Aging and Disease,
Journal Year:
2024,
Volume and Issue:
unknown, P. 0 - 0
Published: Jan. 1, 2024
The
complex
set
of
interactions
between
the
immune
system
and
metabolism,
known
as
immunometabolism,
has
emerged
a
critical
regulator
disease
outcomes
in
central
nervous
system.
Numerous
studies
have
linked
metabolic
disturbances
to
impaired
responses
brain
aging,
neurodegenerative
disorders,
injury.
In
this
review,
we
will
discuss
how
disruptions
immunometabolism
balance
contribute
pathophysiology
dysfunction.
first
part
review
summarizes
contributions
cell
populations
such
microglia,
astrocytes,
infiltrating
cells
mediating
inflammation
metabolism
CNS
disorders.
remainder
addresses
impact
changes
on
activation
progression
Alzheimer's
disease,
Parkinson's
multiple
sclerosis,
stroke,
spinal
cord
injury,
traumatic
Furthermore,
also
address
therapeutic
potential
targeting
immunometabolic
pathways
reduce
neuroinflammation
slow
progression.
By
focusing
among
mechanisms
they
recruit
present
comprehensive
overview
human
health
disease.
Journal of Neurotrauma,
Journal Year:
2024,
Volume and Issue:
41(21-22), P. 2395 - 2412
Published: March 6, 2024
There
is
a
growing
body
of
evidence
that
the
delivery
cell-derived
exosomes
normally
involved
in
intracellular
communication
can
reduce
secondary
injury
mechanisms
after
brain
and
spinal
cord
improve
outcomes.
Exosomes
are
nanometer-sized
vesicles
released
by
Schwann
cells
may
have
neuroprotective
effects
reducing
posttraumatic
inflammatory
processes
as
well
promoting
tissue
healing
functional
recovery.
The
purpose
this
study
was
to
evaluate
beneficial
human
Schwann-cell
(hSC-Exos)
severe
model
penetrating
ballistic-like
(PBBI)
rats
investigate
on
multiple
Human
cell
processing
protocols
followed
Current
Good
Manufacturing
Practices
(cGMP)
with
exosome
extraction
purification
steps
approved
FDA
for
an
expanded
access
single
ALS
patient
IND.
Anesthetized
male
Sprague-Dawley
(280-350g)
underwent
PBBI
surgery
or
sham
procedures
starting
30
min
received
either
dose
hSC-Exos
PBS
through
jugular
vein.
At
48hrs
PBBI,
flow
cytometry
analysis
cortical
revealed
administration
reduced
number
activated
microglia
levels
caspase-1,
marker
inflammasome
activation.
Neuropathological
at
21
days
showed
treatment
significantly
overall
contusion
volume
decreased
frequency
Iba-1
positive
amoeboid
immunocytochemical
analysis.
This
systemic
TBI
reduces
histopathological
damage.
represents
clinically
relevant
cell-based
therapy
limit
detrimental
neurotrauma
other
progressive
neurological
injuries
impacting
pathophysiological
events
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.
Journal of Neuroinflammation,
Journal Year:
2025,
Volume and Issue:
22(1)
Published: April 28, 2025
Immunity
finely
regulates
brain
function.
It
is
directly
involved
in
the
pathological
processes
of
neurodegenerative
diseases
such
as
Parkinson's
and
Alzheimer's
disease,
post-stroke
conditions,
multiple
sclerosis,
traumatic
injury,
psychiatric
disorders
(mood
disorders,
major
depressive
disorder
(MDD),
anxiety
psychosis
schizophrenia,
neurodevelopmental
(NDD)).
Neuromodulation
currently
a
leading
therapeutic
strategy
for
treatment
these
but
little
yet
known
about
its
immune
impact
on
neuronal
function
precise
beneficial
or
harmful
consequences.
We
review
relevant
clinical
preclinical
studies
identify
several
specific
modifications.
These
data
not
only
provide
insights
into
how
neuromodulation
acts
to
optimize
immune-brain
interactions,
also
pave
way
better
understanding
interactions
processes.
Frontiers in Cellular Neuroscience,
Journal Year:
2025,
Volume and Issue:
19
Published: May 7, 2025
White
matter
in
the
central
nervous
system
comprises
bundled
nerve
fibers
myelinated
by
oligodendrocytes.
injury,
characterized
loss
of
oligodendrocytes
and
myelin,
is
common
after
ischemic
brain
inflammatory
demyelinating
diseases
including
multiple
sclerosis,
traumatic
damage
such
as
spinal
cord
injury.
Currently,
no
therapies
have
been
confirmed
to
promote
remyelination
these
diseases.
Over
past
decade,
various
reports
suggested
that
anti-muscarinic
drug
clemastine
can
stimulate
Consequently,
repurposing
a
potential
treatment
for
variety
neurological
disorders
has
gained
significant
attention.
The
therapeutic
effects
demonstrated
animal
models,
its
mechanisms
action
are
currently
being
investigated.
