Parkinson’s
disease
(PD)
is
a
common
multisystem
neurodegenerative
disorder
affecting
1%
of
the
population
above
60
years.
The
main
neuropathological
features
PD
are
loss
dopaminergic
neurons
in
substantia
nigra
pars
compacta
(SNpc)
and
presence
alpha
synuclein
(Syn)-rich
Lewy
bodies
both
manifesting
with
classical
motor
signs.
Syn
has
emerged
as
key
protein
pathology
it
can
spread
through
synaptic
networks
to
reach
several
anatomical
regions
body
contributing
appearance
non-motor
symptoms
(NMS)
considerate
prevalent
among
individuals
before
diagnosis
persisting
throughout
patient’s
life.
NMS
mainly
include
taste
smell,
constipation,
psychiatric
disorders,
dementia,
rapid
eye
movement
(REM)
sleep
behavior
impairment,
urogenital
dysfunction,
cardiovascular
impairment.
This
review
summarizes
more
recent
findings
showing
impact
deposits
on
prodromal
emphasizes
importance
early
detection
toxic
species
biofluids
peripheral
biopsies
prospective
biomarkers
PD.
Frontiers in Aging Neuroscience,
Journal Year:
2024,
Volume and Issue:
16
Published: April 12, 2024
Neuroinflammation
refers
to
a
highly
complicated
reaction
of
the
central
nervous
system
(CNS)
certain
stimuli
such
as
trauma,
infection,
and
neurodegenerative
diseases.
This
is
cellular
immune
response
whereby
glial
cells
are
activated,
inflammatory
mediators
liberated
reactive
oxygen
nitrogen
species
synthesized.
key
process
that
helps
protect
brain
from
pathogens,
but
inappropriate,
or
protracted
inflammation
yields
pathological
states
Parkinson’s
disease,
Alzheimer’s,
Multiple
Sclerosis,
other
disorders
showcase
various
pathways
neurodegeneration
distributed
in
parts
CNS.
review
reveals
major
neuroinflammatory
signaling
associated
with
neurodegeneration.
Additionally,
it
explores
promising
therapeutic
avenues,
stem
cell
therapy,
genetic
intervention,
nanoparticles,
aiming
regulate
neuroinflammation
potentially
impede
decelerate
advancement
these
conditions.
A
comprehensive
understanding
intricate
connection
between
diseases
pivotal
for
development
future
treatment
strategies
can
alleviate
burden
imposed
by
devastating
disorders.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(15), P. 12464 - 12464
Published: Aug. 5, 2023
While
a
certain
level
of
inflammation
is
critical
for
humans
to
survive
infection
and
injury,
prolonged
inflammatory
response
can
have
fatal
consequences.
Pattern
recognition
Toll-like
receptors
(TLRs)
are
key
players
in
the
initiation
an
process.
TLR2
one
most
studied
pattern
(PRRs)
known
form
heterodimers
with
either
TLR1,
TLR4,
TLR6,
TLR10,
allowing
it
recognize
wide
range
pathogens.
Although
large
number
studies
been
conducted
over
past
decades,
there
still
many
unanswered
questions
regarding
mechanisms
health
disease.
In
this
review,
we
provide
up-to-date
overview
TLR2,
including
its
homo-
heterodimers.
Furthermore,
will
discuss
pro-
anti-inflammatory
properties
recent
findings
prominent
TLR2-associated
infectious
neurodegenerative
diseases.
Cureus,
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 13, 2024
This
review
offers
a
comprehensive
of
the
signals
and
paramount
role
neuroinflammation
plays
in
neurodegenerative
diseases
such
as
Alzheimer's,
Parkinson's,
Huntington's,
amyotrophic
lateral
sclerosis.
The
study
explores
sophisticated
interactions
between
microglial,
astrocytic,
dendritic
cells
how
affects
long-term
neuronal
damage
dysfunction.
There
are
specific
pathways
related
to
mentioned
inflammatory
processes,
including
Janus
kinases/signal
transducer
activator
transcriptions,
nuclear
factor-κB,
mitogen-activated
protein
kinases
pathways.
