Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: July 18, 2024
Abstract
Accumulating
evidence
implicates
that
herpes
simplex
virus
type
1
(HSV-1)
has
been
linked
to
the
development
and
progression
of
Alzheimer’s
disease
(AD).
HSV-1
infection
induces
β-amyloid
(Aβ)
deposition
in
vitro
vivo,
but
effect
precise
mechanism
remain
elusive.
Here,
we
show
brains
transgenic
5xFAD
mice
resulted
accelerated
Aβ
deposition,
gliosis,
cognitive
dysfunction.
We
demonstrate
induced
recruitment
microglia
viral
core
trigger
microglial
phagocytosis
HSV-GFP-positive
neuronal
cells.
In
addition,
reveal
NLRP3
inflammasome
pathway
by
played
a
crucial
role
AD
caused
infection.
Blockade
signaling
reduces
alleviates
decline
after
Our
findings
support
notion
is
key
factor
etiology
AD,
demonstrating
activation
functions
interface
AD.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Feb. 16, 2024
Abstract
The
human
gastrointestinal
tract
is
populated
with
a
diverse
microbial
community.
vast
genetic
and
metabolic
potential
of
the
gut
microbiome
underpins
its
ubiquity
in
nearly
every
aspect
biology,
including
health
maintenance,
development,
aging,
disease.
advent
new
sequencing
technologies
culture-independent
methods
has
allowed
researchers
to
move
beyond
correlative
studies
toward
mechanistic
explorations
shed
light
on
microbiome–host
interactions.
Evidence
unveiled
bidirectional
communication
between
central
nervous
system,
referred
as
“microbiota–gut–brain
axis”.
microbiota–gut–brain
axis
represents
an
important
regulator
glial
functions,
making
it
actionable
target
ameliorate
development
progression
neurodegenerative
diseases.
In
this
review,
we
discuss
mechanisms
As
provides
essential
cues
microglia,
astrocytes,
oligodendrocytes,
examine
communications
microbiota
these
cells
during
healthy
states
Subsequently,
diseases
using
metabolite-centric
approach,
while
also
examining
role
microbiota-related
neurotransmitters
hormones.
Next,
targeting
intestinal
barrier,
blood–brain
meninges,
peripheral
immune
system
counteract
dysfunction
neurodegeneration.
Finally,
conclude
by
assessing
pre-clinical
clinical
evidence
probiotics,
prebiotics,
fecal
transplantation
A
thorough
comprehension
will
foster
effective
therapeutic
interventions
for
management
Frontiers in Aging Neuroscience,
Journal Year:
2024,
Volume and Issue:
16
Published: April 12, 2024
Neuroinflammation
refers
to
a
highly
complicated
reaction
of
the
central
nervous
system
(CNS)
certain
stimuli
such
as
trauma,
infection,
and
neurodegenerative
diseases.
This
is
cellular
immune
response
whereby
glial
cells
are
activated,
inflammatory
mediators
liberated
reactive
oxygen
nitrogen
species
synthesized.
key
process
that
helps
protect
brain
from
pathogens,
but
inappropriate,
or
protracted
inflammation
yields
pathological
states
Parkinson’s
disease,
Alzheimer’s,
Multiple
Sclerosis,
other
disorders
showcase
various
pathways
neurodegeneration
distributed
in
parts
CNS.
review
reveals
major
neuroinflammatory
signaling
associated
with
neurodegeneration.
Additionally,
it
explores
promising
therapeutic
avenues,
stem
cell
therapy,
genetic
intervention,
nanoparticles,
aiming
regulate
neuroinflammation
potentially
impede
decelerate
advancement
these
conditions.
A
comprehensive
understanding
intricate
connection
between
diseases
pivotal
for
development
future
treatment
strategies
can
alleviate
burden
imposed
by
devastating
disorders.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 8, 2024
The
increasing
life
expectancy
has
led
to
a
higher
incidence
of
age-related
neurodegenerative
conditions.
Within
this
framework,
neuroinflammation
emerges
as
significant
contributing
factor.
It
involves
the
activation
microglia
and
astrocytes,
leading
release
pro-inflammatory
cytokines
chemokines
infiltration
peripheral
leukocytes
into
central
nervous
system
(CNS).
These
instances
result
in
neuronal
damage
neurodegeneration
through
activated
nucleotide-binding
domain
leucine-rich
repeat
containing
(NLR)
family
pyrin
protein
3
(NLRP3)
nuclear
factor
kappa
B
(NF-kB)
pathways
decreased
erythroid
2-related
2
(Nrf2)
activity.
Due
limited
effectiveness
regarding
inhibition
neuroinflammatory
targets
using
conventional
drugs,
there
is
challenging
growth
search
for
innovative
therapies
alleviating
CNS
diseases
or
even
before
their
onset.
Our
results
indicate
that
interventions
focusing
on
Interleukin-Driven
Immunomodulation,
Chemokine
(CXC)
Receptor
Signaling
Expression,
Cold
Exposure,
Fibrin-Targeted
strategies
significantly
promise
mitigate
processes.
approaches
demonstrate
potential
anti-neuroinflammatory
effects,
addressing
conditions
such
Multiple
Sclerosis,
Experimental
autoimmune
encephalomyelitis,
Parkinson’s
Disease,
Alzheimer’s
Disease.
