The Journals of Gerontology Series A,
Год журнала:
2024,
Номер
79(11)
Опубликована: Авг. 22, 2024
Abstract
Background
Chronic
pain
leads
to
tau
accumulation
and
hippocampal
atrophy,
which
may
be
moderated
through
inflammation.
In
older
men,
we
examined
associations
of
chronic
with
Alzheimer’s
disease
(AD)-related
plasma
biomarkers
volume
as
by
systemic
Methods
Participants
were
men
without
dementia.
was
defined
moderate-to-severe
in
2+
study
waves
at
average
ages
56,
62,
68.
At
age
68,
measured
amyloid-beta
(Aβ42,
n
=
871),
Aβ40
(n
887),
total
(t-tau,
841),
neurofilament
light
chain
(NfL,
915),
serum
high-sensitivity
C-reactive
protein
(hs-CRP,
968),
a
marker
A
subgroup
underwent
structural
MRI
measure
385).
Analyses
adjusted
for
medical
morbidities,
depressive
symptoms,
opioid
use.
Results
related
higher
(β
0.25,
p
.009),
but
hs-CRP
unrelated
AD-related
(ps
>
.05).
There
significant
interaction
such
that
both
levels
had
Aβ42
0.36,
.001)
0.29,
.003).
did
not
interact
predict
Aβ42/Aβ40,
t-tau,
or
NfL.
Furthermore,
there
interactions
associated
lower
volume,
particularly
when
elevated
(hs-CRP
×
Aβ42:
β
−0.19,
.002;
Aβ40:
−0.21,
.001),
regardless
status.
Conclusions
Aβ,
especially
also
elevated.
Higher
Aβ
smaller
volumes.
pain,
accompanied
inflammation,
elevate
the
risk
neurodegeneration
AD-vulnerable
regions.
Abstract
Alzheimer’s
disease
(AD)
is
a
serious
brain
disorder
characterized
by
the
presence
of
beta-amyloid
plaques,
tau
pathology,
inflammation,
neurodegeneration,
and
cerebrovascular
dysfunction.
The
chronic
neuroinflammation,
breaches
in
blood-brain
barrier
(BBB),
increased
levels
inflammatory
mediators
are
central
to
pathogenesis
AD.
These
factors
promote
penetration
immune
cells
into
brain,
potentially
exacerbating
clinical
symptoms
neuronal
death
AD
patients.
While
microglia,
resident
nervous
system
(CNS),
play
crucial
role
AD,
recent
evidence
suggests
infiltration
cerebral
vessels
parenchyma
peripheral
cells,
including
neutrophils,
T
lymphocytes,
B
NK
monocytes
participate
regulation
immunity
which
expected
huge
future
immunotherapy.
Given
this
article
seeks
offer
comprehensive
overview
their
contributions
neuroinflammation
disease.
Understanding
these
neuroinflammatory
response
vital
for
developing
new
diagnostic
markers
therapeutic
targets
enhance
diagnosis
treatment
European journal of medical research,
Год журнала:
2024,
Номер
29(1)
Опубликована: Янв. 24, 2024
Abstract
Background
Alzheimer's
disease
is
one
common
type
of
dementia.
Numerous
studies
have
suggested
a
correlation
between
and
inflammation.
Microglia
mainly
participate
in
the
inflammatory
response
brain.
Currently,
ample
evidence
has
shown
that
microglia
are
closely
related
to
occurrence
development
disease.
Objective
We
opted
for
bibliometric
analysis
comprehensively
summarize
advancements
study
disease,
aiming
provide
researchers
with
current
trends
future
research
directions.
Methods
All
articles
reviews
pertaining
from
2000
2022
were
downloaded
through
Web
Science
Core
Collection.
The
results
subjected
using
VOSviewer
1.6.18
CiteSpace
6.1
R2.
Results
Overall,
7449
publications
included.
number
was
increasing
yearly.
United
States
published
most
publications.
Harvard
Medical
School
papers
all
institutions.
Journal
Alzheimer’s
Disease
o
f
Neuroscience
journals
commonly
cited,
respectively.
Mt
Heneka
author
highest
productivity
co-citation.
After
analysis,
keywords
neuroinflammation,
amyloid-beta,
inflammation,
neurodegeneration.
Gut
microbiota,
extracellular
vesicle,
dysfunction
meta-analysis
hotspots
at
present
stage
likely
continue.
Conclusion
NLRP3
inflammasome,
TREM2,
gut
mitochondrial
dysfunction,
exosomes
hotspots.
relationship
microglia-mediated
neuroinflammation
been
focus
trend
research.
Journal of Orthopaedic Surgery and Research,
Год журнала:
2024,
Номер
19(1)
Опубликована: Май 28, 2024
Sarcopenia
is
associated
with
increased
morbidity
and
mortality.
The
systemic
immune-inflammation
index
(SII)
has
been
correlated
to
a
variety
of
disorders.
present
study
conducted
systematic
review
meta-analysis
investigate
the
relationship
between
SII
sarcopenia.