In
this
review,
we
summarize
relating
administration
white
injury
disease
discuss
promotion.
Clinical Science,
Journal Year:
2024,
Volume and Issue:
138(8), P. 515 - 536
Published: April 1, 2024
Abstract
Once
considered
passive
cells
of
the
central
nervous
system
(CNS),
glia
are
now
known
to
actively
maintain
CNS
parenchyma;
in
recent
years,
evidence
for
glial
functions
physiology
and
pathophysiology
has
only
grown.
Astrocytes,
a
heterogeneous
group
cells,
play
key
roles
regulating
metabolic
inflammatory
landscape
have
emerged
as
potential
therapeutic
targets
variety
disorders.
This
review
will
outline
astrocyte
healthy
ageing,
obesity,
neurodegeneration,
with
focus
on
responses
mitochondrial
function,
address
outlooks.
Neurotherapeutics,
Journal Year:
2024,
Volume and Issue:
unknown, P. e00515 - e00515
Published: Dec. 1, 2024
Traumatic
brain
injury
(TBI)
is
a
leading
cause
of
morbidity
and
mortality
worldwide,
with
limited
effective
therapeutic
options
currently
available.
Recent
research
has
highlighted
the
pivotal
role
mitochondrial
dysfunction
in
pathophysiology
TBI,
making
mitochondria
an
attractive
target
for
intervention.
This
review
comprehensively
examines
advancements
mitochondrial-targeted
therapies
bridging
gap
from
basic
to
clinical
applications.
We
discuss
underlying
mechanisms
damage
including
oxidative
stress,
impaired
bioenergetics,
dynamics,
apoptotic
pathways.
Furthermore,
we
highlight
complex
interplay
between
dysfunction,
inflammation,
blood-brain
barrier
(BBB)
integrity,
elucidating
how
these
interactions
exacerbate
impede
recovery.
also
evaluate
various
preclinical
studies
exploring
pharmacological
agents,
gene
therapy,
novel
drug
delivery
systems
designed
protect
restore
function.
Clinical
trials
their
outcomes
are
assessed
translational
potential
TBI.
By
integrating
findings
bench
bedside,
this
emphasizes
promising
avenues
addresses
remaining
challenges.
It
provides
guidance
future
pave
way
innovative
treatments
that
improve
patient
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: April 28, 2024
Abstract
Pathophysiology
and
outcomes
after
Traumatic
Brain
Injury
(TBI)
are
complex
highly
heterogenous.
Current
classifications
uninformative
about
pathophysiology,
which
limits
prognostication
treatment.
Fluid-based
biomarkers
can
identify
pathways
proteins
relevant
to
TBI
pathophysiology.
Proteomic
approaches
well
suited
exploring
mechanisms
of
disease,
as
they
enable
sensitive
assessment
an
expansive
range
proteins.
We
used
novel
high-dimensional,
multiplex
proteomic
assays
study
changes
in
plasma
protein
expression
acute
moderate-severe
TBI.
analysed
samples
from
88
participants
the
longitudinal
BIO-AX-TBI
cohort
(n=38
within
10
days
injury,
n=22
non-TBI
trauma,
n=28
non-injured
controls)
on
two
platforms:
Alamar
NULISA™
CNS
Diseases
OLINK
®
Target
96
Inflammation.
Participants
also
had
data
available
Simoa
(neurofilament
light,
GFAP,
total
tau,
UCHL1)
Millipore
(S100B).
The
panel
assesses
120
proteins,
most
have
not
been
investigated
before
TBI,
such
differentiate
trauma
controls.
A
subset
(n=29
n=24
subacute
3T
MRI
measures
lesion
volume
white
matter
injury
(fractional
anisotropy,
scanned
6
weeks
injury).
Differential
Expression
analysis
identified
16
with
TBI-specific
significantly
different
expression.
These
were
neuronal
markers
(calbindin2,
UCHL1,
visinin-like
protein1),
astroglial
(S100B,
GFAP),
tau
other
neurodegenerative
disease
(total
pTau231,
PSEN1,
amyloid
beta42,
14-3-3γ),
inflammatory
cytokines
(IL16,
CCL2,
ficolin2),
cell
signalling
(SFRP1),
metabolism
(MDH1)
autophagy
related
(sequestome1)
Acute
levels
pTau231
correlated
volume,
while
sequestome1
was
whole
skeleton
fractional
anisotropy
CCL2
inversely
corpus
callosum
FA.
Neuronal,
astroglial,
each
other,
IL16,
MDH1
sequestome1.
Clustering
(
k
means)
by
3
subgroups
differential
patterns,
but
did
differ
age
or
outcome.
Proteins
that
overlapped
platforms
excellent
r
>0.8)
correlations
between
values.
involved
processing,
cellular
processes
autophagy.
patterns
thus
demonstrating
previously
only
studied
animal
models
human
Our
highlights
potential
improve
classification
understanding
implications
for
treatment
development.