Progress in Neuro-Psychopharmacology and Biological Psychiatry,
Год журнала:
2024,
Номер
135, С. 111114 - 111114
Опубликована: Авг. 5, 2024
The
therapeutic
use
of
many
pharmaceuticals,
including
small
molecules
and
biological
therapies,
has
been
associated
with
the
onset
psychiatric
psychological
adverse
events
(PPAEs),
posing
substantial
concerns
to
patients'
health
safety.
These
events,
which
encompass
mood
(e.g.,
depression,
schizophrenia,
suicidal
ideation)
cognitive
changes
learning
memory
impairment,
dementia)
often
remain
undetected
until
advanced
stages
clinical
trials
or
pharmacovigilance,
mostly
because
mechanisms
underlying
PPAEs
poorly
understood.
In
recent
years,
role
neuroimmune
modulation
(comprising
an
intricate
interplay
between
various
cell
types
signaling
pathways)
in
garnered
interest.
Indeed,
understanding
these
complex
interactions
would
substantially
contribute
increase
ability
predict
potential
during
preclinical
a
new
drug's
R&D.
This
review
provides
comprehensive
summary
most
advances
modulation-related
contributing
their
association
specific
pharmaceuticals.
Reported
data
strongly
support
PPAEs.
Pharmaceuticals
may
target
molecular
pathways
pathway
elements
cholinergic
serotonergic
systems),
turn
directly
indirectly
impact
inflammatory
status
homeostasis
brain,
regulating
inflammation
neuronal
function.
Also,
peripheral
immune
system
by
pharmaceuticals
that
do
not
permeate
blood-brain
barrier
monoclonal
antibodies)
alter
neuroimmunomodulatory
leading
summary,
this
underscores
diverse
through
drugs
can
influence
brain
inflammation,
shedding
light
on
targeted
interventions.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(19), С. 10432 - 10432
Опубликована: Сен. 27, 2024
Neuroinflammation
is
a
critical
factor
that
contributes
to
neurological
impairment
and
closely
associated
with
the
onset
progression
of
neurodegenerative
diseases.
In
central
nervous
system
(CNS),
microglia
play
pivotal
role
in
regulation
inflammation
through
various
signaling
pathways.
Therefore,
mitigating
microglial
considered
promising
strategy
for
restraining
neuroinflammation.
Muscarinic
acetylcholine
receptors
(mAChRs)
are
widely
expressed
CNS
exhibit
clear
neuroprotective
effects
disease
models.
However,
whether
activation
mAChRs
can
harness
benefits
neuroinflammation
remains
largely
unexplored.
this
study,
anti-inflammatory
were
found
mouse
model.
The
expression
cytokines
chemokines
was
regulated
brains
spinal
cords
after
administration
mAChR
agonists.
Microglia
primary
target
cells
which
exerted
their
effects.
results
showed
decreased
pro-inflammatory
phenotypes
microglia,
including
inflammatory
cytokines,
morphological
characteristics,
distribution
density.
Such
modulation
further
neuroprotection,
be
even
more
significant
by
direct
neuronal
mAChRs.
This
study
elucidates
dual
mechanisms
exert
responses,
providing
evidence
application
inflammation-related
disorders.
Immunopharmacology and Immunotoxicology,
Год журнала:
2024,
Номер
46(6), С. 805 - 814
Опубликована: Сен. 16, 2024
Inflammasome
NLR
family
pyrin
domain-containing
3
(NLRP3)
is
associated
with
neurological
disorders.
Neuroinflammation
can
be
suppressed
by
inhibiting
NLRP3
inflammasome
activation,
decreasing
neurodegenerative
disorder
progression.
We
devised
a
therapeutic
technique
that
reduce
neuroinflammation
induced
microglial
avoiding
neurodegeneration.
aimed
to
investigate
the
mechanisms
underlying
pharmacological
effects
of
galantamine
and
wedelolactone
evaluating
response
nuclear
factor
kappa
B
(NF-κB)
signaling
pathway
in
lipopolysaccharide
(LPS)-activated
N9
microglia.
Progress in Neuro-Psychopharmacology and Biological Psychiatry,
Год журнала:
2024,
Номер
135, С. 111114 - 111114
Опубликована: Авг. 5, 2024
The
therapeutic
use
of
many
pharmaceuticals,
including
small
molecules
and
biological
therapies,
has
been
associated
with
the
onset
psychiatric
psychological
adverse
events
(PPAEs),
posing
substantial
concerns
to
patients'
health
safety.
These
events,
which
encompass
mood
(e.g.,
depression,
schizophrenia,
suicidal
ideation)
cognitive
changes
learning
memory
impairment,
dementia)
often
remain
undetected
until
advanced
stages
clinical
trials
or
pharmacovigilance,
mostly
because
mechanisms
underlying
PPAEs
poorly
understood.
In
recent
years,
role
neuroimmune
modulation
(comprising
an
intricate
interplay
between
various
cell
types
signaling
pathways)
in
garnered
interest.
Indeed,
understanding
these
complex
interactions
would
substantially
contribute
increase
ability
predict
potential
during
preclinical
a
new
drug's
R&D.
This
review
provides
comprehensive
summary
most
advances
modulation-related
contributing
their
association
specific
pharmaceuticals.
Reported
data
strongly
support
PPAEs.
Pharmaceuticals
may
target
molecular
pathways
pathway
elements
cholinergic
serotonergic
systems),
turn
directly
indirectly
impact
inflammatory
status
homeostasis
brain,
regulating
inflammation
neuronal
function.
Also,
peripheral
immune
system
by
pharmaceuticals
that
do
not
permeate
blood-brain
barrier
monoclonal
antibodies)
alter
neuroimmunomodulatory
leading
summary,
this
underscores
diverse
through
drugs
can
influence
brain
inflammation,
shedding
light
on
targeted
interventions.
