Immunological Reviews,
Journal Year:
2023,
Volume and Issue:
322(1), P. 259 - 282
Published: Dec. 25, 2023
Summary
From
studies
of
individual
families
to
global
collaborative
efforts,
the
NLRP3
inflammasome
is
now
recognized
be
a
key
regulator
innate
immunity.
Activated
by
panoply
pathogen‐associated
and
endogenous
triggers,
serves
as
an
intracellular
sensor
that
drives
carefully
coordinated
assembly
inflammasome,
downstream
inflammation
mediated
IL‐1
IL‐18.
Initially
discovered
cause
autoinflammatory
spectrum
cryopyrin‐associated
periodic
syndrome
(CAPS),
also
known
play
role
in
more
common
diseases
including
cardiovascular
disease,
gout,
liver
disease.
We
have
seen
cohesion
results
from
clinical
CAPS
patients,
ex
vivo
human
cells
murine
cells,
models
leading
our
understanding
pathways,
cytokine
secretion,
cell
death
pathways
has
solidified
autoinflammation
pathogenesis
Recent
advances
structure
provided
ways
for
us
visualize
normal
mutant
protein
function
pharmacologic
inhibition.
The
subsequent
development
targeted
therapies
successfully
used
treatment
patients
with
completes
bench
bedside
translational
loop
which
defined
study
this
unique
protein.
ABSTRACT
Background
The
COVID‐19
pandemic
has
left
an
indelible
mark
on
the
world,
with
mounting
evidence
suggesting
that
it
not
only
posed
acute
challenges
to
global
healthcare
systems
but
also
unveiled
a
complex
array
of
long‐term
consequences,
particularly
cognitive
impairment
(CI).
As
persistence
post‐COVID‐19
neurological
syndrome
could
evolve
into
next
public
health
crisis,
is
imperative
gain
better
understanding
intricate
pathophysiology
CI
in
patients
and
viable
treatment
strategies.
Methods
This
comprehensive
review
explores
management
across
phases
COVID‐19,
from
infection
Long‐COVID,
by
synthesizing
findings
clinical,
preclinical,
mechanistic
studies
identify
key
contributors
CI,
as
well
current
therapeutic
approaches.
Results
Key
mechanisms
contributing
include
persistent
neuroinflammation,
cerebrovascular
complications,
direct
neuronal
injury,
activation
kynurenine
pathway,
psychological
distress.
Both
pharmacological
interventions,
such
anti‐inflammatory
therapies
agents
targeting
neuroinflammatory
pathways,
non‐pharmacological
strategies,
including
rehabilitation,
show
promise
addressing
these
challenges.
Although
much
derived
preclinical
animal
studies,
provide
foundational
insights
potential
Conclusion
By
knowledge,
this
highlights
importance
COVID‐19‐related
offers
actionable
for
mitigation
recovery
community
continues
grapple
pandemic's
impact.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 7, 2025
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disorder
characterized
by
cognitive
decline,
memory
impairment,
and
neuroinflammation,
with
no
definitive
cure
currently
available.
The
NLRP3
inflammasome,
key
mediator
of
has
emerged
as
critical
player
in
AD
pathogenesis,
contributing
to
the
accumulation
β-amyloid
(Aβ)
plaques,
tau
hyperphosphorylation,
neuronal
damage.
This
review
explores
mechanisms
which
inflammasome
activated
AD,
including
its
interactions
Aβ,
tau,
reactive
oxygen
species
(ROS),
pyroptosis.
Additionally,
it
highlights
role
ubiquitin
system,
ion
channels,
autophagy,
gut
microbiota
regulating
activation.
Therapeutic
strategies
targeting
such
IL-1β
inhibitors,
natural
compounds,
novel
small
molecules,
are
discussed
promising
approaches
mitigate
neuroinflammation
slow
progression.
underscores
potential
inhibition
therapeutic
avenue
for
AD.
British Journal of Pharmacology,
Journal Year:
2023,
Volume and Issue:
181(6), P. 840 - 878
Published: Sept. 14, 2023
Adipose
tissue
has
recently
been
recognized
as
an
important
endocrine
organ
that
plays
a
crucial
role
in
energy
metabolism
and
the
immune
response
many
metabolic
tissues.
With
this
regard,
emerging
evidence
indicates
crosstalk
exists
between
adipose
brain.
However,
contribution
of
to
development
age-related
diseases,
including
Alzheimer's
disease,
remains
poorly
defined.
New
studies
suggest
modulates
brain
function
through
range
endogenous
biologically
active
factors
known
adipokines,
which
can
cross
blood-brain
barrier
reach
target
areas
or
regulate
barrier.
In
review,
we
discuss
effects
several
adipokines
on
physiology
barrier,
their
disease
therapeutic
potential.
LINKED
ARTICLES:
This
article
is
part
themed
issue
From
Disease
Vascular
Dementia:
Different
Roads
Leading
Cognitive
Decline.
To
view
other
articles
section
visit
http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc.
Immunological Reviews,
Journal Year:
2023,
Volume and Issue:
322(1), P. 259 - 282
Published: Dec. 25, 2023
Summary
From
studies
of
individual
families
to
global
collaborative
efforts,
the
NLRP3
inflammasome
is
now
recognized
be
a
key
regulator
innate
immunity.
Activated
by
panoply
pathogen‐associated
and
endogenous
triggers,
serves
as
an
intracellular
sensor
that
drives
carefully
coordinated
assembly
inflammasome,
downstream
inflammation
mediated
IL‐1
IL‐18.
Initially
discovered
cause
autoinflammatory
spectrum
cryopyrin‐associated
periodic
syndrome
(CAPS),
also
known
play
role
in
more
common
diseases
including
cardiovascular
disease,
gout,
liver
disease.
We
have
seen
cohesion
results
from
clinical
CAPS
patients,
ex
vivo
human
cells
murine
cells,
models
leading
our
understanding
pathways,
cytokine
secretion,
cell
death
pathways
has
solidified
autoinflammation
pathogenesis
Recent
advances
structure
provided
ways
for
us
visualize
normal
mutant
protein
function
pharmacologic
inhibition.
The
subsequent
development
targeted
therapies
successfully
used
treatment
patients
with
completes
bench
bedside
translational
loop
which
defined
study
this
unique
protein.
