Aging and Disease,
Journal Year:
2024,
Volume and Issue:
unknown, P. 0 - 0
Published: Jan. 1, 2024
As
a
key
member
of
the
neurotrophin
family
in
central
nervous
system,
brain-derived
neurotrophic
factor
(BDNF)
plays
critical
role
maintenance
and
plasticity
system.
Its
innate
neuroprotective
advantage
can
also
be
shared
with
brain
when
normal
aging-dependent
processes
challenge
neural
circuits.
The
intricate
relationship
between
BDNF
resilience
during
aging
process
signifies
molecular
mechanisms
that
underlie
protection
function,
such
as
cognition,
movement
psychological
well-being.
is
crucial
for
neuronal
growth
survival,
it
promote
against
age-related
functional
decline
frailty,
even
if
fails
to
entirely
prevent
aging-related
decline.
In
present
review,
we
discuss
function
from
perspective
how
may
aging.
We
emphasize
briefly
principal,
well-known
cellular
hallmarks
restrict
disabling
dynamics
enhance
overall
Insight
into
pathways
through
which
reduces
dysfunctions
and/or
improves
resilience,
provides
foundation
developing
targeted
interventions
mental
well-being
an
population.
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(1), P. 71 - 71
Published: Jan. 5, 2024
Chronic
pain
is
sustained,
in
part,
through
the
intricate
process
of
central
sensitization
(CS),
marked
by
maladaptive
neuroplasticity
and
neuronal
hyperexcitability
within
pathways.
Accumulating
evidence
suggests
that
CS
also
driven
neuroinflammation
peripheral
nervous
system.
In
any
chronic
disease,
search
for
perpetuating
factors
crucial
identifying
therapeutic
targets
developing
primary
preventive
strategies.
The
brain-derived
neurotrophic
factor
(BDNF)
emerges
as
a
critical
regulator
synaptic
plasticity,
serving
both
neurotransmitter
neuromodulator.
Mounting
supports
BDNF’s
pro-nociceptive
role,
spanning
from
its
pain-sensitizing
capacity
across
multiple
levels
nociceptive
pathways
to
involvement
neuroinflammation.
Moreover,
consistently
elevated
BDNF
are
observed
various
disorders.
To
comprehensively
understand
profound
impact
pain,
we
delve
into
key
characteristics,
focusing
on
role
underlying
molecular
mechanisms
contributing
pain.
Additionally,
explore
potential
utility
an
objective
biomarker
This
discussion
encompasses
emerging
approaches
aimed
at
modulating
expression,
offering
insights
addressing
complexities
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(11), P. 6023 - 6023
Published: May 30, 2024
Royal
jelly
(RJ)
is
a
highly
nutritious
natural
product
with
great
potential
for
use
in
medicine,
cosmetics,
and
as
health-promoting
food.
This
bee
mixture
of
important
compounds,
such
proteins,
vitamins,
lipids,
minerals,
hormones,
neurotransmitters,
flavonoids,
polyphenols,
that
underlie
the
remarkable
biological
therapeutic
activities
RJ.
Various
bioactive
molecules
like
10-hydroxy-2-decenoic
acid
(10-HDA),
antibacterial
protein,
apisin,
major
royal
specific
peptides
apisimin,
royalisin,
royalactin,
apidaecin,
defensin-1,
jelleins
are
characteristic
ingredients
RJ
shows
numerous
physiological
pharmacological
properties,
including
vasodilatory,
hypotensive,
antihypercholesterolaemic,
antidiabetic,
immunomodulatory,
anti-inflammatory,
antioxidant,
anti-aging,
neuroprotective,
antimicrobial,
estrogenic,
anti-allergic,
anti-osteoporotic,
anti-tumor
effects.
Moreover,
may
reduce
menopause
symptoms
improve
health
reproductive
system,
liver,
kidneys,
promote
wound
healing.
article
provides
an
overview
molecular
mechanisms
underlying
beneficial
effects
various
diseases,
aging,
aging-related
complications,
special
emphasis
on
components
their
properties.
The
data
presented
should
be
incentive
future
clinical
studies
hopefully
will
advance
our
knowledge
about
facilitate
development
novel
RJ-based
opportunities
improving
human
well-being.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(19), P. 10535 - 10535
Published: Sept. 30, 2024
Progress
made
by
the
medical
community
in
increasing
lifespans
comes
with
costs
of
incidence
and
prevalence
age-related
diseases,
neurodegenerative
ones
included.