Neuroinflammation
is
argued
be
double-edged
sword,
being
not
only
protective
agent
that
prevents
further
neuron
but
also
causative
factor
more
cell
injury
development.
concept
contrasting
inflammation
with
neuroprotection
advocates
for
use
therapeutic
techniques
seek
modulate
neuroinflammatory
responses
part
neurodegeneration
treatment.
recent
research
findings
integrated
established
knowledge
help
present
image
neuroinflammation's
impact
on
its
implications
future
therapy.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(7), P. 3951 - 3951
Published: April 2, 2024
The
accumulation
of
misfolded
and
aggregated
α-synuclein
can
trigger
endoplasmic
reticulum
(ER)
stress
the
unfolded
protein
response
(UPR),
leading
to
apoptotic
cell
death
in
patients
with
Parkinson’s
disease
(PD).
As
major
ER
chaperone,
glucose-regulated
78
(GRP78/BiP/HSPA5)
plays
a
key
role
UPR
regulation.
GRP78
overexpression
modulate
UPR,
block
apoptosis,
promote
survival
nigral
dopamine
neurons
rat
model
pathology.
Here,
we
explore
therapeutic
potential
intranasal
exogenous
for
preventing
or
slowing
PD-like
neurodegeneration
lactacystin-induced
model.
We
show
that
intranasally-administered
rapidly
enters
substantia
nigra
pars
compacta
(SNpc)
other
afflicted
brain
regions.
It
is
then
internalized
by
microglia,
development
neurodegenerative
process
nigrostriatal
system.
Lactacystin-induced
disturbances,
such
as
abnormal
phosphorylated
pS129-α-synuclein
activation
pro-apoptotic
GRP78/PERK/eIF2α/CHOP/caspase-3,9
signaling
pathway
are
substantially
reversed
upon
administration.
Moreover,
inhibits
both
microglia
production
proinflammatory
cytokines,
tumor
necrosis
factor-α
(TNF-α)
interleukin-6
(IL-6),
via
nuclear
factor
kappa-light-chain-enhancer
activated
B
cells
(NF-κB)
animals.
neuroprotective
anti-inflammatory
may
inform
effective
agents
PD
synucleinopathies.
Neurobiology of Disease,
Journal Year:
2023,
Volume and Issue:
190, P. 106371 - 106371
Published: Dec. 5, 2023
Neurodegeneration
and
neuroinflammation
are
two
intertwined
mechanisms
contributing
to
the
pathophysiology
of
Parkinson's
disease.
Whether
circulating
biomarkers
reflecting
those
processes
differ
according
disease
duration
remains
be
established.
The
present
study
was
conducted
characterize
individuals
with
PD
short
(≤5
years)
or
long
(>5
years).
We
consecutively
enrolled
104
patients
evaluated
them
using
validated
clinical
scales
(MDS-UPDRS,
Hoehn
Yahr
staging,
MMSE).
Serum
samples
were
assayed
for
following
biomarkers:
neurofilament
light
chain
(NfL),
brain-derived
neurotrophic
factor
(BDNF),
interleukin
(IL-)
1β,
4,
5,
6,
10,
17,
interferon-γ,
tumor
necrosis
α.
Mean
age
participants
66.0
±
9.6
years
45
(34%)
women.
average
8
5
(range
1
19
Patients
(≤
showed
a
pro-inflammatory
profile,
significantly
higher
levels
IL-1β
lower
concentrations
IL-5,
IL-10
IL-17
(p
<
0.05).
NfL
serum
positive
correlation
(respectively
rho
=
0.248,
p
0.014
0.559,
0.001)
while
an
opposite
pattern
detected
BDNF
−0,187,
0.034
−0.245,
0.014).
Our
findings
suggest
that
status
may
observed
in
early
phases
disease,
independently
from
age.
