Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
177, P. 117031 - 117031
Published: June 25, 2024
An
expanding
body
of
research
indicates
a
correlation
between
the
gut
microbiota
and
various
diseases.
Metabolites
produced
by
act
as
mediators
host,
interacting
with
multiple
systems
in
human
to
regulate
physiological
or
pathological
functions.
However,
further
investigation
is
still
required
elucidate
underlying
mechanisms.
One
such
metabolite
involved
choline
metabolism
microbes
trimethylamine
(TMA),
which
can
traverse
intestinal
epithelial
barrier
enter
bloodstream,
ultimately
reaching
liver
where
it
undergoes
oxidation
catalyzed
flavin-containing
monooxygenase
3
(FMO3)
form
N-oxide
(TMAO).
While
some
TMAO
eliminated
through
renal
excretion,
remaining
amounts
circulate
leading
systemic
inflammation,
endoplasmic
reticulum
(ER)
stress,
mitochondrial
disruption
normal
functions
humans.
As
representative
microbial
originating
from
gut,
has
significant
potential
both
biomarker
for
monitoring
disease
occurrence
progression
tailoring
personalized
treatment
strategies
patients.
This
review
provides
an
extensive
overview
sources
its
blood,
well
impact
on
several
major
Additionally,
we
explore
latest
areas
related
along
future
directions.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: July 12, 2023
Abstract
Studies
in
neurodegenerative
diseases,
including
Alzheimer’s
disease,
Parkinson’s
disease
and
Amyotrophic
lateral
sclerosis,
Huntington’s
so
on,
have
suggested
that
inflammation
is
not
only
a
result
of
neurodegeneration
but
also
crucial
player
this
process.
Protein
aggregates
which
are
very
common
pathological
phenomenon
can
induce
neuroinflammation
further
aggravates
protein
aggregation
neurodegeneration.
Actually,
even
happens
earlier
than
aggregation.
Neuroinflammation
induced
by
genetic
variations
CNS
cells
or
peripheral
immune
may
deposition
some
susceptible
population.
Numerous
signaling
pathways
range
been
to
be
involved
the
pathogenesis
neurodegeneration,
although
they
still
far
from
being
completely
understood.
Due
limited
success
traditional
treatment
methods,
blocking
enhancing
inflammatory
considered
promising
strategies
for
therapy
many
them
got
exciting
results
animal
models
clinical
trials.
Some
them,
few,
approved
FDA
usage.
Here
we
comprehensively
review
factors
affecting
major
pathogenicity
sclerosis.
We
summarize
current
strategies,
both
clinic,
diseases.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(7), P. 6328 - 6328
Published: March 28, 2023
Neuroinflammation
is
a
critical
factor
in
developing
and
progressing
numerous
brain
diseases,
including
neurodegenerative
diseases.
Chronic
or
excessive
neuroinflammation
can
lead
to
neurotoxicity,
causing
damage
contributing
the
onset
progression
of
various
Therefore,
understanding
mechanisms
strategies
control
them
crucial
for
treating
Studies
have
shown
that
plays
vital
role
such
as
Alzheimer's
(AD)
Parkinson's
(PD),
stroke.
Additionally,
effects
PM
Frontiers in Endocrinology,
Journal Year:
2023,
Volume and Issue:
14
Published: April 3, 2023
Obesity
has
been
associated
with
oxidative
stress.
Obese
patients
are
at
increased
risk
for
diabetic
cognitive
dysfunction,
indicating
a
pathological
link
between
obesity,
stress,
and
dysfunction.
can
induce
the
biological
process
of
stress
by
disrupting
adipose
microenvironment
(adipocytes,
macrophages),
mediating
low-grade
chronic
inflammation,
mitochondrial
dysfunction
(mitochondrial
division,
fusion).
Furthermore,
be
implicated
in
insulin
resistance,
inflammation
neural
tissues,
lipid
metabolism
disorders,
affecting
diabetics.
CNS Neuroscience & Therapeutics,
Journal Year:
2023,
Volume and Issue:
29(4), P. 1094 - 1108
Published: Jan. 10, 2023
Abstract
Background
A
growing
body
of
research
shows
that
drug
monomers
from
traditional
Chinese
herbal
medicines
have
antineuroinflammatory
and
neuroprotective
effects
can
significantly
improve
the
recovery
motor
function
after
spinal
cord
injury
(SCI).
Here,
we
explore
role
molecular
mechanisms
Alpinetin
on
activating
microglia‐mediated
neuroinflammation
neuronal
apoptosis
SCI.
Methods
Stimulation
microglia
with
lipopolysaccharide
(LPS)
to
simulate
models
in
vitro,
effect
release
pro‐inflammatory
mediators
LPS‐induced
its
mechanism
were
detected.
In
addition,
a
co‐culture
system
cells
was
constructed
assess
apoptosis.
Finally,
rat
used
study
inflammation,
apoptosis,
axonal
regeneration,
Alpinetin.
Results
inhibits
activity
JAK2/STAT3
pathway.
also
reverse
activated
reactive
oxygen
species
(ROS)
production
decrease
mitochondrial
membrane
potential
(MMP)
PC12
cells.
vivo
inflammatory
response
improves
function.
Conclusion
be
treat
neurodegenerative
diseases
is
novel
candidate
for
treatment
neuroinflammation.