Aging
is
associated
a
series
morphological
changes
at
tissue
cellular
levels
brain,
as
well
impairments
signaling
pathways
gene
transcription,
which
lead
to
synaptic
dysfunction
cognitive
decline.
Although
we
are
not
able
pinpoint
exact
differences
between
healthy
aging
neurodegeneration,
research
increasingly
highlights
involvement
neuroinflammation
chronic
systemic
inflammation
(inflammaging)
development
age-associated
via
pathogenic
cascades,
triggered
dysfunctions
circadian
clock,
gut
dysbiosis,
immunosenescence,
or
impaired
cholinergic
signaling.
In
addition,
gender
susceptibility
course
neurodegeneration
that
appear
be
mediated
glial
cells
emphasize
need
for
future
this
area
an
individualized
therapeutic
approach.
rejuvenation
still
its
very
early
infancy,
accumulated
knowledge
on
various
involved
promoting
senescence
opens
perspective
interfering
these
preventing
delaying
senescence.
Journal of Personalized Medicine,
Journal Year:
2024,
Volume and Issue:
14(5), P. 488 - 488
Published: May 3, 2024
Interleukin-8
(IL-8/CXCL8),
an
essential
CXC
chemokine,
significantly
influences
psychoneuroimmunological
processes
and
affects
neurological
psychiatric
health.
It
exerts
a
profound
effect
on
immune
cell
activation
brain
function,
suggesting
potential
roles
in
both
neuroprotection
neuroinflammation.
IL-8
production
is
stimulated
by
several
factors,
including
reactive
oxygen
species
(ROS)
known
to
promote
inflammation
disease
progression.
Additionally,
CXCL8
gene
polymorphisms
can
alter
production,
leading
differences
susceptibility,
progression,
severity
across
populations.
levels
vary
among
neuropsychiatric
conditions,
demonstrating
sensitivity
psychosocial
stressors
severity.
be
detected
blood
circulation,
cerebrospinal
fluid
(CSF),
urine,
making
it
promising
candidate
for
broad-spectrum
biomarker.
This
review
highlights
the
need
further
research
diverse
effects
of
associated
implications
personalized
medicine.
A
thorough
understanding
its
complex
role
could
lead
development
more
effective
treatment
strategies
conditions.
Frontiers in Neurology,
Journal Year:
2024,
Volume and Issue:
15
Published: Aug. 1, 2024
Neuroplasticity
as
a
mechanism
to
overcome
central
nervous
system
injury
resulting
from
different
neurological
diseases
has
gained
increasing
attention
in
recent
years.
However,
deficiency
of
these
repair
mechanisms
leads
the
accumulation
neuronal
damage
and
therefore
long-term
disability.
To
date,
by
which
remyelination
occurs
why
extent
differs
interindividually
between
multiple
sclerosis
patients
regardless
disease
course
are
unclear.
A
member
neurotrophins
family,
brain-derived
neurotrophic
factor
(BDNF)
received
particular
this
context
it
is
thought
play
role
thus
neuroplasticity,
neuroprotection,
memory.
Journal of Lipid and Atherosclerosis,
Journal Year:
2024,
Volume and Issue:
13(2), P. 122 - 122
Published: Jan. 1, 2024
Vascular
dementia
(VaD)
is
the
second
most
common
type
of
and
characterized
by
memory
impairment,
blood-brain
barrier
disruption,
neuronal
cell
loss,
glia
activation,
impaired
synaptic
plasticity,
cholinergic
system
abnormalities.
To
effectively
prevent
treat
VaD
a
good
understanding
mechanisms
underlying
its
neuropathology
needed.
Brain-derived
neurotrophic
factor
(BDNF)
an
important
with
multiple
functions
in
systemic
circulation
central
nervous
known
to
regulate
survival,
formation,
cognitive
decline.
Recent
studies
indicate
that
when
compared
normal
subjects,
patients
have
low
serum
BDNF
levels
deficiency
cerebrospinal
fluid
indicator
VaD.
Here,
we
review
current
knowledge
on
role
signaling
pathology
VaD,
such
as
cerebrovascular
dysfunction,
impairment.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: June 4, 2024
Abstract
Background
Neuroinflammation
is
widely
acknowledged
as
a
characteristic
feature
of
almost
all
neurological
disorders
and
specifically
in
depression-
anxiety-like
disorders.
