Scientific Reports,
Journal Year:
2023,
Volume and Issue:
13(1)
Published: Dec. 14, 2023
Abstract
Traumatic
brain
injury
(TBI)
is
a
major
cause
of
mortality
and
disability
worldwide,
particularly
among
individuals
under
the
age
45.
It
complex,
heterogeneous
disease
with
multifaceted
pathophysiology
that
remains
to
be
elucidated.
Metabolomics
has
potential
identify
metabolic
pathways
unique
biochemical
profiles
associated
TBI.
Herein,
we
employed
longitudinal
metabolomics
approach
study
TBI
in
weight
drop
mouse
model
reveal
changes
pathogenesis,
severity,
secondary
injury.
Using
proton
nuclear
magnetic
resonance
(
1
H
NMR)
spectroscopy,
biochemically
profiled
post-mortem
from
mice
suffered
mild
(N
=
25;
13
male
12
female),
severe
24;
11
female)
sham
controls
16;
5
at
baseline,
day
7
following
NMR-based
metabolomics,
combination
bioinformatic
analyses,
highlights
few
significant
metabolites
severity
perturbed
metabolism
related
We
report
concentrations
taurine
,
creatinine
adenine
dimethylamine
histidine
N-Acetyl
aspartate
glucose
1-phosphate
are
all
severity.
Longitudinal
observation
tissue
revealed
lead
distinct
profile
changes.
A
multi-class
was
able
classify
as
well
time
after
estimated
86%
accuracy.
Further,
identified
high
degree
correlation
between
respective
hemisphere
(r
>
0.84,
p
<
0.05,
Pearson
correlation).
This
underlying
While
comprehensive,
future
studies
should
investigate
whether:
(a)
highlighted
here
recapitulated
sufferers
(b)
if
panel
biomarkers
also
effective
less
invasively
harvested
biomatrices,
for
objective
rapid
identification
prognosis.
Journal of Neuroscience Research,
Journal Year:
2025,
Volume and Issue:
103(4)
Published: April 1, 2025
Traumatic
brain
injury
(TBI)
is
an
insult
to
the
that
impacts
neuronal
and
non-neuronal
cells/tissues.
The
study
aimed
understand
TBI-induced
early
changes
in
systemic
physiology.
male
rats
were
subjected
mild
moderate
TBI,
where
serum
urine
metabolic
fingerprints
of
TBI
showed
a
hypermetabolic
response
with
increased
energy
metabolites,
amino
acids,
gut
metabolites
TCA
cycle
intermediates
urine.
In
contrast,
decreased
lactate,
pyruvate,
acids
(glycine
leucine)
[trimethylamine
N
OXIDE
(TMAO),
choline
acetate]
serum.
creatinine,
allantoin
levels.
To
brain's
role
altered
physiology,
hypothalamus
structure
was
assessed
using
diffusion
tensor
imaging
(DTI)
stress
levels
observed
corticosterone.
injured
exhibited
DTI
metrics
hypothalamus,
suggesting
potential
disruption
regulation
hypothalamus-pituitary-adrenal
axis
(HPA)
axis.
These
alterations
accompanied
by
TNF-α
after
TBI.
induced
allostatic
overload,
impaired
hypothalamic
structure,
physiology
also
microbiome
dysbiosis.
Firmicutes:
Bacteroidetes
ratio
injury,
variable
composition
both
injuries.
Therefore,
present
provides
insight
into
interplay
between
HPA
axis,
metabolism,
following
Importantly,
this
crosstalk
regulatory
systems
different
highlighting
need
assess
phenotype
based
on
severity.
Indian Journal of Neurosurgery,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 2, 2025
Abstract
Traumatic
brain
injury
(TBI)
has
profound
effects
that
extend
beyond
the
brain,
affecting
other
body
systems
via
secondary
pathways
and
leading
to
various
complications,
including
gastrointestinal
(GI)
dysfunction
during
after
hospitalization.
While
advances
in
TBI
management
have
improved
overall
outcomes,
absence
of
effective
treatments
for
these
systemic
highlights
urgent
need
innovative
therapeutic
strategies.
A
critical
aspect
this
context
is
brain–gut
axis
(BGA),
a
bidirectional
communication
network
connecting
GI
system
through
complex
neuronal,
hormonal,
immune
pathways.
results
increased
intestinal
permeability
hypercatabolic
state
bacterial
translocation,
dysregulation,
septic
multiorgan
failure.
These
complications
significantly
heighten
risk
morbidity
mortality
patients.
Emerging
evidence
suggests
gut
dysbiosis
plays
pivotal
role
post-TBI
complications.
The
microbiome,
diverse
community
commensal
microorganisms,
integral
physiology,
performing
key
functions
such
as
metabolic
regulation,
maintaining
barrier,
modulating
responses.
Disruptions
microbiota
can
exacerbate
dysfunction,
potentially
severe
outcomes.
This
review
examines
mechanisms
underlying
BGA
following
TBI,
focusing
on
contributing
dysregulation.
Additionally,
it
discusses
strategies
aimed
at
mitigating
dysbiosis.
Potential
interventions
include
approaches
restore
microbial
balance,
enhance
barrier
integrity,
support
modulation.
By
targeting
areas,
therapies
may
reduce
improve
patient
Acta Neuropathologica Communications,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: May 3, 2025
Traumatic
brain
injury
(TBI)
occurs
in
2-3
million
Americans
each
year
and
is
a
leading
cause
of
death
disability.
Among
the
many
physiological
consequences
TBI,
hypothalamic
pituitary
axis
(HPA)
particularly
vulnerable,
including
reduction
growth
hormone
(GH)
insulin-like
factor
(IGF-1).
