Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Июль 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
Medicine,
Год журнала:
2023,
Номер
102(25), С. e34009 - e34009
Опубликована: Июнь 23, 2023
Neuroinflammation
after
traumatic
brain
injury
(TBI)
is
related
to
chronic
neurodegenerative
diseases
and
one
of
the
causes
acute
secondary
TBI.
Therefore,
it
particularly
important
clarify
role
cellular
mechanisms
in
neuroinflammatory
response
The
objective
this
article
understand
involvement
cells
during
TBI
inflammatory
(for
instance,
astrocytes,
microglia,
oligodendrocytes)
shed
light
on
recent
progress
stimulation
interaction
granulocytes
lymphocytes,
provide
a
novel
approach
for
clinical
research.
We
searched
articles
PubMed
published
between
1950
2023,
using
following
keywords:
TBI,
neuroinflammation,
cells,
neuroprotection,
clinical.
Articles
inclusion
paper
were
finalized
based
their
novelty,
representativeness,
relevance
main
arguments
review.
found
that
includes
activation
glial
release
mediators
brain,
recruitment
peripheral
immune
cells.
These
responses
not
only
induce
damage,
but
also
have
repairing
nervous
system
some
extent.
However,
all
cell-to-cell
interactions
been
well
studied.
After
treatment
cannot
simply
suppress
response,
phenotype
patients’
needs
be
defined
according
specific
conditions
injury.
Clinical
trials
personalized
inflammation
regulation
therapy
patients
should
carried
out
order
improve
prognosis
patients.
Journal of Alzheimer s Disease,
Год журнала:
2024,
Номер
98(3), С. 837 - 857
Опубликована: Март 12, 2024
A
hypothesis
of
Alzheimer’s
disease
etiology
is
proposed
describing
how
cellular
stress
induces
excessive
polyamine
synthesis
and
recycling
which
can
disrupt
nucleoli.
Polyamines
are
essential
in
nucleolar
functions,
such
as
RNA
folding
ribonucleoprotein
assembly.
Changes
the
pool
anionic
cationic
polyamines
acting
counterions
cause
significant
dynamics.
Polyamine
reduces
S-adenosylmethionine
which,
at
low
levels,
triggers
tau
phosphorylation.
Also,
acetyl-CoA
needed
for
acetylcholine,
disease.
Extraordinary
expansion
and/or
contraction
epigenetic
control
peri-nucleolar
chromatin,
chromosome
14
with
presenilin-1
gene;
21
amyloid
precursor
protein
17
19
APOE4
inactive
X
(Xi;
aka
“nucleolar
satellite”)
normally
silent
spermine
synthase
(polyamine
synthesis)
spermidine/spermine-N1-acetyltransferase
recycling)
alleles.
Chromosomes
17,
Xi
have
high
concentrations
Alu
elements
be
transcribed
by
polymerase
III
if
positioned
nucleosomes
displaced
from
elements.
sudden
flood
transcripts
competitively
bind
nucleolin
usually
bound
to
sequences
structural
RNAs
that
stabilize
heterochromatic
shell.
This
competition
leads
loss
integrity
leaking
aggregation
phosphorylated
tau.
The
was
developed
key
word
searches
(e.g.,
PubMed)
using
relevant
terms
Alzheimer’s,
lupus,
nucleolin)
based
on
a
systems
biology
approach
exploring
autoimmune
tautology,
gaining
synergistic
insights
other
diseases.
One
of
the
main
causes
death
and
disability
worldwide
is
brain
neurological
disorder/disease.
According
to
total
DALYs
(disability-adjusted
life
years),
burden
illnesses
will
continue
rise.
The
prevalence
condition
rising
with
age
as
population
ages
grows,
placing
a
significant
financial
strain
on
government
agencies
that
provide
assistance,
treatment,
rehabilitation.
prevention
diseases
therapeutic
approaches
are
therefore
subject
extensive
research.
In
this
book
chapter,
exosomes
defined
membrane-bound
nanovesicles
(30–100
nm)
endosomal
origins
contain
mRNAs,
proteins,
lipids.
Within
body,
they
take
part
in
intricate
intercellular
communication
system.
They
expelled
from
many
cell
types
healthy
or
setting,
by
transporting
active
signals,
influence
activity
receiving
cells.
addition
serving
potential
drug
delivery
systems,
also
serve
molecular
payloads,
novel
messengers,
coordinators
complex
regenerative
processes,
surface
biomarkers
for
detection
numerous
chronic
disorders.
Exosomes
have
low
immunogenicity,
long
biological
half-life,
ability
pass
blood–brain
barrier.
can
be
both
beneficial
detrimental
treatment
impact
central
nervous
system,
such
traumatic
encephalopathy,
Alzheimer's
disease,
Parkinson's
stroke,
prion
disease.
