Cells,
Journal Year:
2021,
Volume and Issue:
10(7), P. 1584 - 1584
Published: June 23, 2021
Increased
life
expectancy
in
combination
with
modern
style
and
high
prevalence
of
obesity
are
important
risk
factors
for
development
neurodegenerative
diseases.
Neuroinflammation
is
a
feature
diseases,
microglia,
the
innate
immune
cells
brain,
central
players
it.
The
present
review
discusses
effects
obesity,
chronic
peripheral
inflammation
obesity-associated
metabolic
endocrine
perturbations,
including
insulin
resistance,
dyslipidemia
increased
glucocorticoid
levels,
on
microglial
function.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: June 30, 2023
Abstract
Amyloid
β
protein
(Aβ)
is
the
main
component
of
neuritic
plaques
in
Alzheimer’s
disease
(AD),
and
its
accumulation
has
been
considered
as
molecular
driver
pathogenesis
progression.
Aβ
prime
target
for
development
AD
therapy.
However,
repeated
failures
Aβ-targeted
clinical
trials
have
cast
considerable
doubt
on
amyloid
cascade
hypothesis
whether
drug
followed
correct
course.
recent
successes
targeted
assuaged
those
doubts.
In
this
review,
we
discussed
evolution
over
last
30
years
summarized
application
diagnosis
modification.
particular,
extensively
pitfalls,
promises
important
unanswered
questions
regarding
current
anti-Aβ
therapy,
well
strategies
further
study
more
feasible
approaches
optimization
prevention
treatment.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(7), P. 6518 - 6518
Published: March 30, 2023
Alzheimer’s
disease
is
one
of
the
most
commonly
diagnosed
cases
senile
dementia
in
world.
It
an
incurable
process,
often
leading
to
death.
This
multifactorial,
and
factor
this
inflammation.
Numerous
mediators
secreted
by
inflammatory
cells
can
cause
neuronal
degeneration.
Neuritis
may
coexist
with
other
mechanisms
disease,
contributing
progression,
also
directly
underlie
AD.
Although
much
has
been
established
about
processes
pathogenesis
AD,
many
aspects
remain
unexplained.
The
work
devoted
particular
pathomechanism
inflammation
its
role
diagnosis
treatment.
An
in-depth
detailed
understanding
neuroinflammation
help
development
diagnostic
methods
for
early
contribute
new
therapeutic
strategies
disease.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(18), P. 10572 - 10572
Published: Sept. 12, 2022
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disorder;
it
the
most
common
cause
of
dementia
and
has
no
treatment.
It
characterized
by
two
pathological
hallmarks,
extracellular
deposits
amyloid
beta
(Aβ)
intraneuronal
Neurofibrillary
tangles
(NFTs).
Yet,
those
hallmarks
do
not
explain
full
pathology
seen
with
AD,
suggesting
involvement
other
mechanisms.
Neuroinflammation
could
offer
another
explanation
for
progression
disease.
This
review
provides
an
overview
recent
advances
on
role
immune
cells'
microglia
astrocytes
in
neuroinflammation.
In
become
reactive
several
mechanisms
leading
to
release
proinflammatory
cytokines
that
further
neuronal
damage.
We
then
provide
updates
neuroinflammation
diagnostic
markers
investigational
therapeutics
currently
clinical
trials
target
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(5), P. 4354 - 4354
Published: Feb. 22, 2023
Alzheimer's
disease
(AD)
is
the
main
type
of
dementia
and
a
with
profound
socioeconomic
burden
due
to
lack
effective
treatment.
In
addition
genetics
environmental
factors,
AD
highly
associated
metabolic
syndrome,
defined
as
combination
hypertension,
hyperlipidemia,
obesity
2
diabetes
mellitus
(T2DM).
Among
these
risk
connection
between
T2DM
has
been
deeply
studied.
It
suggested
that
mechanism
linking
both
conditions
insulin
resistance.
Insulin
an
important
hormone
regulates
not
only
peripheral
energy
homeostasis
but
also
brain
functions,
such
cognition.
desensitization,
therefore,
could
impact
normal
function
increasing
developing
neurodegenerative
disorders
in
later
life.
Paradoxically,
it
demonstrated
decreased
neuronal
signalling
can
have
protective
role
aging
protein-aggregation-associated
diseases,
case
AD.
This
controversy
fed
by
studies
focused
on
signalling.
However,
action
other
cell
types,
astrocytes,
still
unexplored.
