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.
Frontiers in Aging Neuroscience,
Journal Year:
2024,
Volume and Issue:
16
Published: Feb. 28, 2024
Sensorineural
hearing
loss
(SNHL)
is
a
category
of
that
often
leads
to
difficulty
in
understanding
speech
and
other
sounds.
Auditory
system
dysfunction,
including
deafness
auditory
trauma,
results
cognitive
deficits
via
neuroplasticity.
Cognitive
impairment
(CI)
refers
an
abnormality
the
brain’s
higher
intellectual
processes
related
learning,
memory,
thinking
judgment
can
lead
severe
learning
memory
deficits.
Studies
have
established
strong
correlation
between
SNHL
CI,
but
it
remains
unclear
how
contributes
CI.
The
purpose
this
article
describe
three
hypotheses
regarding
relationship,
mainstream
load
hypothesis,
co-morbidity
sensory
deprivation
as
well
latest
research
progress
each
hypothesis.
Pharmaceutics,
Journal Year:
2024,
Volume and Issue:
16(6), P. 708 - 708
Published: May 24, 2024
Neurodegenerative
diseases
(NDs)
are
a
set
of
progressive,
chronic,
and
incurable
characterized
by
the
gradual
loss
neurons,
culminating
in
decline
cognitive
and/or
motor
functions.
Alzheimer’s
disease
(AD)
Parkinson’s
(PD)
most
common
NDs
represent
an
enormous
burden
both
terms
human
suffering
economic
cost.
The
available
therapies
for
AD
PD
only
provide
symptomatic
palliative
relief
limited
period
unable
to
modify
diseases’
progression.
Over
last
decades,
research
efforts
have
been
focused
on
developing
new
pharmacological
treatments
these
NDs.
However,
date,
no
breakthrough
treatment
has
discovered.
Hence,
development
disease-modifying
drugs
able
halt
or
reverse
progression
remains
unmet
clinical
need.
This
review
summarizes
major
hallmarks
treatment.
It
also
sheds
light
potential
directions
that
can
be
pursued
develop
new,
treat
PD,
describing
as
representative
examples
some
advances
drug
candidates
targeting
oxidative
stress
adenosine
A2A
receptors.
Frontiers in Molecular Neuroscience,
Journal Year:
2023,
Volume and Issue:
16
Published: May 12, 2023
Recent
advances
highlight
that
inflammation
is
critical
to
Alzheimer
Disease
(AD)
pathogenesis.
Indeed,
several
diseases
characterized
by
are
considered
risk
factors
for
AD,
such
as
type
2
diabetes,
obesity,
hypertension,
and
traumatic
brain
injury.
Moreover,
allelic
variations
in
genes
involved
the
inflammatory
cascade
AD.
AD
also
mitochondrial
dysfunction,
which
affects
energy
homeostasis
of
brain.
The
role
dysfunction
has
been
mostly
neuronal
cells.
However,
recent
data
demonstrating
occurs
cells,
promoting
secretion
pro-inflammatory
cytokines,
turn
induce
neurodegeneration.
In
this
review,
we
summarize
finding
supporting
hypothesis
inflammatory-amyloid
describe
demonstrate
link
between
altered
cascade.
We
focus
summarizing
Drp1,
fission,
showing
Drp1
activation
leads
NLRP3
inflammasome,
cascade,
aggravates
Amyloid
beta
(Ab)
deposition
tau-induced
neurodegeneration,
relevance
pathway
an
early
event
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 10, 2025
Abstract
Background
Alzheimer’s
disease
(AD)
is
the
most
common
neurodegenerative
disorder,
NLRP3
inflammasome
has
been
shown
to
play
a
pivotal
role
in
pathogenesis
of
AD,
and
with
increasing
attention
its
involvement
AD.
Therefore,
we
applied
bibliometric
methods
describe
current
research
status
This
study
aims
analyze
trends
hotspots
this
field
from
2013
2024,
providing
valuable
insights
for
AD
research.
Methods
We
have
selected
on
Web
Science
Core
Collection,
time
range
January
1,
2013,
November
30,
exported
all
publications
plain
text
format.