Neuro-inflammation
associated
proinflammatory
cytokines,
T
B
lymphocytes,
β-amyloid
peptides
1–42,
tau
protein,
well
neuronal
damage
aberrant
protein
aggregation.
There
growing
evidence
peripheral
system
(PNS)
(CNS)
communicate.
Extracellular
vehicles
(EVs),
which
regarded
state-of-the-art
information
transport
produced
almost
all
Proteins,
lipids,
nucleic
acids,
range
other
bioactive
regulators
present
transported
EVs.
Additionally,
it
has
been
established
EVs
mediating
role
between
systems
due
their
cross
barrier
(BBB).
Along
carrying
molecules
either
sick
state,
exceptional
promise
targeted
administration
medications.
mechanisms
behind
EV
migration,
connections
contrasting
immune
interactions
organs
during
CNS
disorders
neurodegenerative
diseases,
strokes,
trauma
explored
chapter.
Involvement
function
creation
novel,
minimally
intrusive
techniques,
discussed.
Molecular Neurobiology,
Год журнала:
2024,
Номер
unknown
Опубликована: Июль 16, 2024
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disease.
The
accumulation
of
amyloid-β
(Aβ)
plaques
and
tau
neurofibrillary
tangles
are
the
key
players
responsible
for
pathogenesis
Aβ
affect
balance
in
chemical
neurotransmitters
brain.
Thus,
current
review
examined
role
discusses
alterations
neurochemical
activity
cross
talk
with
their
receptors
transporters.
In
presence
tangles,
changes
may
occur
expression
neuronal
which
turn
triggers
excessive
release
glutamate
into
synaptic
cleft
contributing
to
cell
death
damage.
GABAergic
system
also
be
affected
by
AD
pathology
similar
way.
addition,
decreased
cholinergic
dysfunction
dopamine
neurotransmission
contribute
damage
cognitive
function.
Moreover,
deficiencies
noradrenergic
neurons
within
locus
coeruleus
suggests
that
stimulation
could
useful
addressing
its
pathophysiology.
regulation
melatonin,
known
effectiveness
enhancing
function
preventing
accumulation,
along
involvement
serotonergic
histaminergic
cognition
memory,
becomes
remarkable
promoting
AD.
Additionally,
nitric
oxide
adenosine-based
therapeutic
approaches
play
protective
neuroinflammation.
Overall,
neurotransmitter-based
strategies
emerge
as
pivotal
neurotransmitter
homeostasis
context
This
discussed
potential
drugs
effective
slowing
correcting
processes
targeting
imbalance
Therefore,
serve
future
strategy
tackle
Frontiers in Neuroscience,
Год журнала:
2025,
Номер
19
Опубликована: Фев. 25, 2025
Cognitive
dysfunction
after
traumatic
brain
injury
(TBI)
significantly
reduces
quality
of
life
and
imposes
a
heavy
burden
on
society.
A
detailed
examination
research
trends
cognitive
following
TBI
has
not
yet
been
conducted.
This
study
aimed
to
examine
the
bibliometric
analysis
over
past
20
years.
Literature
was
retrieved
from
Web
Science
Core
Collection
(WoSCC)
Citation
Index
Expanded
(SCI-E)
2004
2023.
The
type
literature
language
were
refined.
total
1,902
articles
used
for
analysis,
including
1,543
(81.1%)
original
359
(18.9%)
review
articles.
Data
June
5,
2024.
publication
volume
increasing
year
by
year,
with
published
in
537
journals.
Journal
Neurotrauma,
130
articles,
most
productive
influential
journal.
University
California
System
led
number
published.
There
9,002
authors
62
countries/regions.
USA
China
top-ranked
countries
article
count.
Pandharipande
PP
authored
highly
cited
article.
Pick
CG,
as
author
highest
h-index.
top
three
keywords
injury,
impairment,
mild
injury.
topics
ferroptosis,
decline,
spinal
cord
prognosis.
Our
findings
provide
valuable
insights
into
highlight
emerging
future
research.
Abstract
Axon
pruning
is
a
unique
process
neurons
utilize
to
selectively
degenerate
axon
branches
while
keeping
the
neuronal
cell
body
intact.
The
mechanisms
of
have
much
in
common
with
those
apoptosis.
Both
and
apoptosis
pathways
require
key
apoptotic
proteins
(Bax,
Caspase-9,
Caspase-3).
Interestingly,
does
not
Apaf-1,
member
apoptosome
complex.
As
such,
exactly
how
caspases
are
activated
an
apoptosome-independent
manner
during
unknown.
Here
we
show
that
NLRP1
inflammasome,
innate
immune
sensor
pathogens,
specifically
for
pruning.
Strikingly,
NLRP1b-deficient
were
unable
prune
axons
both
vitro
vivo,
but
fully
capable
degenerating
Our
results
reveal
as
molecule
engaged
by
unexpected
physiological
function
independent
its
pathogen-induced
proinflammatory
role.
