This
reduction
in
miR-
185
expression
contributed
to
dendritic
and
spine
development
deficits
in
hippocampal
neurons
.
In
addition
,
miR-
185
has
two
validated
targets
(
RhoA
,
Cdc
42
)
,
both
of
which
have
been
associated
with
altered
expression
levels
in
schizophrenia
.
These
combined
data
support
the
involvement
of
miR-
185
and
its
down-stream
pathways
in
schizophrenia
.
This
review
summarizes
evidence
implicating
microRNA-mediated
dysregulation
in
schizophrenia
in
both
22
q
11
.
2
DS
-related
and
idiopathic
cases
.
Diseases
Validation
Diseases presenting
"demonstrated alterations in brain microrna biogenesis"
symptom
22q11.2 deletion syndrome
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