Biomedical Papers,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 17, 2024
Traumatic
brain
injury
(TBI)
has
long-term
consequences,
including
neurodegenerative
disease
risk.
Current
diagnostic
tools
are
limited
in
detecting
subtle
damage.
This
review
explores
emerging
biomarkers
for
TBI,
those
related
to
neuronal
injury,
inflammation,
EVs,
and
ncRNAs,
evaluating
their
potential
predict
clinical
outcomes
like
mortality,
recovery,
cognitive
impairment.
It
addresses
challenges
opportunities
implementing
practice,
aiming
improve
TBI
diagnosis,
prognosis,
treatment.
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
Biomedicines,
Journal Year:
2024,
Volume and Issue:
12(2), P. 293 - 293
Published: Jan. 26, 2024
Mild
traumatic
brain
injury
(mTBI)
accounts
for
most
TBI
cases,
the
leading
cause
of
morbidity
and
mortality
worldwide.
Despite
its
high
incidence,
mTBI
pathophysiology
remains
largely
unknown.
Recent
studies
have
shown
that
inflammatory
response
is
activated
early
after
can
persist
several
weeks
or
months.
However,
limited
evidence
on
utility
biomarkers
as
predictors
clinical
outcomes
in
has
been
previously
provided.
Thus,
this
systematic
review
meta-analysis
aims
to
provide
an
overview
current
knowledge
role
inflammation
pathogenesis
potential
some
biomolecules
mTBI.
In
regard,
eight
comprising
1184
individuals
were
selected.
it
was
increase
IL-6,
TNF-α,
IL-1β
plasma
levels
could
be
implicated
development
post-concussion
symptoms.
On
other
hand,
persistence
increased
plasmatic
concentrations
IL-10
IL-8
long
six
months
following
event
suggest
chronic
neuroinflammation
late
persistent
context,
our
findings
showed
relevant
diagnosing
predicting
recovery
long-term
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Feb. 9, 2024
Traumatic
encephalopathy
syndrome
(TES)
is
defined
as
the
clinical
manifestation
of
neuropathological
entity
chronic
traumatic
(CTE).
A
core
feature
TES
neurobehavioral
dysregulation
(NBD),
a
neuropsychiatric
in
repetitive
head
impact
(RHI)-exposed
individuals,
characterized
by
poor
regulation
emotions/behavior.
To
discover
biological
correlates
for
NBD,
we
investigated
association
between
biomarkers
inflammation
(interleukin
(IL)-1β,
IL-6,
IL-8,
IL-10,
C-reactive
protein
(CRP),
tumor
necrosis
factor
(TNF)-α)
cerebrospinal
fluid
(CSF)
and
NBD
symptoms
former
American
football
players
unexposed
individuals.
Journal of Neurotrauma,
Journal Year:
2023,
Volume and Issue:
41(7-8), P. 862 - 878
Published: Dec. 20, 2023
The
aim
of
our
study
was
to
investigate
the
biological
underpinnings
persistent
post-concussion
symptoms
(PPCS)
at
3
months
following
mild
traumatic
brain
injury
(mTBI).
Patients
(
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 6, 2025
Abstract
Common
psychological
disorders
related
to
stress,
depression
and
anxiety
pose
serious
disease
economic
burden
globally
especially
in
lower
middle-income
countries.
Existing
pharmacotherapies
mostly
target
neurotransmitter
systems
are
partially
effective
across
a
range
of
diagnostic
categories.
However,
it
is
also
long-standing
finding
that
low
grade
inflammation
persistently
present
systemic
circulation
as
well
the
brain
anxiety.
Specifically,
neuroinflammation
driven
by
Interleukin-1β
(IL-1β)
pleiotropic
cytokine.
has
recently
been
focus
keen
interest
research.
IL-1β
probably
most
prominent
proinflammatory
cytokine
long
associated
with
these
conditions.
We
on
molecules
cause
be
synthesized
from
its
precursor,
namely
Caspase
1,
through
activation
large
multiprotein
complex
known
NLRP3
inflammasome
complex.
Using
two
different
rat
models
physical
psychosocial
we
validate
our
earlier
findings
induction
BTK/NLRP3/Caspase
1
Canonical
Pathway
stressed
animals.
show
involvement
Gasdermin
D/Caspase11
non
canonical
pathway
contributes
enhanced
leakage
cells
pyroptosis,
absence
lytic
cell
death.
Stressed
rats
display
robust
neuroinflammatory
phenotype,
reduction
CA3
Hippocampal
spine
density,
number
mature
mushroom
spines,
functional
impairments
multiple
domains
behavior.
Finally
employ
FDA
approved
drugs,
Ibrutinib
Disulfiram
mitigate
neural,
phenotype
behavioral
dysfunctions,
individually
combination.
The
combination
therapy
proved
more
efficacious,
suggesting
joint
inhibition
mitigates
pathological
sequelae
stress.
Taken
together
data
provides
preclinical
argues
for
amelioration
dependent
release
considered
an
alternative
therapeutic
strategy
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: June 12, 2024
Abstract
Traumatic
Brain
Injury
(TBI)
induces
neuroinflammatory
response
that
can
initiate
epileptogenesis,
which
develops
into
epilepsy.
Recently,
we
identified
anti-convulsive
effects
of
naltrexone,
a
mu-opioid
receptor
(MOR)
antagonist,
used
to
treat
drug
addiction.
While
blocking
opioid
receptors
reduce
inflammation,
it
is
unclear
if
post-TBI
seizures
be
prevented
by
MORs.
Here,
tested
naltrexone
prevents
neuroinflammation
and/or
post-TBI.
TBI
was
induced
modified
Marmarou
Weight-Drop
(WD)
method
on
4-week-old
C57BL/6J
male
mice.
Mice
were
placed
in
two
groups:
non-telemetry
assessing
the
acute
or
telemetry
monitoring
for
interictal
events
and
spontaneous
both
following
naltrexone.
Molecular,
histological
neuroimaging
techniques
evaluate
neuroinflammation,
neurodegeneration
fiber
track
integrity
at
8
days
3
months
Peripheral
immune
responses
assessed
through
serum
chemokine/cytokine
measurements.
Our
results
show
an
increase
MOR
expression,
nitro-oxidative
stress,
mRNA
expression
inflammatory
cytokines,
microgliosis,
neurodegeneration,
white
matter
damage
neocortex
Video-EEG
revealed
increased
mice,
with
71%
mice
developing
post-traumatic
(PTS).
Naltrexone
treatment
ameliorated
reduced
all
makes
promising
candidate
against
PTS,
TBI-associated
epileptogenesis
WD
model
TBI.
