Molecular Psychiatry,
Journal Year:
2020,
Volume and Issue:
26(1), P. 103 - 117
Published: Nov. 3, 2020
Abstract
Depression
is
a
common
mental
illness,
affecting
more
than
300
million
people
worldwide.
Decades
of
investigation
have
yielded
symptomatic
therapies
for
this
disabling
condition
but
not
led
to
consensus
about
its
pathogenesis.
There
are
data
support
several
different
theories
causation,
including
the
monoamine
hypothesis,
hypothalamic–pituitary–adrenal
axis
changes,
inflammation
and
immune
system
alterations,
abnormalities
neurogenesis
conducive
environmental
milieu.
Research
in
these
areas
others
has
greatly
advanced
current
understanding
depression;
however,
there
other,
less
widely
known
Oligodendrocyte
lineage
cells,
oligodendrocyte
progenitor
cells
mature
oligodendrocytes,
numerous
important
functions,
which
include
forming
myelin
sheaths
that
enwrap
central
nervous
axons,
supporting
axons
metabolically,
mediating
certain
forms
neuroplasticity.
These
specialized
glial
been
implicated
psychiatric
disorders
such
as
depression.
In
review,
we
summarize
recent
findings
shed
light
on
how
might
participate
pathogenesis
depression,
discuss
new
approaches
targeting
novel
strategy
treat
The Lancet,
Journal Year:
2020,
Volume and Issue:
396(10250), P. 565 - 582
Published: Aug. 1, 2020
Clinicians
can
encounter
sex
and
gender
disparities
in
diagnostic
therapeutic
responses.
These
are
noted
epidemiology,
pathophysiology,
clinical
manifestations,
disease
progression,
response
to
treatment.
This
Review
discusses
the
fundamental
influences
of
as
modifiers
major
causes
death
morbidity.
We
articulate
how
genetic,
epigenetic,
hormonal
biological
influence
physiology
disease,
social
constructs
affect
behaviour
community,
clinicians,
patients
health-care
system
interact
with
pathobiology.
aim
guide
clinicians
researchers
consider
their
approach
diagnosis,
prevention,
treatment
diseases
a
necessary
step
towards
precision
medicine,
which
will
benefit
men's
women's
health.
Science,
Journal Year:
2018,
Volume and Issue:
362(6420)
Published: Dec. 13, 2018
Most
genetic
risk
for
psychiatric
disease
lies
in
regulatory
regions,
implicating
pathogenic
dysregulation
of
gene
expression
and
splicing.
However,
comprehensive
assessments
transcriptomic
organization
diseased
brains
are
limited.
In
this
work,
we
integrated
genotypes
RNA
sequencing
brain
samples
from
1695
individuals
with
autism
spectrum
disorder
(ASD),
schizophrenia,
bipolar
disorder,
as
well
controls.
More
than
25%
the
transcriptome
exhibits
differential
splicing
or
expression,
isoform-level
changes
capturing
largest
effects
enrichments.
Coexpression
networks
isolate
disease-specific
neuronal
alterations,
microglial,
astrocyte,
interferon-response
modules
defining
previously
unidentified
neural-immune
mechanisms.
We
genomic
data
to
perform
a
transcriptome-wide
association
study,
prioritizing
loci
likely
mediated
by
cis
on
expression.
This
characterization
molecular
pathology
across
three
major
disorders
provides
resource
mechanistic
insight
therapeutic
development.
