Immunological Investigations,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 23
Published: Dec. 16, 2024
Background
Immune
homeostasis
plays
a
crucial
role
in
immunology
andis
dependent
on
both
central
and
peripheral
tolerance.
Centraltolerance
tolerance
occur
the
thymus
thesecondary
lymphoid
tissues,
respectively.
Tolerance
breakdown
andimmune
regulation
defects
can
lead
to
autoimmune
disorders.
In
thisreview
article,
we
aimed
describe
of
exosomes
inregulating
provide
summary
their
effectson
pathogenesis,
diagnosis,
therapeutic
potential
inmyasthenia
gravis
(MG).
Frontiers in Cell and Developmental Biology,
Journal Year:
2025,
Volume and Issue:
12
Published: Jan. 6, 2025
Graves
disease
(GD),
an
autoimmune
affects
the
thyroid
gland,
results
in
hyperthyroidisms
and
goiter.
The
main
cause
of
GD
is
not
clearly
defined;
however,
stimulating
autoantibodies
for
hormone
receptor
(TSHR)
known
as
thyroid-stimulating
immunoglobulins
(TSIs)
are
primary
proposed
mechanism.
TSI
activation
TSHRs
gland
excessive
release
hormones
with
subsequent
development
hyperthyroidism
cellular
process
macroautophagy/autophagy
implicated
pathogenesis
other
diseases.
Autophagy
plays
a
critical
role
many
diseases
different
stages
same
through
modulation
immunity
inflammatory
response.
In
addition,
autophagy
also
thyroid-associated
ophthalmopathy
(TAO).
However,
exact
well
explained.
Therefore,
this
review
discusses
how
intricately
involved
regarding
its
protective
harmful
effects.
Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
221, P. 111189 - 111189
Published: Jan. 5, 2025
Epilepsy
is
a
neurological
disease
characterized
by
unprovoked
recurrent
epileptic
seizures.
Temporal
lobe
epilepsy
(TLE)
the
commonest
type
of
focal
in
adults
that
resist
to
conventional
anti-seizure
medications
(ASMs).
Interestingly,
ASMs
do
not
affect
epileptogenesis
and
progression
disease.
Therefore,
repurposing
natural
products
with
anti-inflammatory,
anti-oxidant
effects
such
as
berberine
(BRB)
may
be
logical
treating
refractory
TLE.
However,
molecular
mechanism
BRB
against
development
seizure
mainly
TLE
was
fully
elucidated.
we
attempt
this
review
discuss
potential
underlying
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(5)
Published: March 1, 2025
Alzheimer's
disease
(AD)
is
a
neurodegenerative
caused
by
the
progressive
deposition
of
extracellular
amyloid
beta
(Aβ)
and
intracellular
neurofibrillary
tangles
(NFTs).
Of
note,
metabolic
disorders
such
as
insulin
resistance
(IR)
type
2
diabetes
(T2D)
are
associated
with
development
brain
IR
neurodegeneration.
In
addition,
AD
neuropathology
linked
cognitive
impairment
accelerate
peripheral
progression
T2D.
Therefore,
there
bidirectional
relationship
between
T2D
AD.
It
has
been
demonstrated
that
induce
dysregulation
peroxisome
proliferator-activated
receptor
alpha
(PPAR-α)
leading
to
central
disturbances.
Hence,
dysregulated
PPAR-α
could
be
shared
mechanism
in
both
T2D,
restoration
signalling
agonist
fenofibrate
(FN)
may
alleviate
this
review
aims
shed
light
on
potential
involvement
AD,
how
FN
effective
management
seems
dual
neuroprotective
antidiabetic
effects
can
mitigate
T2D-related
complications
modulating
various
cellular
processes
inflammatory
pathways.
conclusion,
possible
candidate
different
pathways
involved
pathogenesis
these
conditions.
European Journal of Pharmacology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 177510 - 177510
Published: March 1, 2025
Humanin
(HN)
is
an
endogenous
micropeptide
also
known
as
a
mitochondria-derived
peptide.
It
has
neuroprotective
effect
against
Alzheimer's
disease
(AD)
and
other
neurodegenerative
diseases
by
improving
hippocampal
acetylcholine
attenuating
the
development
of
oxidative
stress
associated
neurotoxicity.
HN
protects
neuron
from
toxic
effects
amyloid
beta
(Aβ).
regarded
biomarker
mitochondrial
stress.
Interestingly,
aging
reduces
brain
expression
HN,
leading
to
cognitive
impairment
elevating
risk
neurodegeneration,
including
AD.
However,
in
old
subjects
AD
patients,
circulating
levels
increase
compensatory
mechanism
reduce
neurodegeneration
dysfunction
Conversely,
studies
demonstrated
reduction
These
findings
indicated
controversial
points
regarding
precise
mechanistic
role
Therefore,
aim
this
review
was
discuss
exact
neuropathology
molecular
mechanisms
Brain-derived
neurotrophic
factor
(BDNF)
is
a
neurotrophin,
acting
as
signal
and
neuromodulator
in
the
central
nervous
system
(CNS).
BDNF
synthesized
from
its
precursor
proBDNF
within
CNS
peripheral
tissues.
Through
activation
of
NTRK2/TRKB
(neurotrophic
receptor
tyrosine
kinase
2),
promotes
neuronal
survival,
synaptic
plasticity,
growth,
whereas
it
inhibits
microglial
release
pro-inflammatory
cytokines.
dysregulated
different
neurodegenerative
diseases
depressions.
However,
there
major
controversy
concerning
levels
stages
multiple
sclerosis
(MS).
Therefore,
this
review
discusses
potential
role
signaling
MS,
how
modulators
affect
pathogenesis
outcomes
disease.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 20, 2024
Abstract
Myasthenia
gravis
(MG),
a
rare
autoimmune
disorder,
presents
complex
pathogenesis
involving
various
immune
molecules.
The
modification
of
N6-methyladenosine
(m6A)
regulates
diverse
metabolic
and
immunopathological
processes;
however,
its
role
in
MG
remains
unclear.
We
downloaded
dataset
GSE85452
from
the
GEO
database
to
identify
differentially
expressed
genes
regulated
by
m6A.
Random
Forest
(RF)
method
was
utilized
pivotal
regulatory
associated
with
m6A
modification.
Subsequently,
prognostic
model
crafted
confirmed
using
this
gene
set.
Patients
were
stratified
according
expression
levels
these
key
genes.
Additionally,
MG-specific
signatures
delineated
examining
cell
infiltration
patterns
their
correlations.
Further
functional
annotation,
protein-protein
interaction
mapping,
molecular
docking
analyses
performed
on
biomarkers,
leading
discovery
three
that
exhibited
significant
differential
within
dataset:
RBM15,
CBLL1,
YTHDF1.The
random
forest
algorithm
as
MG,
validated
constructing
clinical
prediction
model.
Based
expression,
we
divided
patients
into
two
groups,
revealing
distinct
varying
abundances.
also
discovered
61
phenotype
conducted
an
in-depth
exploration
biological
roles.
YTHDF1
found
positively
correlated
CD56dim
natural
killer
cells,
T
type
1
helper
cells.
These
stable
diagnostic
m6A-related
markers
both
validation
cohorts.
Our
findings
suggest
for
MG.
analysis
may
elucidate
roles
microenvironment