Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: July 16, 2024
Abstract
Post-traumatic
epilepsy
(PTE)
is
one
of
the
most
debilitating
consequences
traumatic
brain
injury
(TBI)
and
drug-resistant
forms
epilepsy.
Novel
therapeutic
treatment
options
are
an
urgent
unmet
clinical
need.
The
current
focus
in
healthcare
has
been
shifting
to
disease
prevention,
rather
than
treatment,
though,
not
much
progress
made
due
a
limited
understanding
pathogenesis.
Neuroinflammation
implicated
pathophysiology
may
impact
neurological
sequelae
following
TBI
including
functional
behavior
post-traumatic
development.
Inflammasome
signaling
major
components
neuroinflammatory
response,
which
increasingly
being
explored
for
its
contribution
epileptogenic
mechanisms
novel
target
against
This
review
discusses
role
inflammasomes
as
possible
connecting
link
between
PTE
with
particular
on
preclinical
evidence
inflammasome
targeting
downstream
effector
molecules
their
epileptogenesis.
Finally,
we
also
discuss
emerging
indicating
potential
evaluating
proteins
biofluids
by
non-invasive
neuroimaging,
biomarkers
predicting
npj Parkinson s Disease,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: April 25, 2025
Parkinson's
disease
(PD)
is
associated
with
chronic
sterile
inflammation
and
persistent
inflammasome
activation
involving
α-synuclein
ASC
protein
aggregates,
but
the
underlying
mechanisms
of
neuroinflammatory
response
remain
unclear.
Here,
we
used
midbrain
postmortem
samples
from
donors
without
α-synucleinopathies
to
assess
expression
proteins
in
patients
Parkinsonism.
We
show
that
dopaminergic
neurons
exhibit
increased
ASC,
NOD-like
receptor
(NLRP)
1,
modification
phosphorylation
at
serine129
(pS129)
within
Lewy
body
inclusions,
whereas
NLRP3
was
identified
mainly
microglial.
Moreover,
treatment
LRRK2
cells
specks
PD
dementia
induced
cytotoxicity
blocked
by
IC100.
Administration
preformed
aggregates
microglia
resulted
a
significant
elevation
pS129,
this
effect
also
Thus,
IC100
may
be
promising
therapeutic
strategy
for
inflammatory
synucleinopathies
other
diseases.
Neurotherapeutics,
Journal Year:
2023,
Volume and Issue:
20(6), P. 1508 - 1528
Published: Aug. 23, 2023
Traumatic
brain
injury
is
a
common
type
of
acquired
varying
severity
carrying
potentially
deleterious
consequences
for
the
afflicted
individuals,
families,
and
society.
Following
initial,
traumatically
induced
insult,
cellular
processes
ensue.
These
are
believed
to
be
amenable
treatment.
Among
such
injuries,
neuroinflammation
has
gained
interest
become
specific
focus
both
experimental
clinical
researchers.
Neuroinflammation
elicited
almost
immediately
following
trauma,
extend
long
time,
possibly
years,
after
primary
injury.
In
acute
phase,
inflammatory
response
characterized
by
innate
mechanisms
as
activation
microglia
which
among
else
mediates
cytokine
production.
earliest
cytokines
emerge
interleukin-
(IL-)
1
family
members,
comprising,
example,
agonist
IL-1β
its
competitive
antagonist,
IL-1
receptor
antagonist
(IL-1ra).
Because
early
emergence
trauma
increased
concentrations
also
human
TBI,
been
hypothesized
tractable
treatment
target
TBI.
Ample
data
supports
this,
demonstrates
restored
neurological
behavior,
diminished
lesion
zones,
an
attenuated
modulation
either
through
knock-out
experiments,
inhibition,
or
IL-1ra
Of
these,
likely
most
physiological.
addition,
recombinant
(anakinra)
already
approved
utilization
across
few
rheumatologic
disorders.
As
today,
one
randomized
controlled
trial
utilized
inhibition
intervention
demonstrated
safety.
Further
trials
powered
patient
outcome
needed
in
order
demonstrate
efficacy.
this
review,
we
summarize
biology
relation
neuroinflammatory
TBI
with
particular
on
current
evidence
context.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: July 16, 2024
Abstract
Post-traumatic
epilepsy
(PTE)
is
one
of
the
most
debilitating
consequences
traumatic
brain
injury
(TBI)
and
drug-resistant
forms
epilepsy.
Novel
therapeutic
treatment
options
are
an
urgent
unmet
clinical
need.
The
current
focus
in
healthcare
has
been
shifting
to
disease
prevention,
rather
than
treatment,
though,
not
much
progress
made
due
a
limited
understanding
pathogenesis.
Neuroinflammation
implicated
pathophysiology
may
impact
neurological
sequelae
following
TBI
including
functional
behavior
post-traumatic
development.
Inflammasome
signaling
major
components
neuroinflammatory
response,
which
increasingly
being
explored
for
its
contribution
epileptogenic
mechanisms
novel
target
against
This
review
discusses
role
inflammasomes
as
possible
connecting
link
between
PTE
with
particular
on
preclinical
evidence
inflammasome
targeting
downstream
effector
molecules
their
epileptogenesis.
Finally,
we
also
discuss
emerging
indicating
potential
evaluating
proteins
biofluids
by
non-invasive
neuroimaging,
biomarkers
predicting