While
findings
are
promising,
immunomodulatory
often
face
limitations
due
Immune-Related
Adverse
Events.
Therefore,
conduction
randomized
clinical
trials
matter
mandatory,
will
pave
way
promising
future
development
new
medicines
with
specific
therapeutic
targets.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(2), P. 240 - 240
Published: Feb. 16, 2024
Neurodegenerative
diseases
(NDs)
encompass
an
assorted
array
of
disorders
such
as
Alzheimer's
disease,
Parkinson's
and
amyotrophic
lateral
sclerosis,
each
characterised
by
distinct
clinical
manifestations
underlying
pathological
mechanisms.
While
some
cases
have
a
genetic
basis,
many
NDs
occur
sporadically.
Despite
their
differences,
these
commonly
feature
chronic
neuroinflammation
hallmark.
Consensus
has
recently
been
reached
on
the
possibility
that
mitochondria
dysfunction
protein
aggregation
can
mutually
contribute
to
activation
neuroinflammatory
response
thus
onset
progression
disorders.
In
present
review,
we
discuss
contribution
aetiology
NDs,
highlighting
new
potential
therapeutic
targets
be
identified
tackle
neurodegenerative
processes
alleviate
pathologies.
Gut Microbes,
Journal Year:
2024,
Volume and Issue:
16(1)
Published: July 7, 2024
With
the
increasing
of
aging
population
and
consumption
high-fat
diets
(HFD),
incidence
Alzheimer's
disease
(AD)
has
skyrocketed.
Natural
antioxidants
show
promising
potential
in
prevention
AD,
as
oxidative
stress
neuroinflammation
are
two
hallmarks
AD
pathogenesis.
Here,
we
showed
that
quinic
acid
(QA),
a
polyphenol
derived
from
millet,
significantly
decreased
HFD-induced
brain
levels
Aβ
p-Tau.
Examination
gut
microbiota
suggested
improvement
composition
HFD
mice
after
QA
treatment.
Metabolomic
analysis
significant
increase
microbial
tryptophan
metabolites
indole-3-acetic
(IAA)
kynurenic
(KYNA)
by
QA.
In
addition,
IAA
KYNA
negative
correlation
with
pro-inflammatory
factors
indicators.
Further
experiments
on
proved
could
reproduce
effects
suppress
inflammation
decrease
Transcriptomics
administration
revealed
inhibition
DR3/IKK/NF-κB
signaling
pathway
IAA.
conclusion,
this
study
demonstrated
counteract
regulating
inflammatory
via
metabolites.
Neuron,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 1, 2024
Autophagy
is
a
conserved
mechanism
that
degrades
damaged
or
superfluous
cellular
contents
and
enables
nutrient
recycling
under
starvation
conditions.
Many
neurodegeneration-associated
proteins
are
autophagy
substrates,
upregulation
ameliorates
disease
in
many
animal
models
of
neurodegeneration
by
enhancing
the
clearance
toxic
proteins,
proinflammatory
molecules,
dysfunctional
organelles.
inhibition
also
induces
neuronal
glial
senescence,
phenomenon
occurs
with
increasing
age
non-diseased
brains
as
well
response
to
stresses.
However,
aging
mutations
impair
autophagy.
This
creates
potentially
detrimental
feedback
loop
whereby
accumulation
these
disease-associated
impairs
their
autophagic
clearance,
facilitating
further
aggregation.
Thus,
understanding
how
interacts
aging,
neurodegenerative
diseases
temporal,
cellular,
genetic
context
important
for
future
clinical
application
autophagy-modulating
therapies
neurodegeneration.
Cell Communication and Signaling,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 3, 2025
Oxidative
stress
and
neuroinflammation
are
recognized
as
key
factors
in
the
development
of
neurodegenerative
diseases,
yet
effective
interventions
biomarkers
to
address
oxidative
these
conditions
limited.
Uric
acid
(UA),
traditionally
associated
with
gout,
is
now
gaining
prominence
a
potential
target
diseases.
Soluble
UA
stands
out
one
most
vital
antioxidant
compounds
produced
by
human
body,
accounting
for
up
55%
extracellular
capacity
neutralize
free
radicals.
While
there
increasing
evidence
supporting
neuroprotective
properties
Parkinson's
disease
Alzheimer's
disease,
gaps
knowledge
still
exist
regarding
underlying
mechanisms
how
effectively
translate
benefits
into
clinical
practice.
Moreover,
current
elevation
therapy
exhibits
unstable
properties,
individual
variability,
even
adverse
effects,
limiting
its
applications.
This
review
consolidates
recent
advancements
understanding
exerts
effects
on
diseases
emphasizes
dual
roles
managing
neuroinflammation.
Additionally,
elucidates
through
which
confers
neuroprotection.
Based
this,
underscores
significance
biomarker
aims
provide
comprehensive
therapeutic
target,
while
also
addressing
possible
challenges
implementation.