Therefore,
worthwhile
exploring
involvement
astrocytic
receptor
cognition,
well
onset
and/or
development
Annals of Neurosciences,
Journal Year:
2021,
Volume and Issue:
28(3-4), P. 191 - 200
Published: July 1, 2021
Background:
Innate
immunity
is
mediated
by
a
variety
of
cell
types,
including
microglia,
macrophages,
and
neutrophils,
serves
as
the
immune
system's
first
line
defense.
There
are
numerous
pathways
involved
in
innate
immunity,
interferon
(IFN)
pathway,
TRK
mitogen-activated
protein
kinase
(MAPK)
Janus
kinase/signal
transducer
activator
transcription
(JAK/STAT)
interleukin
(IL)
pathways,
chemokine
(CCR5),
GSK
signaling,
Fas
signaling.
Summary:
JAK/STAT
one
these
important
signaling
this
review
focused
on
pathway
only.
The
overactivation
microglia
astrocytes
influences
JAK/STAT's
role
neuroinflammatory
disease
initiating
orchestrating
adaptive
mechanisms,
ultimately
constraining
inflammatory
immunological
responses.
critical
factors
that
promotes
neuroinflammation
neurodegenerative
diseases.
Key
message:
Given
importance
disease,
discussed
feasibility
targeting
neuroprotective
therapy
for
diseases
near
future.
Journal of Alzheimer s Disease,
Journal Year:
2020,
Volume and Issue:
78(2), P. 619 - 626
Published: Sept. 29, 2020
Background:
Alzheimer’s
disease
(AD)
is
increasingly
prevalent
and
over
99%
of
drugs
developed
for
AD
have
failed
in
clinical
trials.
A
growing
body
literature
suggests
that
potent
inhibitors
tumor
necrosis
factor-α
(TNF-α)
potential
to
improve
cognitive
performance.
Objective:
In
this
review,
we
summarize
the
evidence
regarding
TNF-α
inhibition
prevent
function
people
at
risk
dementia.
Methods:
We
conducted
a
review
PubMed,
screening
all
articles
published
before
July
7,
2019
related
TNF
blocking
agents
curcumin
(another
inhibitor)
context
pathology.
The
keywords
search
included:
AD,
dementia,
memory,
cognition,
TNF-α,
inhibitors,
etanercept,
infliximab,
adalimumab,
golimumab,
curcumin.
Results:
Three
large
epidemiology
studies
reported
etanercept
treated
patients
had
60
70%
lower
odds
ratio
(OR)
developing
AD.
Two
small-randomized
control
trials
(RCTs)
demonstrated
an
improvement
performance
with
etanercept.
Studies
using
animal
models
dementia
also
similar
findings
(etanercept,
Theracurmin),
which
appeared
cognition.
small
human
RCT
Theracurmin,
well-absorbed
form
lowers
showed
enhanced
decreased
brain
levels
amyloid-β
plaque
tau
tangles.
Conclusion:
targeted
therapy
biologically
plausible
approach
preservation
warrants
larger
prospective
RCTs
further
investigate
benefits
populations
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: July 22, 2022
Neurological
disorders
(NDs)
are
one
of
the
leading
causes
global
death.
A
sustained
neuroinflammatory
response
has
been
reported
to
be
associated
with
pathogenesis
multiple
NDs,
including
Parkinson’s
disease
(PD),
sclerosis
(MS),
Alzheimer’s
(AD),
amyotrophic
lateral
(ALS),
and
major
depressive
disorder
(MDD).
Accumulating
evidence
shows
that
recruitment
abundant
lymphocytes
in
central
nervous
system
may
contribute
promoting
development
progress
inflammation
neurological
disorders.
As
subset
T
lymphocytes,
CD4
+
cells
have
a
critical
impact
on
helper
(Th)
17
is
most
studied
Th
subpopulations
produces
cytokines
(e.g.,
IL-17A,
IL-23,
IL-21,
IL-6,
IFN-γ),
abnormal
excessive
activation
microglia
other
immune
cell
types.
All
these
factors
involved
several
However,
possible
mechanisms
Th17
their
immunopathology
abovementioned
not
clarified
completely.
This
review
will
summarize
by
which
encephalitogenic
inflammatory
related
strongly
chronic
neuroinflammation,
thus
perpetuating
neurodegenerative
processes
NDs.
Finally,
potential
therapeutic
prospects
NDs
also
discussed.
