Current Pharmaceutical Design,
Год журнала:
2024,
Номер
30(5), С. 323 - 332
Опубликована: Фев. 1, 2024
Abstract:
Neuroinflammation
represents
a
critical
immune
response
within
the
brain,
playing
pivotal
role
in
defense
against
injury
and
infection.
However,
when
this
becomes
chronic,
it
can
contribute
to
development
of
various
neurodegenerative
psychiatric
disorders.
This
bibliographic
review
delves
into
vitamin
D
modulating
neuroinflammation
its
implications
for
brain
health,
particularly
context
neurological
While
is
traditionally
associated
with
calcium
homeostasis
bone
also
exerts
immunomodulatory
neuroprotective
effects
central
nervous
system.
Through
comprehensive
analysis
preclinical
clinical
studies,
we
uncover
how
D,
acting
through
receptors
glial
cells,
may
influence
production
proinflammatory
cytokines
antioxidants,
potentially
mitigating
cascade
events
leading
neuronal
damage.
Clinical
research
has
identified
deficiency
as
common
thread
increased
risks
multiple
sclerosis,
Parkinson's
disease,
Alzheimer's,
depression,
among
others.
Furthermore,
models
suggest
D's
regulatory
capacity
over
inflammatory
mediators,
protective
apoptosis,
contribution
neurogenesis
synaptic
plasticity.
These
insights
underscore
potential
supplementation
not
only
slowing
progression
diseases
but
improving
quality
life
patients
suffering
from
conditions.
Future
studies
are
essential
validate
these
findings
further
our
understanding
prevent
or
alleviate
symptoms,
opening
new
avenues
therapeutic
strategies
neuroinflammation-related
pathologies.
crucial
injuries
infections,
persistence
lead
such
Parkinson's,
depression.
Cholecalciferol
(Vitamin
D3)
emerges
regulator
neuroinflammation,
present
cells
astrocytes
microglia,
function.
Vitamin
mechanisms
action
include
cytokine
modulation
regulation
nuclear
mitochondrial
genes.
It
adjusts
mediators
resulting
effects.
Additionally,
impacts
neurotransmitter
synthesis
positions
adjunct
treating
like
Alzheimer's
Parkinson's.
Lastly,
intestinal
microbiota
serotonin
contributes
disorders
schizophrenia
Thus,
presents
novel
approach
neuroinflammatory,
neurodegenerative,
neuropsychiatric
diseases.
Journal of Neuroinflammation,
Год журнала:
2025,
Номер
22(1)
Опубликована: Фев. 7, 2025
Mitochondrial
dysfunction
is
a
pivotal
instigator
of
neuroinflammation,
with
mitochondrial
DNA
(mtDNA)
leakage
as
critical
intermediary.
This
review
delineates
the
intricate
pathways
leading
to
mtDNA
release,
which
include
membrane
permeabilization,
vesicular
trafficking,
disruption
homeostatic
regulation,
and
abnormalities
in
dynamics.
The
escaped
activates
cytosolic
sensors,
especially
cyclic
gmp-amp
synthase
(cGAS)
signalling
inflammasome,
initiating
neuroinflammatory
cascades
via
pathways,
exacerbating
spectrum
neurological
pathologies.
therapeutic
promise
targeting
discussed
detail,
underscoring
necessity
for
multifaceted
strategy
that
encompasses
preservation
homeostasis,
prevention
leakage,
reestablishment
dynamics,
inhibition
activation
sensors.
Advancing
our
understanding
complex
interplay
between
neuroinflammation
imperative
developing
precision
interventions
disorders.
Pharmaceutics,
Год журнала:
2023,
Номер
16(1), С. 60 - 60
Опубликована: Дек. 29, 2023
Alzheimer’s
disease
is
a
neurodegenerative
condition
marked
by
the
progressive
deterioration
of
cognitive
abilities,
memory
impairment,
and
accumulation
abnormal
proteins,
specifically
beta-amyloid
plaques
tau
tangles,
within
brain.
Despite
extensive
research
efforts,
remains
without
cure,
presenting
significant
global
healthcare
challenge.
Recently,
there
has
been
an
increased
focus
on
antibody-based
treatments
as
potentially
effective
method
for
dealing
with
disease.