Visualization
analysis
was
performed
using
CiteSpace
6.4.R1,
VOSviewer
1.6.20,
Scimago
Graphica
1.0.46.
Results
A
total
759
related
were
included
study.
The
number
annual
showed
general
upward
trend.
top
three
countries
terms
publication
volume
China,
United
States,
Italy.
University
Manchester
institution
highest
publications.
author
Michael
Heneka,
while
cited
Eicke
Latz.
International
Journal
Molecular
Sciences
published
articles
also
frequently
journal.
keywords
disease,
inflammasome,
neuroinflammation,
Aβ,
microglia.
Conclusion
primary
focus
pathology,
potential
as
therapeutic
target,
strategies
modulate
neuroinflammation
through
targeting
inflammasome.
Future
should
further
investigate
interactions
between
other
molecular
pathways,
assess
clinical
potential,
provide
new
early
diagnosis
treatment
Pharmaceuticals,
Journal Year:
2025,
Volume and Issue:
18(1), P. 133 - 133
Published: Jan. 20, 2025
Neuroinflammation
is
a
key
factor
in
the
progression
of
neurodegenerative
diseases,
driven
by
dysregulation
molecular
pathways
and
activation
brain’s
immune
system,
resulting
release
pro-inflammatory
oxidative
molecules.
This
chronic
inflammation
exacerbated
peripheral
leukocyte
infiltration
into
central
nervous
system.
Medicinal
plants,
with
their
historical
use
traditional
medicine,
have
emerged
as
promising
candidates
to
mitigate
neuroinflammation
offer
sustainable
alternative
for
addressing
conditions
green
healthcare
framework.
review
evaluates
effects
medicinal
plants
on
neuroinflammation,
emphasizing
mechanisms
action,
effective
dosages,
clinical
implications,
based
systematic
search
databases
such
PubMed,
SCOPUS,
Web
Science.
The
findings
highlight
that
like
Cleistocalyx
nervosum
var.
paniala,
Curcuma
longa,
Cannabis
sativa,
Dioscorea
nipponica
reduce
cytokines
(TNF-α,
IL-6,
IL-1β),
inhibit
enzymes
(COX-2
iNOS),
activate
antioxidant
pathways,
particularly
Nrf2.
NF-κB
primary
pathway
inhibited
across
studies.
While
anti-inflammatory
potential
these
significant,
variability
dosages
phytochemical
compositions
limits
translation.
Here,
we
are
modulators
underscoring
therapeutic
potential.
Future
research
should
focus
animal
models,
standardized
protocols,
safety
assessments,
integrating
advanced
methodologies,
genetic
studies
nanotechnology,
enhance
applicability
disease
management.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(7), P. 2906 - 2906
Published: March 23, 2025
Interferon
Regulatory
Factors
(IRFs)
are
critical
modulators
of
immune
and
inflammatory
responses,
yet
their
roles
in
Alzheimer's
disease
(AD)
other
neurodegenerative
disorders
remain
incompletely
understood.
While
IRFs
recognized
for
regulatory
functions
neuroinflammation,
microglial
activation,
neuronal
survival,
dual
as
both
drivers
pathological
inflammation
mediators
neuroprotective
pathways
underscore
a
sophisticated
paradox
disorders.
This
review
aims
to
synthesize
current
evidence
on
IRF-mediated
neuroinflammation
AD
related
diseases,
focusing
the
multifaceted
key
IRF
family
members,
including
IRF1,
IRF3,
IRF7.
We
critically
evaluate
divergent
roles:
IRF1
instance,
exacerbate
neuroinflammatory
cascades
amyloid-beta
(Aβ)
pathology
AD,
whereas
IRF7
may
paradoxically
suppress
under
specific
conditions.
Additionally,
we
explore
dysregulation
Parkinson's
disease,
multiple
sclerosis,
amyotrophic
lateral
Huntington's
emphasizing
shared
distinct
mechanisms
across
Restoring
balance
through
genetic
manipulation,
small-molecule
inhibitors,
or
microbiome-derived
could
attenuate
enhance
Aβ
clearance,
protect
integrity.
Ultimately,
this
work
provides
framework
future
research
harness
signaling
development
precision
therapies
diseases.