Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: June 13, 2024
Repetitive
mild
traumatic
brain
injuries
(rmTBI)
sustained
within
a
window
of
vulnerability
can
result
in
long
term
cognitive
deficits,
depression,
and
eventual
neurodegeneration
associated
with
tau
pathology,
amyloid
beta
(Aβ)
plaques,
gliosis,
neuronal
functional
loss.
However,
comprehensive
study
relating
acute
changes
immune
signaling
glial
reactivity
to
pathological
markers
after
single
repetitive
mTBIs
is
currently
lacking.
In
the
current
study,
we
addressed
question
how
repeated
affect
neuroimmune
response
phase
injury
(<
24
h)
by
exposing
3xTg-AD
mouse
model
Aβ
pathology
successive
(1x-5x)
once-daily
weight
drop
closed-head
quantifying
markers,
transcriptional
profiles
at
30
min,
4
h,
h
each
injury.
We
used
young
adult
2-4
month
old
mice
effects
rmTBI
absence
significant
pathology.
identified
pronounced
sexual
dimorphism
this
model,
females
eliciting
more
diverse
compared
males.
Specifically,
showed:
(1)
caused
decrease
neuron-enriched
genes
inversely
correlated
inflammatory
protein
expression
an
increase
AD-related
(2)
significantly
increased
group
cortical
cytokines
(IL-1α,
IL-1β,
IL-2,
IL-9,
IL-13,
IL-17,
KC)
MAPK
phospho-proteins
(phospho-Atf2,
phospho-Mek1),
several
which
co-labeled
neurons
phospho-tau,
(3)
astrocyte
macrophage-associated
function.
Collectively
our
data
suggest
that
respond
while
other
cell
types,
including
astrocytes,
transition
phenotypes
days
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(3), P. 2272 - 2272
Published: Jan. 23, 2023
Occupational
injuries
and
toxicant
exposures
lead
to
the
development
of
neuroinflammation
by
activating
distinct
mechanistic
signaling
cascades
that
ultimately
culminate
in
disruption
neuronal
function
leading
neurological
neurodegenerative
disorders.
The
entry
toxicants
into
brain
causes
subsequent
activation
glial
cells,
a
response
known
as
‘reactive
gliosis’.
Reactive
cells
secrete
wide
variety
molecules
perturbations
thus
play
crucial
role
progression
regulation
central
nervous
system
(CNS)
injury.
In
parallel,
roles
protein
phosphorylation
cell
eliciting
are
evolving.
However,
there
is
limited
understanding
molecular
underpinnings
associated
with
toxicant-
or
occupational
injury-mediated
neuroinflammation,
gliosis,
outcomes.
has
biological
significance,
including
promotion
inhibition
disease
mechanisms.
Nevertheless,
regulatory
mechanisms
synergism
antagonism
among
intracellular
pathways
remain
elusive.
This
review
highlights
research
focusing
on
direct
interaction
between
immune
injury-induced
gliosis.
Specifically,
injuries,
e.g.,
trips,
slips,
falls
resulting
traumatic
injury,
toxicants,
volatile
organic
compounds,
metals,
nanoparticles/nanomaterials
diseases
highlighted.
Further,
this
recapitulates
recent
advancement
related
characterization
comprising
signaling,
culminating
neuroinflammation.
Journal of Personalized Medicine,
Journal Year:
2025,
Volume and Issue:
15(1), P. 33 - 33
Published: Jan. 17, 2025
A
significant
proportion
of
patients
who
sustain
a
concussion/mild
traumatic
brain
injury
endorse
persisting,
lingering
symptoms.
The
symptoms
associated
with
concussion
are
nonspecific,
and
many
other
medical
conditions
present
similar
Medical
that
overlap
symptomatically
include
anxiety,
depression,
insomnia,
chronic
pain,
fatigue,
fibromyalgia,
cervical
strain
injuries.
One
the
factors
may
account
for
these
similarities
is
all
disturbances
in
optimal
functioning
autonomic
nervous
system
its
intricate
interactions
endocrine
immune
system—the
three
primary
regulatory
systems
body.
When
clinicians
working
presenting
persisting
after
concussion,
evidence-based
treatment
options
drawn
from
literature
limited.
We
framework
assessment
following
based
on
available
evidence
(treatment
trials),
neuroanatomical
principles
(research
into
physiology
concussion),
clinical
judgment.
review
research
supporting
premise
behavioral
interventions
designed
to
stabilize
optimize
body
have
potential
reduce
improve
patients.