This
paper
offers
comprehensive
overview
current
status
molecules
therapies
We
will
briefly
mention
their
mechanisms
action,
therapeutic
efficacy,
safety
profiles
while
addressing
challenges
limitations
encountered
during
development.
also
highlight
some
crucial
considerations
in
treatment
development,
including
patient
selection
criteria,
dosing
regimens,
or
concerns.
In
conclusion,
present
hopeful
outlook
While
remain,
accumulating
evidence
suggests
that
these
may
offer
substantial
promise
ameliorating
preventing
progression
this
debilitating
condition,
thus
enhancing
quality
life
millions
individuals
families
affected
worldwide.
Journal of Cerebral Blood Flow & Metabolism,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 12, 2025
Extracellular
vesicles
(EVs)
convey
complex
signals
between
cells
that
can
be
used
to
promote
neuronal
plasticity
and
neurological
recovery
in
brain
disease
models.
These
EV
are
multimodal
context-dependent,
making
them
unique
therapeutic
principles.
This
review
analyzes
how
EVs
released
from
various
cell
sources
control
metabolic
function,
survival
plasticity.
Preferential
sites
of
communication
the
interfaces
pre-
postsynaptic
neurons
at
synapses,
astrocytes
plasma
membranes
or
tripartite
oligodendrocytes
axons,
microglial
cells/macrophages
neurons,
cerebral
microvascular
neurons.
At
each
these
interfaces,
support
mitochondrial
function
metabolism
under
physiological
conditions
orchestrate
response
injury.
In
injured
brain,
promotion
by
is
tightly
linked
with
actions
on
metabolism,
oxidative
stress
immune
responses.
Via
stabilization
balance,
responses
activated
functional
induced.
As
such,
lay
ground
for
Gliomas
pose
a
significant
challenge
in
oncology
due
to
their
malignant
nature,
aggressive
growth,
frequent
recurrence,
and
complications
posed
by
the
blood-brain
barrier.
Emerging
research
has
revealed
critical
role
of
gut
microbiota
influencing
health
disease,
indicating
its
possible
impact
on
glioma
pathogenesis
treatment
responsiveness.
This
review
focused
existing
evidence
hypotheses
relationship
between
from
progression
invasion.
By
discussing
mechanisms
through
which
may
affect
biology,
this
paper
offers
new
avenues
for
targeted
therapies
precision
medicine
oncology.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(14), С. 7893 - 7893
Опубликована: Июль 19, 2024
Alzheimer's
disease
(AD)
represents
the
most
common
form
of
dementia
and
affects
million
people
worldwide,
with
a
high
social
burden
considerable
economic
costs.
AD
diagnosis
benefits
from
well-established
panel
laboratory
tests
that
allow
ruling-in
patients,
along
FDG
amyloid
PET
imaging
tools.
The
main
used
to
identify
patients
are
Aβ40,
Aβ42,
Aβ42/Aβ40
ratio,
phosphorylated
Tau
181
(pTau181)
total
(tTau).
Although
they
measured
preferentially
in
cerebrospinal
fluid
(CSF),
some
evidence
about
possibility
for
blood-based
determination
enter
clinical
practice
is
growing
up.
Unfortunately,
CSF
biomarkers
and,
even
more,
ones,
present
few
flaws,
twenty
years
research
this
field
did
not
overcome
these
pitfalls.
tale
worsens
when
issue
treating
addressed
due
lack
effective
strategies
despite
many
decades
attempts
by
pharmaceutic
industries
scientists.
Amyloid-based
drugs
failed
stop
disease,
no
neuroinflammation-based
have
been
demonstrated
work
so
far.
Hence,
only
symptomatic
therapy
available,
disease-modifying
treatment
on
hand.
Such
desolate
situation
fully
justifies
active
search
novel
be
as
reliable
molecular
targets
patients.
Recently,
group
molecules
has
identified
follow-up,
nuclei
acid-based
biomarkers.
Nucleic
composite
extracellular
consisting
DNA
RNA
alone
or
combination
other
molecules,
including
proteins.
This
review
article
reports
findings
studies
carried
out
during
AD,
highlights
their
advantages
limitations.
Biomolecules,
Год журнала:
2023,
Номер
13(11), С. 1568 - 1568
Опубликована: Окт. 24, 2023
Alzheimer’s
disease
(AD)
is
a
complex
neurodegenerative
disorder
characterized
by
progressive
cognitive
decline
and
memory
impairment.