Clinical
preclinical
supplementation
IGF-1
after
TBI
has
exhibited
beneficial
effects.
receptors
are
prominently
observed
tissues,
gastrointestinal
(GI)
system.
In
addition
to
causing
damage
brain,
also
induces
GI
system
damage,
inflammation
alterations
intestinal
permeability
gut
microbiome.
The
goal
this
study
was
assess
effects
systemic
treatment
rat
model
on
outcomes.
Because
dysfunction
been
linked
hippocampal
dysfunction,
we
examined
proliferation
immature
granule
cells
dentate
gyrus.
10-week-old
male
rats
were
treated
with
an
intraperitoneal
(i.p.)
dose
at
4
24
h
lateral
fluid
percussion
(FPI).
At
3-
35-days
post-injury
(DPI),
permeability,
dysmorphia,
fecal
microbiome,
hippocampus
assessed.
FPI-induced
blood-gut-barrier,
as
measured
by
elevated
metabolites
blood,
prevented
treatment.
Gut
dysmorphia
microbiome
FPI
these
ameliorated
IGF-1,
increase
hippocampus.
These
findings
suggest
that
can
target
its
role
influencing
adult
neurogenesis.
Journal of Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
14(10), P. 3488 - 3488
Published: May 16, 2025
Background:
Gut
microbiome
composition
may
influence
the
risk
of
intracranial
aneurysm
rupture.
Methods:
This
study
analyzed
gut
microbiota
48
patients—24
with
ruptured
aneurysms
(RA)
and
24
unruptured
(UIA)—using
next-generation
sequencing.
Results:
While
alpha
diversity
was
similar
between
groups,
beta
revealed
significant
taxonomic
differences
(Bray–Curtis:
p
=
0.02;
unweighted
UniFrac:
0.0291).
Both
groups
were
dominated
by
phyla
Bacillota,
Bacteroidota,
Proteobacteria,
but
genus-
family-level
observed.
RA
patients
showed
higher
abundances
Anaerotruncus,
Coprobacillus,
Sellimonas,
Hungatella,
Ruthenibacterium,
whereas
UIA
exhibited
greater
levels
Faecalibacterium,
Brotolimicola,
Clostridiaceae,
Roseburia,
Agathobaculum.
Linear
discriminant
analysis
identified
one
class,
10
genera,
17
species
that
differed
significantly
groups.
Notably,
Faecalibacterium
prausnitzii
Agathobaculum
butyriciproducens—bacteria
known
for
their
anti-inflammatory
neuroprotective
properties—were
enriched
in
patients.
Conclusions:
These
findings
suggest
microbiota,
particularly
short-chain
fatty
acid–producing
bacteria,
contribute
to
vascular
protection
pathophysiology.
Microbiome-based
therapeutic
strategies
could
offer
new
avenues
prevention
cerebrovascular
disease.
PLoS ONE,
Journal Year:
2022,
Volume and Issue:
17(11), P. e0278259 - e0278259
Published: Nov. 30, 2022
Dysregulation
of
the
gut
microbiome
has
been
shown
to
perpetuate
neuroinflammation,
alter
intestinal
permeability,
and
modify
repetitive
mild
traumatic
brain
injury
(RmTBI)-induced
deficits.
However,
there
have
no
investigations
regarding
comparative
effects
that
may
on
RmTBI
in
adolescents
adults.
Therefore,
we
examined
influence
depletion
prior
microbial
composition
metabolome,
adolescent
adult
Sprague
Dawley
rats.
Rats
were
randomly
assigned
standard
or
antibiotic
drinking
water
for
14
days,
subsequent
sham
RmTBIs.
The
metabolome
analysed
at
baseline,
1
day
after
first
mTBI,
euthanasia
(11
days
following
third
mTBI).
At
euthanasia,
samples
also
collected
quantify
tight
junction
protein
(
TJP1
occludin
)
expression.
Adolescents
significantly
more
susceptible
via
administration
which
increased
pro-inflammatory
metabolites.
Furthermore,
induced
a
transient
increase
‘beneficial
bacteria’
Lachnospiraceae
Faecalibaculum
only
indicate
compensatory
action
response
injury.
Finally,
generated
exemplified
potentially
chronic
pathogenic
inflammatory
state
as
demonstrated
by
Clostridium
innocuum
Erysipelatoclostridium
reductions
Bacteroides
Sensu
Stricto
.
Results
highlight
are
vulnerable
compared
adults
dysbiosis
exacerbate
secondary
cascades.
Journal of Clinical Medicine,
Journal Year:
2024,
Volume and Issue:
13(15), P. 4546 - 4546
Published: Aug. 3, 2024
Traumatic
brain
injury
(TBI)
is
a
serious
global
public
health
issue,
recognized
as
chronic
and
progressive
disease
that
can
affect
multiple
organs,
including
the
gastrointestinal
(GI)
tract.
Research
shows
there
specific
link
between
GI
tract
central
nervous
system,
termed
gut-brain
axis,
which
consists
of
bidirectional
exchange
these
two.
Several
preclinical
clinical
studies
have
demonstrated
intestinal
barrier
dysfunction,
inflammation
gut
dysbiosis
in
patients
with
TBI.
It
proven
probiotics
modulate
inflammatory
process
modify
microbiota.
Numerous
animal
human
trials
effectiveness
selected
bacterial
strains
an
adjuvant
treatment
reducing
inflammation,
infection
rates
time
spent
intensive
care
hospitalized
suffering
from
injury.
Thus,
this
review
summarizes
current
evidence
regarding
beneficial
effects
probiotic
administration
TBI-related
complications.
This
will
help
identify
novel
therapeutic
strategies
future
extensive
history
apparently
safe
use.