Foundational
rehabilitation
strategies
areas
sleep
stabilization,
fatigue
management,
physical
exercise,
nutrition,
relaxation
protocols,
activation
outlined
along
practical
implementing
intervention
modules
Frontiers in Neurology,
Journal Year:
2023,
Volume and Issue:
14
Published: May 12, 2023
Mild
traumatic
brain
injuries
(mTBIs)
trigger
a
neuroinflammatory
response,
which
leads
to
perturbations
in
the
levels
of
inflammatory
cytokines,
resulting
distinctive
profile.
A
systematic
review
and
meta-analysis
were
conducted
synthesize
data
related
cytokines
patients
with
mTBI.
The
electronic
databases
EMBASE,
MEDLINE,
PUBMED
searched
from
January
2014
December
12,
2021.
total
5,138
articles
screened
using
approach
based
on
PRISMA
R-AMSTAR
guidelines.
Of
these
articles,
174
selected
for
full-text
26
included
final
analysis.
results
this
study
demonstrate
that
within
24
hours,
mTBI
have
significantly
higher
Interleukin-6
(IL-6),
Interleukin-1
Receptor
Antagonist
(IL-1RA),
Interferon-γ
(IFN-γ)
blood,
compared
healthy
controls
majority
studies.
Similarly
one
week
following
injury,
circulatory
Monocyte
Chemoattractant
Protein-1/C-C
Motif
Chemokine
Ligand
2
(MCP-1/CCL2),
also
confirmed
findings
by
demonstrating
elevated
blood
IL-6,
MCP-1/CCL2,
beta
(IL-1β)
population
(
p
<
0.0001),
particularly
acute
stages
(<7
days).
Furthermore,
it
was
found
Tumor
Necrosis
Factor-alpha
(TNF-α),
IL-1RA,
IL-10,
MCP-1/CCL2
associated
poor
clinical
outcomes
Finally,
research
highlights
lack
consensus
methodology
studies
measure
provides
direction
future
research.
NeuroImage Clinical,
Journal Year:
2024,
Volume and Issue:
43, P. 103647 - 103647
Published: Jan. 1, 2024
Mild
traumatic
brain
injury
(mTBI),
often
called
concussion,
is
a
prevalent
condition
that
can
have
significant
implications
for
people's
health,
functioning
and
well-being.
Current
clinical
practice
relies
on
self-reported
symptoms
to
guide
decision-making
regarding
return
sport,
employment,
education.
Unfortunately,
reliance
subjective
evaluations
may
fail
accurately
reflect
the
resolution
of
neuropathology,
exposing
individuals
with
mTBI
an
increased
risk
further
head
trauma.
No
objective
technique
currently
exists
assess
microstructural
alterations
tissue
which
characterise
mTBI.
MRI-based
T2
relaxation
quantitative
imaging
susceptible
detecting
fluid
properties
in
hypothesised
indicate
neuroinflammation.
This
study
aimed
investigate
potential
individual-level
relaxometry
evaluate
cellular
damage
from
20
male
participants
acute
sports-related
(within
14
days
post-injury)
44
healthy
controls
were
recruited
this
study.
Each
participant's
voxel-wise
map
was
analysed
against
control
averages
using
z-test
false
discovery
rate
correction.
Five
re-scanned
after
recovery
results
compared
their
maps
reduction
times
significantly
19/20
(95
%)
controls,
regions
including
hippocampus,
frontal
cortex,
parietal
insula,
cingulate
cortex
cerebellum.
Results
suggest
presence
cerebral
Longitudinal
indicated
all
five
participants,
indicating
possible
over
time.
research
highlights
MRI
as
non-invasive
method
assessing
subtle
pathology
Identifying
monitoring
changes
content
could
aid
predicting
developing
individualised
treatment
plans
Future
should
validate
measure
other
markers
inflammation
(e.g.
blood
biomarkers)
test
whether
T2-relaxometry
related
In
addition,
future
utilise
larger
groups
establish
normative
ranges
compute
robust
z-score
analyses.
Frontiers in Neuroscience,
Journal Year:
2023,
Volume and Issue:
17
Published: April 3, 2023
Repetitive
physical
insults
to
the
head,
including
those
that
elicit
mild
traumatic
brain
injury
(mTBI),
are
a
known
risk
factor
for
variety
of
neurodegenerative
conditions
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
and
chronic
encephalopathy
(CTE).
Although
most
individuals
who
sustain
mTBI
typically
achieve
seemingly
full
recovery
within
few
weeks,
subset
experience
delayed-onset
symptoms
later
in
life.