Many
possible
factors
might
contribute
to
the
development
of
AD,
including
amyloid
peptide
tau
deposition,
but
more
recent
evidence
suggests
that
neuroinflammation
may
also
play
an—at
least
partial—role
in
its
pathogenesis.
In
years,
emerging
research
has
explored
involvement
external,
invading
pathogens
starting
or
accelerating
neuroinflammatory
processes
AD.
this
narrative
review,
we
advance
hypothesis
AD
be
partially
caused
viral,
bacterial,
fungal
entering
brain
through
nose
olfactory
system.
The
system
represents
plausible
route
for
pathogen
entry,
given
direct
anatomical
connection
early
stages
We
discuss
potential
mechanisms
which
exploit
pathway
initiate
neuroinflammation,
one
them
being
accidental
exposure
mucosa
hands
contaminated
with
soil
feces
when
picking
one’s
nose.
Frontiers in Neuroscience,
Год журнала:
2024,
Номер
18
Опубликована: Дек. 2, 2024
Cell
loss
and
mitochondrial
dysfunction
are
key
pathological
features
of
idiopathic
Parkinson's
disease
(PD)
multiple
system
atrophy
(MSA).
It
remains
unclear
whether
disease-specific
changes
in
plasma
circulating
cell-free
nuclear
DNA
(cf-nDNA)
(cf-mtDNA)
occur
patients
with
PD
MSA.
In
this
study,
we
investigated
cf-nDNA,
cf-mtDNA
levels,
as
well
integrity,
altered
DNA repair,
Год журнала:
2023,
Номер
131, С. 103581 - 103581
Опубликована: Окт. 6, 2023
Cells
possess
an
inherent
and
evolutionarily
conserved
ability
to
detect
respond
the
presence
of
foreign
pathological
'self'
nucleic
acids.
The
result
is
stimulation
innate
immune
responses,
signalling
host
system
that
defence
mechanisms
are
necessary
protect
organism.
To
date,
there
a
vast
body
literature
describing
responses
various
acid
species,
including
dsDNA,
ssDNA
ssRNA
etc.,
however,
limited
information
available
on
R-loops.
R-loops
3-stranded
structures
form
during
transcription,
upon
DNA
damage
in
other
settings.
Emerging
evidence
suggests
may
also
exist
for
detection
R-loop
related
structures,
implicating
as
drivers
inflammatory
states.
In
this
review,
we
aim
summarise
indicating
immunogenic
species
can
trigger
physiological
settings
discuss
implications
study
diseases
therapeutic
development.
Journal of Advanced Research,
Год журнала:
2024,
Номер
unknown
Опубликована: Июль 1, 2024
Nav1.6
is
closely
related
to
the
pathology
of
Alzheimer's
Disease
(AD),
and
astrocytes
have
recently
been
identified
as
a
significant
source
β-amyloid
(Aβ).
However,
little
known
about
connection
between
astrocyte-derived
Aβ.
This
study
explored
crucial
role
in
mediated
Aβ
AD
knockdown
astrocytic
alleviates
progression
by
promoting
autophagy
lysosome-APP
fusion.
A
mouse
model
for
was
constructed
effects
on
amyloidosis.
The
lysosome-APP(amyloid
precursor
protein)
fusion
used
transmission
electron
microscope,
immunostaining,
western
blot
patch
clamp.
Glial
cell
activation
detected
using
immunostaining.
Neuroplasticity
neural
network
were
assessed
patch-clamp,
Golgi
stain
EEG
recording.
Behavioral
experiments
performed
evaluate
cognitive
defects.
Astrocytic
reduces
amyloidosis,
glial
morphological
complexity,
improves
neuroplasticity
abnormal
networks,
well
promotes
learning
memory
abilities
APP/PS1
mice.
itself-derived
lysosome-
APP
fusion,
which
attenuating
reverse
Na+-Ca2+
exchange
current
thus
reducing
intracellular
Ca2+
facilitate
autophagic
through
AKT/mTOR/ULK
pathway.
Our
findings
unveil
astrocyte-specific
Aβ,
highlighting
its
potential
cell-specific
target
modulating
progression.