In
recent
years,
there
has
been
significant
attention
on
natural
compounds
with
potent
anti-inflammatory
effects
due
to
their
potential
mitigating
neuroinflammation
neuroplasticity.
Methods
the
present
study,
we
aimed
evaluate
neuroprotective
oleacein
(OC),
rare
secoiridoid
derivative
found
extra
virgin
olive
oil.
Our
goal
was
explore
BDNF/TrkB
neurotrophic
activity
OC
subsequently
assess
its
for
modulating
neuroinflammatory
response
using
human
neuroblastoma
cells
(SH-SY5Y
cells)
an
vivo
model
depression
induced
by
lipopolysaccharide
(LPS)-mediated
inflammation.
Results
SH-SY5Y
cells,
exhibited
dose-dependent
increase
BDNF
expression.
This
enhancement
absent
when
were
co-treated
inhibitors
BDNF's
receptor
TrkB,
well
downstream
molecules
PI3K
MEK.
Whole-transcriptomics
analysis
revealed
that
upregulated
cell
cycle-related
genes
under
normal
conditions,
while
downregulating
inflammation-associated
LPS-induced
conditions.
Furthermore,
surface
plasmon
resonance
(SPR)
assays
demonstrated
stronger
more
stable
binding
affinity
TrkB
compared
positive
control,
7,8-dihydroxyflavone.
Importantly,
bioluminescence
imaging
single
oral
dose
significantly
increased
expression
brains
Bdnf-IRES-AkaLuc
mice.
administration
at
dosage
10
mg/kg
body
weight
days
reduced
immobility
time
tail
suspension
test
LPS-treated
group.
RT-qPCR
decreased
pro-inflammatory
cytokines
Tnfα
,
Il6
Il1β
simultaneously
enhancing
Bdnf
expression,
both
pro
mature
protein
levels
mice
hippocampus.
These
changes
comparable
those
control
antidepressant
drug
fluoxetine.
Additionally,
microarray
mouse
confirmed
could
counteract
inflammatory
biological
events.
Conclusion
Altogether,
our
study
represents
first
report
antineuroinflammatory
properties
via
modulation
activity.
finding
underscores
therapeutic
agent
anxiety-related
Abstract
Background
Sleep
deprivation
(SD)
is
a
growing
global
health
problem
with
many
deleterious
effects,
such
as
cognitive
impairment.
Microglia
activation‐induced
neuroinflammation
may
be
an
essential
factor
in
this.
Propofol
has
been
shown
to
clear
sleep
debt
after
SD
rats.
This
study
aims
evaluate
the
effects
of
propofol‐induced
on
ameliorating
quality
impairment
and
decline
48
h
SD.
Methods
Almost
8–12‐week‐old
rats
were
placed
system
for
natural
or
continuous
Afterwards,
received
propofol
(20
mg·kg
−1
·h
,
6
h)
via
tail
slept
naturally.
The
Morris
water
maze
(MWM)
Y‐maze
test
assessed
spatial
learning
memory
abilities.
Rat
EEG/EMG
monitored
sleep.
expression
brain
muscle
Arnt‐like
protein
1
(BMAL1),
brain‐derived
neurotrophic
(BDNF)
hippocampus
BMAL1
hypothalamus
by
western
blot.
Enzyme‐linked
immunosorbent
assay
detected
IL‐6,
IL‐1β,
arginase
(Arg1),
IL‐10
levels
hippocampus.
Immunofluorescence
was
used
determine
microglia
well
morphological
changes.
Results
Compared
control
group,
sleep‐deprived
showed
poor
performance
both
MWM
test,
accompanied
disturbances
structure,
including
increased
total
time,
time
spent
delta
power
non‐rapid
eye
movement
In
addition,
induces
abnormal
circadian
rhythm
BMAL1,
activates
microglia,
causes
nerve
damage.
reversed
these
changes
saved
Furthermore,
treatment
significantly
reduced
hippocampal
IL‐1β
IL‐6
levels,
BDNF,
Arg1,
switched
surface
markers
from
inflammatory
M1
type
anti‐inflammatory
M2
type.
Conclusion
reduces
SD‐induced
disruption,
possibly
lowering
neuronal
inflammation
switching
phenotype
activated
state,
thus
exerting
neuroprotective
effects.