Frontiers in Neurology,
Journal Year:
2024,
Volume and Issue:
15
Published: Oct. 25, 2024
Many
patients
experience
persistent
symptoms
after
COVID-19,
a
syndrome
referred
to
as
Long
COVID
(LC).
The
goal
of
this
study
was
identify
novel
new
or
worsening
comorbidities
self-reported
in
with
LC.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(4), P. 1634 - 1634
Published: Feb. 14, 2025
Aging
and
age-related
neurodegenerative
disorders
are
characterized
by
the
dysfunction
or
loss
of
brain
nicotinic
acetylcholine
receptors
(nAChRs),
these
changes
may
be
related
to
other
senescence
markers,
such
as
oxidative
stress
DNA
repair
dysfunction.
However,
mechanism
nAChR
in
aging
modification
this
process
drugs
(e.g.,
memantine,
Mem)
not
yet
fully
understood.
To
study
whether
differences
expression
rat
occur
due
modulated
Mem,
we
analyzed
subunits
(at
RNA
protein
levels)
biomarkers
real-time
quantitative
polymerase
chain
reaction
(RQ-PCR)
Western
blot
validation.
Twenty-one
female
Wistar
rats
were
divided
into
four
groups,
depending
on
age,
oldest
group
received
injections
Mem
water
with
use
intragastric
catheters.
We
studied
cerebral
grey
matter
(CGM),
subcortical
white
(SCWM),
cerebellum
(Ce).
Results
showed
an
decrease
α7
mRNA
level
SCWM.
The
was
accompanied
reduced
8-oxoguanine
glycosylase
1
(OGG1)
increased
tumor
necrosis
factor
alpha
(TNFα)
level.
In
group,
observed
a
higher
SCWM
Ce.
Biomarker
levels
changed,
but
different
extent
area.
Importantly,
antioxidative
status
stopped
even
regressed
under
treatment.
After
two
weeks
treatment,
increase
TP53
8-oxo-2'deoxyguanosine
(8-oxo-2'dG)
observed.
conclude
that
administration
protective
against
mechanisms.
Viruses,
Journal Year:
2025,
Volume and Issue:
17(3), P. 405 - 405
Published: March 12, 2025
Background:
The
Zika
virus
(ZIKV)
is
an
arbovirus
linked
to
“Congenital
Syndrome”
and
a
range
of
neurodevelopmental
disorders
(NDDs),
with
microcephaly
as
the
most
severe
manifestation.
Milder
NDDs,
such
autism
spectrum
delays
in
neuropsychomotor
language
development,
often
go
unnoticed
neonates,
resulting
long-term
social
academic
difficulties.
Murine
models
ZIKV
infection
can
be
used
mimic
part
motor
cognitive
deficits
observed
humans.
These
evaluated
through
behavioral
tests,
enabling
comparison
gene
expression
profiles
aiding
characterization
ZIKV-induced
NDDs.
Objectives:
This
study
aimed
identify
genes
associated
changes
following
subtle
juvenile
BALB/c
mice.
Methods:
Neonatal
mice
were
subcutaneously
inoculated
(MH544701.2)
on
postnatal
day
1
(DPN)
at
dose
6.8
×
103
PFU.
Viral
presence
cerebellum
cortex
was
quantified
10-
30-days
post-infection
(DPI)
using
RT-qPCR.
Neurobehavioral
assessed
30
DPI
T-maze,
rotarod,
open
field
tests.
Next-Generation
Sequencing
(NGS)
performed
differentially
expressed
(DEGs),
which
analyzed
Gene
Ontology
(GO)
KEGG
enrichment.
interaction
networks
then
constructed
explore
interactions
enriched
biological
categories.
Results:
A
model
successfully
established,
brain
while
allowing
survival
beyond
DPI.
induced
mild
changes,
though
motivational
functions
remained
unaffected.
functional
repression
synaptic
vesicles
alterations
neuronal
structure,
suggesting
potential
disruptions
plasticity.