As
research
has
focused
on
acute
phase
injury,
there
is
an
incomplete
understanding
mechanisms
related
late-life
emergence
neurodegeneration
after
early
exposure
head
trauma.
The
recent
adoption
Drosophila
-based
models
provides
several
unique
advantages
over
existing
preclinical
animal
models,
tractable
framework
amenable
high-throughput
assays
short
relative
lifespan
conducive
lifelong
mechanistic
investigation.
use
flies
also
opportunity
investigate
important
factors
associated
with
conditions,
specifically
age
sex.
In
this
review,
we
survey
current
literature
examines
sex
as
contributing
trauma-mediated
humans
mammalian
models.
We
discuss
similarities
disparities
between
human
fly
aging,
differences,
pathophysiology.
Finally,
highlight
effective
tool
investigating
underlying
trauma-induced
identifying
therapeutic
targets
treatment
recovery.
Environmental
insults,
including
mild
head
trauma,
significantly
increase
the
risk
of
neurodegeneration.
However,
it
remains
challenging
to
establish
a
causative
connection
between
early-life
exposure
trauma
and
late-life
emergence
neurodegenerative
deficits,
nor
do
we
know
how
sex
age
compound
outcome.
Using
Drosophila
model,
demonstrate
that
causes
conditions
emerge
late
in
life
disproportionately
affect
females.
Increasing
age-at-injury
further
exacerbates
this
effect
sexually
dimorphic
manner.
We
identify
peptide
signaling
as
key
factor
female
susceptibility
post-injury
brain
deficits.
RNA
sequencing
highlights
reduction
innate
immune
defense
transcripts
specifically
mated
females
during
life.
Our
findings
causal
relationship
early
neurodegeneration,
emphasizing
differences
injury
response
impact
age-at-injury.
Finally,
our
reveal
reproductive
adversely
impacts
insults
elevates
vulnerability
Frontiers in Neurology,
Journal Year:
2024,
Volume and Issue:
15
Published: July 11, 2024
Objectives
Inflammatory
biomarkers,
as
indicators
of
biological
states,
provide
a
valuable
approach
for
accurate
and
reproducible
measurements,
crucial
the
effective
management
mild
traumatic
brain
injury
(mTBI)
in
pediatric
patients.
This
study
aims
to
assess
diagnostic
utility
blood-based
inflammatory
markers
IL6,
IL8,
IL10
children
with
mTBI,
including
those
who
did
not
undergo
computed
tomography
(CT)
scans.
Methods
A
prospective
multicentric
cohort
involving
285
mTBI
patients
was
conducted,
stratified
into
CT-scanned
non-CT-scanned
groups
within
24
h
post-trauma,
alongside
74
control
subjects.
Biomarker
levels
were
quantitatively
analyzed
using
ELISA.
Sensitivity
specificity
metrics
calculated
determine
efficacy
each
biomarker.
Results
total
223
(78%)
CT
scan
examination
but
kept
observation
symptoms
monitoring
at
emergency
department
(ED)
more
than
6
(in-hospital-observation
patients).
Among
(
n
=
62),
14
(23%)
positive
(CT+).
Elevated
IL6
found
compared
controls.
Within
patients,
significantly
increased
CT+
both
CT–
in-hospital-observation
No
significant
differences
observed
IL8
among
groups.
yielded
48%
identifying
100%
sensitivity
excluding
all
cases.
These
performances
maintained
whether
measured
or
after
trauma.
Conclusion
The
marker
emerges
robust
biomarker,
showing
promising
stratification
value
undergoing
scans
staying
ED.
Journal of Neuroscience Research,
Journal Year:
2025,
Volume and Issue:
103(4)
Published: April 1, 2025
Mild
traumatic
brain
injury
(mTBI)
is
a
common
condition,
particularly
pervasive
in
contact
sports
environments.
A
range
of
symptoms
can
accompany
this
type
and
negatively
impact
people's
lives.
As
mTBI
diagnosis
recovery
largely
rely
on
subjective
reports,
more
objective
markers
are
needed.
The
current
study
compared
structural
MRI-T2
relaxometry
between
group
40
male
athletes
with
within
14
days
age-matched
controls.
Voxel-averaged
T2
the
gray
matter
was
increased
for
to
controls
(p
<
0.001),
statistically
significant
superior
cortical
regions.
Our
findings
indicate
subtle
abnormalities
be
identified
acute
using
relaxometry.
These
may
reflect
inflammation
present
could
constitute
an
marker
supplement
methods
that
dominate
clinical
decisions
regarding
prognosis.
Future
research
should
validate
potential
other
data
types,
such
as
blood
biomarkers
or
histological
samples.