Frontiers in Nutrition,
Год журнала:
2024,
Номер
11
Опубликована: Авг. 1, 2024
Catechins,
a
class
of
phytochemicals
found
in
various
fruits
and
tea
leaves,
have
garnered
attention
for
their
diverse
health-promoting
properties,
including
potential
combating
neurodegenerative
diseases.
Among
these
catechins,
(-)-epigallocatechin-3-gallate
(EGCG),
the
most
abundant
polyphenol
green
tea,
has
emerged
as
promising
therapeutic
agent
due
to
its
potent
antioxidant
anti-inflammatory
effects.
Chronic
neuroinflammation
oxidative
stress
are
key
pathological
mechanisms
diseases
such
Alzheimer's
disease
(AD)
Parkinson's
(PD).
EGCG
neuroprotective
efficacy
scavenging
free
radicals,
reducing
attenuating
neuroinflammatory
processes.
This
review
discusses
molecular
EGCG's
anti-oxidative
chronic
neuroinflammation,
emphasizing
effects
on
autoimmune
responses,
neuroimmune
system
interactions,
focusing
related
AD
PD.
By
elucidating
action
impact
processes,
this
underscores
intervention
AD,
PD,
possibly
other
Overall,
emerges
natural
compound
stress,
offering
novel
avenues
strategies
treatment
disorders.
Bioelectronic Medicine,
Год журнала:
2025,
Номер
11(1)
Опубликована: Янв. 20, 2025
Abstract
The
field
of
bioelectronic
medicine
has
advanced
rapidly
from
rudimentary
electrical
therapies
to
cutting-edge
closed-loop
systems
that
integrate
real-time
physiological
monitoring
with
adaptive
neuromodulation.
Early
innovations,
such
as
cardiac
pacemakers
and
deep
brain
stimulation,
paved
the
way
for
these
sophisticated
technologies.
This
review
traces
historical
technological
progression
medicine,
culminating
in
emerging
potential
devices
multiple
disorders
body.
We
emphasize
both
invasive
techniques,
implantable
brain,
spinal
cord
autonomic
regulation,
while
we
introduce
new
prospects
non-invasive
neuromodulation,
including
focused
ultrasound
newly
developed
neurography
enabling
precise
detection
titration
inflammatory
immune
responses.
case
neuromodulation
(incorporating
splenic
stimulation)
is
presented
through
its
applications
conditions
sepsis
chronic
inflammation,
illustrating
capacity
revolutionize
personalized
healthcare.
Today,
or
have
yet
be
dynamically
modulate
nervous
system
function
by
responding
molecular
signals;
it
represents
a
transformative
approach
therapeutic
interventions
major
opportunity
which
may
advance.
Knowledge
gaps
remain
likely
contribute
lack
available
closed
loop
systems,
namely,
(1)
significant
exogenous
endogenous
noise
must
filtered
out,
(2)
drift
signal
due
temporal
change
disease
severity
and/or
therapy
induced
neuroplasticity,
(3)
confounding
effects
(e.g.,
concurrent
medications
dysregulate
functions).
Leveraging
continuous
feedback
adjustments
overcome
many
barriers,
next
generation
stand
at
forefront
precision
offering
avenues
individualized
treatment.
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 18, 2025
Abstract
The
Cri
du
Chat
Syndrome
(CdCS),
a
devastating
genetic
disorder
caused
by
deletion
on
chromosome
5p,
faces
challenges
in
finding
effective
treatments
and
accurate
animal
models.
Using
CRISPR‐Cas9,
novel
CdCS
rat
model
with
2q22
is
developed,
mirroring
common
alteration
patients.
This
exhibits
pronounced
deficits
social
behavior,
cognition,
anxiety,
accompanied
neuronal
abnormalities
immune
dysregulation
key
brain
regions
such
as
the
hippocampus
medial
prefrontal
cortex
(mPFC).
immunostaining
RNA‐seq
analyses
provide
new
insights
into
pathogenesis,
revealing
inflammatory
processes.
Importantly,
it
demonstrated
that
early
gene
replacement
therapy
AAV‐
Ctnnd2
alleviates
cognitive
impairments
rats,
highlighting
potential
for
intervention.
However,
effectiveness
of
this
confined
to
developmental
stages
does
not
fully
restore
all
symptoms.
findings
deepen
understanding
pathogenesis
suggest
promising
therapeutic
directions.
Biomolecules,
Год журнала:
2023,
Номер
13(6), С. 967 - 967
Опубликована: Июнь 8, 2023
Alzheimer's
disease
(AD)
is
the
most
prevalent
kind
of
dementia
with
roughly
135
million
cases
expected
in
world
by
2050.
Unfortunately,
current
medications
for
treatment
AD
can
only
relieve
symptoms
but
they
do
not
act
as
disease-modifying
agents
that
stop
course
AD.