Conclusions:
Moderate
circulating
strains
from
2016
epidemic
may
cause
dysregulation
related
immune
response,
cytoskeletal
organization,
modifications
cellular
transport
mediated
by
vesicles.
Despite
viral
control,
neurocognitive
effects
persisted,
including
memory
anxiety-like
behaviors,
highlighting
neurological
consequences
that
show
no
apparent
malformations.
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: March 19, 2025
Currently,
the
treatment
and
prevention
of
multiple
sclerosis
(MS)
continue
to
encounter
significant
challenges.
Mendelian
randomization
(MR)
analysis
has
emerged
as
a
crucial
research
method
in
pursuit
new
therapeutic
strategies.
Accordingly,
we
hypothesize
that
there
exists
causal
association
between
genetic
variants
specific
plasma
proteins
MS
through
MR
mechanisms,
key
targets
can
be
precisely
identified
by
integrating
multi-omics
analytical
approaches.
In
this
study,
developed
comprehensive
framework
aimed
at
identifying
validating
potential
for
MS.
The
commenced
with
two-sample
study
utilizing
two
large
protein
quantitative
trait
locus
(pQTL)
datasets.
Building
on
foundation,
performed
Bayesian
co-localization
coding
genes,
followed
full
phenotype-wide
(PheWAS)
co-positive
genes
both
methods.
This
approach
allowed
us
explore
functions
mechanisms
co-morbidity
associated
disease.
Subsequently,
integrated
protein-protein
interaction
(PPI)
network
analysis,
gene
ontology
(GO)
Kyoto
Encyclopedia
Genes
Genomes
(KEGG)
pathway
facilitate
drug
prediction
molecular
docking
studies.
conducted
systematic
pQTLs
datasets
Icelandic
88
positive
proteins,
while
UK
Biobank
database
122
proteins.
By
comparison,
uroporphyrinogen
III
synthase
(UROS)
glutathione
S-transferase
theta
2B
(GSTT2B)
were
found
shared
After
false
discovery
rate
(FDR)
correction,
signal
transducer
activator
transcription
3
(STAT3)
was
significantly
pQTLs.
pQTLs,
advanced
glycosylation
end
product-specific
receptor
(AGER),
allograft
inflammatory
factor
1
(AIF1),
butyrophilin
subfamily
member
A1
(BTN1A1),
cluster
differentiation
58
(CD58),
desmoglein
4
(DSG4),
ecotropic
viral
integration
site
5
(EVI5),
tumor
necrosis
(TNF),
superfamily
14
(TNFRSF14)
Bonferroni
AGER,
CD58,
EVI5,
TNF
remained
colocalization
EVI5
(PPH4
=
0.9800),
O-GlcNAcase
(OGA)
0.8569),
TNFRSF14
0.8904)
common
conclusion,
OGA,
may
Through
application
have
successfully
These
findings
provide
scientific
basis
development
novel
immunotherapies,
combination
regimens,
or
targeted
intervention
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Aug. 26, 2024
Mast
cells
serve
as
crucial
effector
within
the
innate
immune
system
and
are
predominantly
localized
in
skin,
airways,
gastrointestinal
tract,
urinary
reproductive
tracts,
well
brain.
Under
physiological
conditions,
brain-resident
mast
secrete
a
diverse
array
of
neuro-regulatory
mediators
to
actively
participate
neuroprotection.
Meanwhile,
primary
source
molecules
causing
brain
inflammation,
also
function
“first
responders”
injury.
They
interact
with
neuroglial
neurons
facilitate
release
numerous
inflammatory
mediators,
proteases,
reactive
oxygen
species.
This
process
initiates
amplifies
immune-inflammatory
responses
brain,
thereby
contributing
regulation
neuroinflammation
blood-brain
barrier
permeability.
article
provides
comprehensive
overview
potential
mechanisms
through
which
may
modulate
neuroprotection
their
pathological
implications
various
neurological
disorders.
It
is
our
contention
that
inhibition
cell
activation
disorders
could
represent
novel
avenue
for
therapeutic
breakthroughs.