British Journal of Pharmacology,
Journal Year:
2019,
Volume and Issue:
176(18), P. 3544 - 3557
Published: Jan. 24, 2019
Background
and
purpose
Alzheimer's
disease
(AD)
is
a
common
neurodegenerative
characterized
by
neuroinflammatory
state,
to
date,
there
no
cure
its
treatment
represents
large
unmet
clinical
need.
The
involvement
of
Th17
cells
in
the
pathogenesis
AD‐related
neuroinflammation
has
been
reported
several
studies.
However,
role
cytokine,
IL‐17
not
well
addressed.
Herein,
we
investigate
effects
neutralizing
antibody
(IL‐17Ab)
injected
i.c.v.
or
intranasal
(IN)
routes
on
amyloid‐β
(Aβ)‐induced
memory
impairment
mice.
Experimental
approach
Aβ
1–42
was
into
cerebral
ventricles
adult
CD1
These
mice
received
IL‐17Ab
via
either
at
1
h
prior
injection
IN
5
12
days
after
injection.
After
7
14
administration,
evaluated
olfactory,
spatial
working
performed
biochemical
analyses
whole
brain
specific
areas.
Key
results
Pretreatment
with
IL‐17Ab,
given,
i.c.v.,
markedly
reduced
‐induced
neurodegeneration,
improved
function,
prevented
increase
pro‐inflammatory
mediators
dose‐dependent
manner
days.
Similarly,
double
administration
decline,
levels
proinflammatory
cytokines.
Conclusion
implications
findings
suggest
that
behavioural
symptoms
induced
Aβ.
efficacy
reducing
neurodegeneration
points
possible
future
therapeutic
patients
AD.
Linked
Articles
This
article
part
themed
section
Therapeutics
for
Dementia
Disease:
New
Directions
Precision
Medicine.
To
view
other
articles
this
visit
http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.18/issuetoc
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: July 12, 2023
Abstract
Studies
in
neurodegenerative
diseases,
including
Alzheimer’s
disease,
Parkinson’s
disease
and
Amyotrophic
lateral
sclerosis,
Huntington’s
so
on,
have
suggested
that
inflammation
is
not
only
a
result
of
neurodegeneration
but
also
crucial
player
this
process.
Protein
aggregates
which
are
very
common
pathological
phenomenon
can
induce
neuroinflammation
further
aggravates
protein
aggregation
neurodegeneration.
Actually,
even
happens
earlier
than
aggregation.
Neuroinflammation
induced
by
genetic
variations
CNS
cells
or
peripheral
immune
may
deposition
some
susceptible
population.
Numerous
signaling
pathways
range
been
to
be
involved
the
pathogenesis
neurodegeneration,
although
they
still
far
from
being
completely
understood.
Due
limited
success
traditional
treatment
methods,
blocking
enhancing
inflammatory
considered
promising
strategies
for
therapy
many
them
got
exciting
results
animal
models
clinical
trials.
Some
them,
few,
approved
FDA
usage.
Here
we
comprehensively
review
factors
affecting
major
pathogenicity
sclerosis.
We
summarize
current
strategies,
both
clinic,
diseases.
Frontiers in Neuroendocrinology,
Journal Year:
2019,
Volume and Issue:
55, P. 100788 - 100788
Published: Sept. 9, 2019
Neuroinflammation
is
a
physiological
protective
response
in
the
context
of
infection
and
injury.
However,
neuroinflammation,
especially
if
chronic,
may
also
drive
neurodegeneration.
Neurodegenerative
diseases,
such
as
multiple
sclerosis
(MS),
Alzheimer's
disease
(AD),
Parkinson's
(PD)
traumatic
brain
injury
(TBI),
display
inflammatory
activation
microglia
astrocytes.
Intriguingly,
central
nervous
system
(CNS)
highly
steroidogenic
environment
synthesizing
steroids
de
novo,
well
metabolizing
deriving
from
circulation.
Neurosteroid
synthesis
can
be
substantially
affected
by
while,
turn,
several
steroids,
17β-estradiol,
dehydroepiandrosterone
(DHEA)
allopregnanolone,
regulate
neuroinflammatory
responses.
Here,
we
review
role
neurosteroids
neuroinflammation
MS,
AD,
PD
TBI
describe
underlying
molecular
mechanisms.
Moreover,
introduce
concept
that
synthetic
neurosteroid
analogues
could
potentially
utilized
for
treatment
neurodegenerative
diseases
future.
Frontiers in Aging Neuroscience,
Journal Year:
2021,
Volume and Issue:
13
Published: Feb. 12, 2021
A
wide
range
of
comorbid
diseases
is
associated
with
Alzheimer's
disease
(AD),
the
most
common
neurodegenerative
worldwide.
Evidence
from
clinical
and
molecular
studies
suggest
that
chronic
diseases,
including
diabetes,
cardiovascular
disease,
depression,
inflammatory
bowel
may
be
an
increased
risk
AD
in
different
populations.
Disruption
several
shared
biological
pathways
has
been
proposed
as
underlying
mechanism
for
association
between
these
comorbidities.
Notably,
inflammation
a
dysregulated
pathway
by
comorbidities
AD.
Some
drugs
commonly
prescribed
to
patients
diabetes
have
shown
promising
results
patients.
Systems-based
biology
identified
genetic
factors
explain
relationship
disorders
Nonetheless,
precise
mechanisms
occurrence
are
not
entirely
understood.
Here,
we
discuss
impact
management
Biomedicine & Pharmacotherapy,
Journal Year:
2022,
Volume and Issue:
148, P. 112681 - 112681
Published: Feb. 14, 2022
Alzheimer's
disease
(AD)
is
the
most
common
neurodegenerative
disease,
with
cognitive
decline
as
primary
clinical
feature.
According
to
epidemiological
statistics,
50
million
people
worldwide
are
currently
affected
by
disease.
Although
new
drugs
such
aducanumab
have
been
approved
for
use
in
treatment
of
AD,
none
them
reversed
progression
AD.
MicroRNAs
(miRNAs)
small
molecule
RNAs
that
exert
their
biological
functions
regulating
expression
intracellular
proteins,
and
differential
abundance
varieties
found
between
central
peripheral
tissues
AD
patients
healthy
controls.
This
article
will
summarise
changes
miRNAs
process,
potential
role
diagnostic
markers
therapeutic
targets
be
explored.
