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.
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(24), P. 4359 - 4359
Published: Dec. 18, 2024
Traumatic
brain
injury
(TBI)
represents
a
multifaceted
pathological
condition
resulting
from
external
forces
that
disrupt
neuronal
integrity
and
function.
This
narrative
review
explores
the
intricate
relationship
between
dietary
macronutrients,
gut
microbiota
(GM),
neuroinflammation
in
TBI.
We
delineate
dual
aspects
of
TBI:
immediate
mechanical
damage
(primary
injury)
subsequent
biological
processes
(secondary
exacerbate
damage.
Dysregulation
gut–brain
axis
emerges
as
critical
factor
neuroinflammatory
response,
emphasizing
role
GM
mediating
immune
responses.
Recent
evidence
indicates
specific
including
lipids,
proteins,
probiotics,
can
influence
composition
turn
modulate
neuroinflammation.
Moreover,
specialized
interventions
may
promote
resilience
against
secondary
insults
support
neurological
recovery
post-TBI.
aims
to
synthesize
current
preclinical
clinical
on
potential
strategies
mitigating
pathways,
suggesting
targeted
nutrition
health
optimization
could
serve
promising
therapeutic
modalities
TBI
management.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(13), P. 10820 - 10820
Published: June 28, 2023
Traumatic
brain
injury
refers
to
the
damage
caused
intracranial
tissues
by
an
external
force
acting
on
head,
leading
both
immediate
and
prolonged
harmful
effects.
Neuroinflammatory
responses
play
a
critical
role
in
exacerbating
primary
during
acute
chronic
phases
of
TBI.
Research
has
demonstrated
that
numerous
neuroinflammatory
are
mediated
through
“microbiota–gut–brain
axis,”
which
signifies
functional
connection
between
gut
microbiota
brain.
The
aryl
hydrocarbon
receptor
(AhR)
plays
vital
facilitating
communication
host
recognizing
specific
ligands
produced
directly
or
indirectly
microbiota.
Tryptophan
(trp),
indispensable
amino
acid
animals
humans,
represents
one
key
endogenous
for
AhR.
metabolites
trp
have
significant
effects
functioning
central
nervous
system
(CNS)
activating
AHR
signalling,
thereby
establishing
bidirectional
These
interactions
immune,
metabolic,
neural
signalling
mechanisms.
In
this
review,
we
emphasize
co-metabolism
tryptophan
pathway
following
Furthermore,
discuss
impact
these
mechanisms
underlying
processes
involved
traumatic
injury,
while
also
addressing
potential
future
targets
intervention.
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.