Acta Neuropathologica Communications,
Journal Year:
2023,
Volume and Issue:
11(1)
Published: Aug. 2, 2023
Astrocytes
are
one
of
the
brain's
major
cell
types
and
responsible
for
maintaining
neuronal
homeostasis
via
regulating
extracellular
environment,
providing
metabolic
support,
modulating
synaptic
activity.
In
neurodegenerative
diseases,
such
as
Alzheimer's
disease,
astrocytes
can
take
on
a
hypertrophic
appearance.
These
reactive
canonically
associated
with
increases
in
cytoskeletal
proteins,
glial
fibrillary
acidic
protein
vimentin.
However,
molecular
alterations
that
characterize
human
disease
tissues
have
not
been
extensively
studied
single
resolution.
Using
nucleus
RNA
sequencing
data
from
normal,
pathologic
aging,
brains,
we
identified
transcriptomic
changes
astrocytes.
Deep
learning-based
clustering
algorithms
denoised
expression
17,012
genes
clustered
15,529
astrocyte
nuclei,
identifying
protoplasmic,
gray
matter
fibrous,
white
clusters.
trajectory
analyses
revealed
spectrum
reactivity
within
protoplasmic
characterized
by
modest
increase
marked
decrease
homeostatic
genes.
Amyloid
but
tau
pathology
correlated
reactivity.
To
identify
reactivity-associated
genes,
linear
regressions
gene
versus
were
used
to
top
52
upregulated
144
downregulated
Gene
Ontology
analysis
cellular
growth,
responses
metal
ions,
inflammation,
proteostasis.
Downregulated
involved
interactions,
development,
ERBB
signaling,
synapse
regulation.
Transcription
factors
significantly
enriched
among
co-immunofluorescence
staining
brain
tissues,
confirmed
downregulation
ERBB4
transcription
factor
NFIA
Our
findings
reveal
exist
is
strong
loss
normal
function.
Phytotherapy Research,
Journal Year:
2024,
Volume and Issue:
38(6), P. 3169 - 3189
Published: April 14, 2024
Abstract
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disorder
characterized
by
the
accumulation
of
amyloid‐beta
plaques
and
neurofibrillary
tangles,
leading
to
neuronal
loss.
Curcumin,
polyphenolic
compound
derived
from
Curcuma
longa
,
has
shown
potential
neuroprotective
effects
due
its
anti‐inflammatory
antioxidant
properties.
This
review
aims
synthesize
current
preclinical
data
on
anti‐neuroinflammatory
mechanisms
curcumin
in
context
AD,
addressing
pharmacokinetics,
bioavailability,
as
therapeutic
adjunct.
An
exhaustive
literature
search
was
conducted,
focusing
recent
studies
within
last
10
years
related
curcumin's
impact
neuroinflammation
role
AD.
The
methodology
included
sourcing
articles
specialized
databases
using
specific
medical
subject
headings
terms
ensure
precision
relevance.
Curcumin
demonstrates
significant
properties
modulating
neuroinflammatory
pathways,
scavenging
reactive
oxygen
species,
inhibiting
production
pro‐inflammatory
cytokines.
Despite
potential,
challenges
remain
regarding
limited
bioavailability
scarcity
comprehensive
human
clinical
trials.
emerges
promising
adjunct
AD
multimodal
benefits.
However,
further
research
required
overcome
establish
effective
dosing
regimens
subjects.
Developing
novel
delivery
systems
formulations
may
enhance
treatment.
Cellular and Molecular Neurobiology,
Journal Year:
2024,
Volume and Issue:
44(1)
Published: Feb. 19, 2024
Abstract
Neuroinflammation
is
an
important
pathogenesis
of
neurological
diseases
and
causes
a
series
physiopathological
changes,
such
as
abnormal
activation
glial
cells,
neuronal
degeneration
death,
disruption
the
blood‒brain
barrier.
Therefore,
modulating
inflammation
may
be
therapeutic
tool
for
treating
diseases.
Mesenchymal
stem
cells
(MSCs),
pluripotent
have
great
potential
due
to
their
regenerative
ability,
immunity,
ability
regulate
inflammation.
However,
recent
studies
shown
that
MSC-derived
exosomes
(MSC-Exos)
play
major
role
in
this
process
key
neuroprotection
by
regulating
neuroglia.
This
review
summarizes
progress
made
neuroinflammation
focusing
on
mechanisms
which
MSC-Exos
are
involved
regulation
through
signaling
pathways
TLR,
NF-κB,
MAPK,
STAT,
NLRP3
provide
some
references
subsequent
research
therapy.
Graphical
Exosomes
derived
from
MSCs
exhibit
neuroprotective
effects
mitigating
triggered
cells.
International Journal of Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
53(5)
Published: April 2, 2024
Chronic
neuroinflammation
serves
a
key
role
in
the
onset
and
progression
of
neurodegenerative
disorders.
Mitochondria
serve
as
central
regulators
neuroinflammation.
In
addition
to
providing
energy
cells,
mitochondria
also
participate
immunoinflammatory
response
disorders
including
Alzheimer's
disease,
Parkinson's
multiple
sclerosis
epilepsy,
by
regulating
processes
such
cell
death
inflammasome
activation.
Under
inflammatory
conditions,
mitochondrial
oxidative
stress,
epigenetics,
dynamics
calcium
homeostasis
imbalance
may
underlying
regulatory
mechanisms
for
these
diseases.
Therefore,
investigating
related
dysfunction
result
therapeutic
strategies
against
chronic
neurodegeneration.
The
present
review
summarizes
neuroinflammatory
diseases
current
treatment
approaches
that
target