Caffeine
one
widely
used
drugs
today,
and
a
number
clinical
studies
suggest
drinking
coffee
may
be
good
health,
especially
fight
against
neurodegenerative
conditions
such
Experimental
works
conducted
"in
vivo"
vitro"
provide
intriguing
evidence
caffeine
exerts
its
neuroprotective
effects
antagonistically
binding
to
A2A
receptors
(A2ARs),
subset
GPCRs
are
triggered
endogenous
nucleoside
adenosine.
This
review
provides
summary
scientific
data
supporting
critical
role
A2ARs
play
memory
loss
cognitive
decline,
well
protective
benefits
neurodegeneration
attained
caffeine's
antagonistic
action
on
these
receptors.
They
novel
fascinating
target
regulating
enhancing
synaptic
activity,
achieving
symptomatic
potentially
effects,
protecting
neurodegeneration.
Life,
Год журнала:
2023,
Номер
13(7), С. 1466 - 1466
Опубликована: Июнь 28, 2023
Alzheimer’s
disease
(AD)
is
characterized
by
the
accumulation
of
specific
proteins
in
brain.
A
recent
study
revealed
that
manipulating
gut
microbiota
(GM)
significantly
reduced
tau
pathology
and
neurodegeneration
an
apolipoprotein
E
isoform-dependent
manner.
The
resilience
a
healthy
protects
it
from
variety
dysbiosis-related
pathologies.
Convincing
evidence
has
demonstrated
roles
GM
pathogenesis
AD,
which
are
partly
mediated
modified
microglial
activity
Therefore,
modulation
may
be
promising
therapeutic
option
for
AD
prevention.
In
addition
to
providing
cells
with
energy
affecting
maturation,
these
microbial
metabolites
appear
influence
neuronal
function.
One
potential
approaches
targeting
involve
using
probiotics.
Additionally,
human
its
have
also
become
targets
developing
interventions
prevention
disorders.
Synbiotics
postbiotics
can
used
treat
modulating
GM.
addition,
physical
activity,
exercise,
fitness
being
considered
as
nonpharmacological
therapies
reduce
signaling
pathways
related
neuroinflammation.
might
strategies
health
promotion.
Frontiers in Aging Neuroscience,
Год журнала:
2023,
Номер
15
Опубликована: Авг. 17, 2023
Article
purpose
The
clinical
approach
to
Alzheimer's
disease
(AD)
is
challenging,
particularly
in
high-functioning
individuals.
Accurate
diagnosis
crucial,
especially
given
the
significant
side
effects,
including
brain
hemorrhage,
of
newer
monoclonal
antibodies
approved
for
treating
earlier
stages
Alzheimer's.
Although
early
treatment
more
effective,
also
difficult.
Several
mimickers
AD
exist
either
separately,
or
conjunction
with
pathology,
adding
diagnostic
complexity.
To
illustrate
decision-making
process,
this
study
includes
de-identified
cases
and
reviews
underlying
etiology
pathology
available
therapies
exemplify
subtleties.
Problem
presentation
complex
varied.
Multiple
other
primary
pathologies
present
phenotypes
that
can
be
difficult
distinguish
from
AD.
Furthermore,
rarely
exists
isolation,
as
almost
all
patients
show
evidence
pathologies,
Lewy
body
argyrophilic
grain
disease.
phenotype
progression
vary
based
on
regions
affected
by
coexistence
severity
presence
systemic
comorbidities
such
cardiac
disease,
common
co-occurrence
psychiatric
diagnoses,
genetic
risk
factors.
Additionally,
symptoms
are
influenced
an
individual's
reserve
cognitive
reserve,
well
timing
diagnosis,
which
depends
demographics
both
patient
diagnosing
physician,
availability
biomarkers.
Methods
optimal
biomarker
strategy
accurately
AD,
neuropathologic
co-morbidities
mimickers,
medication
non-medication-based
treatments
discussed.
Real-life
examples
loss
process
illustrative
responses.
Implications
best
considered
a
syndromic
disorder,
multitude
environmental
characteristics.
existing
alone
unicorn,
there
nearly
always
coexisting
pathologies.
biomarkers
essential.
Treatment
response
variables
involved,
effective
its
prevention,
requires
individualized,
precision
medicine
strategy.
Antioxidants,
Год журнала:
2023,
Номер
12(8), С. 1564 - 1564
Опубликована: Авг. 4, 2023
Although
the
trigger
for
neurodegenerative
disease
process
is
unknown,
relevance
of
aging
stands
out
as
a
major
risk
development
neurodegeneration.
In
this
review,
we
highlighted
relationship
between
different
cellular
mechanisms
that
occur
consequence
and
transcription
factor
nuclear
erythroid-2-related
2
(NRF2)
connection
with
TAU
protein.
We
focused
on
NRF2
in
main
processes
involved
neurodegeneration
associated
aging,
such
genomic
instability,
protein
degradation
systems
(proteasomes/autophagy),
senescence,
stem
cell
exhaustion,
well
inflammation.
also
analyzed
effect
levels
its
aggregation
spread
process.
Finally,
investigated
interconnection
alterations
signaling
pathway
both
primary
secondary
tauopathies.
All
these
points
highlight
possible
therapeutic
target