Journal of Parkinson s Disease,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 29
Published: Sept. 25, 2024
Increasing
evidence
suggests
a
potential
role
for
infectious
pathogens
in
the
etiology
of
synucleinopathies,
group
age-related
neurodegenerative
disorders
including
Parkinson’s
disease
(PD),
multiple
system
atrophy
and
dementia
with
Lewy
bodies.
In
this
review,
we
discuss
link
between
infections
synucleinopathies
from
historical
perspective,
present
emerging
that
supports
link,
address
current
research
challenges
focus
on
neuroinflammation.
Infectious
can
elicit
neuroinflammatory
response
modulate
genetic
risk
PD
related
synucleinopathies.
The
mechanisms
how
might
be
linked
as
well
overlap
immune
cellular
pathways
affected
by
virulent
disease-related
factors
are
discussed.
Here,
an
important
α-synuclein
against
is
emerging.
Critical
methodological
knowledge
gaps
addressed,
provide
new
future
perspectives
to
these
gaps.
Understanding
neuroinflammation
influence
will
essential
development
early
diagnostic
tools
novel
therapies.
Cells,
Journal Year:
2024,
Volume and Issue:
13(15), P. 1265 - 1265
Published: July 27, 2024
Parkinson's
disease
(PD)
is
a
common
multisystem
neurodegenerative
disorder
affecting
1%
of
the
population
over
age
60
years.
The
main
neuropathological
features
PD
are
loss
dopaminergic
neurons
in
substantia
nigra
pars
compacta
(SNpc)
and
presence
alpha
synuclein
(αSyn)-rich
Lewy
bodies
both
manifesting
with
classical
motor
signs.
αSyn
has
emerged
as
key
protein
pathology
it
can
spread
through
synaptic
networks
to
reach
several
anatomical
regions
body
contributing
appearance
non-motor
symptoms
(NMS)
considered
prevalent
among
individuals
prior
diagnosis
persisting
throughout
patient's
life.
NMS
mainly
includes
taste
smell,
constipation,
psychiatric
disorders,
dementia,
impaired
rapid
eye
movement
(REM)
sleep,
urogenital
dysfunction,
cardiovascular
impairment.
This
review
summarizes
more
recent
findings
on
impact
deposits
prodromal
emphasizes
importance
early
detection
toxic
species
biofluids
peripheral
biopsies
prospective
biomarkers
PD.
Parkinson’s
disease
(PD)
is
a
common
multisystem
neurodegenerative
disorder
affecting
1%
of
the
population
above
60
years.
The
main
neuropathological
features
PD
are
loss
dopaminergic
neurons
in
substantia
nigra
pars
compacta
(SNpc)
and
presence
alpha
synuclein
(Syn)-rich
Lewy
bodies
both
manifesting
with
classical
motor
signs.
Syn
has
emerged
as
key
protein
pathology
it
can
spread
through
synaptic
networks
to
reach
several
anatomical
regions
body
contributing
appearance
non-motor
symptoms
(NMS)
considerate
prevalent
among
individuals
before
diagnosis
persisting
throughout
patient’s
life.
NMS
mainly
include
taste
smell,
constipation,
psychiatric
disorders,
dementia,
rapid
eye
movement
(REM)
sleep
behavior
impairment,
urogenital
dysfunction,
cardiovascular
impairment.
This
review
summarizes
more
recent
findings
showing
impact
deposits
on
prodromal
emphasizes
importance
early
detection
toxic
species
biofluids
peripheral
biopsies
prospective
biomarkers
PD.
Immunity Inflammation and Disease,
Journal Year:
2023,
Volume and Issue:
11(8)
Published: Aug. 1, 2023
Polysulfides
are
reported
to
be
involved
in
various
important
biological
processes.
N-acetyl-l-cysteine
polysulfide
with
2
sulfane
sulfur
atoms
(NAC-S2)
regulates
diverse
toll-like
receptor
(TLR)
signaling
pathways.
Here,
we
aimed
determine
the
role
of
NAC-S2
periodontitis
and
explore
potential
mechanism.
