The Indissociable Triad: Vascular Impairment, Muscle Atrophy, and Cognitive Decline
Enzo Pereira de Lima,
No information about this author
Masaru Tanaka,
No information about this author
Caroline Barbalho Lamas
No information about this author
et al.
Published: Aug. 12, 2024
The
triad
of
vascular
impairment,
muscle
atrophy,
and
cognitive
decline
represents
critical
age-related
conditions
that
significantly
impact
health.
Vascular
impairment
disrupts
blood
flow,
precipitating
mass
reduction
seen
in
sarcopenia
the
neuronal
functions
characteristic
neurodegeneration.
Our
limited
understanding
intricate
relationships
within
this
hinders
accurate
diagnosis
effective
treatment
strategies.
This
review
ana-lyzes
interrelated
mechanisms
contribute
to
these
conditions,
with
a
specific
focus
on
ox-idative
stress,
chronic
inflammation,
impaired
nutrient
delivery.
aim
is
understand
common
pathways
involved
suggest
comprehensive
therapeutic
approaches.
dysfunctions
hinder
circulation
transportation
nutrients,
resulting
sar-copenia
characterized
by
atrophy
weakness.
dysfunction
have
negative
physical
function
quality
life.
Neurodegenerative
diseases
exhibit
comparable
pathophysiological
affect
motor
functions.
Preventive
approaches
encompass
lifestyle
adjustments,
addressing
oxidative
in-flammation,
integrated
therapies
improving
muscular
well-being.
Better
links
can
refine
strategies
yield
better
patient
out-comes.
study
emphasizes
complex
interplay
between
dysfunction,
de-generation,
decline,
highlighting
necessity
for
multidisciplinary
ap-proaches.
Advances
domain
promise
improved
diagnostic
accuracy,
more
thera-peutic
options,
enhanced
preventive
measures,
all
contributing
higher
life
elderly
population.
Language: Английский
Current evidence of synaptic dysfunction after stroke: Cellular and molecular mechanisms
Chuan Li,
No information about this author
Min Jiang,
No information about this author
Zhi‐Ting Fang
No information about this author
et al.
CNS Neuroscience & Therapeutics,
Journal Year:
2024,
Volume and Issue:
30(5)
Published: May 1, 2024
Stroke
is
an
acute
cerebrovascular
disease
in
which
brain
tissue
damaged
due
to
sudden
obstruction
of
blood
flow
the
or
rupture
vessels
brain,
can
prompt
ischemic
hemorrhagic
stroke.
After
stroke
onset,
ischemia,
hypoxia,
infiltration
components
into
parenchyma,
and
lysed
cell
fragments,
among
other
factors,
invariably
increase
blood-brain
barrier
(BBB)
permeability,
inflammatory
response,
edema.
These
changes
lead
neuronal
death
synaptic
dysfunction,
latter
poses
a
significant
challenge
treatment.
Language: Английский
Vascular Impairment, Muscle Atrophy, and Cognitive Decline: Critical Age-Related Conditions
Enzo Pereira de Lima,
No information about this author
Masaru Tanaka,
No information about this author
Caroline Barbalho Lamas
No information about this author
et al.
Biomedicines,
Journal Year:
2024,
Volume and Issue:
12(9), P. 2096 - 2096
Published: Sept. 13, 2024
The
triad
of
vascular
impairment,
muscle
atrophy,
and
cognitive
decline
represents
critical
age-related
conditions
that
significantly
impact
health.
Vascular
impairment
disrupts
blood
flow,
precipitating
the
mass
reduction
seen
in
sarcopenia
neuronal
function
characteristic
neurodegeneration.
Our
limited
understanding
intricate
relationships
within
this
hinders
accurate
diagnosis
effective
treatment
strategies.
This
review
analyzes
interrelated
mechanisms
contribute
to
these
conditions,
with
a
specific
focus
on
oxidative
stress,
chronic
inflammation,
impaired
nutrient
delivery.
aim
is
understand
common
pathways
involved
suggest
comprehensive
therapeutic
approaches.
dysfunctions
hinder
circulation
transportation
nutrients,
resulting
characterized
by
atrophy
weakness.
dysfunction
have
negative
physical
quality
life.
Neurodegenerative
diseases
exhibit
comparable
pathophysiological
affect
motor
functions.
Preventive
approaches
encompass
lifestyle
adjustments,
addressing
integrated
therapies
improving
muscular
well-being.
Better
links
can
refine
strategies
yield
better
patient
outcomes.
study
emphasizes
complex
interplay
between
dysfunction,
degeneration,
decline,
highlighting
necessity
for
multidisciplinary
Advances
domain
promise
improved
diagnostic
accuracy,
more
options,
enhanced
preventive
measures,
all
contributing
higher
life
elderly
population.
Language: Английский
ATP11C as a key regulator of neuronal loss following intracerebral hemorrhage in mice
Peng Lü,
No information about this author
Zilan Wang,
No information about this author
Qing Sun
No information about this author
et al.
Biochemical and Biophysical Research Communications,
Journal Year:
2025,
Volume and Issue:
756, P. 151531 - 151531
Published: March 5, 2025
Language: Английский
Interleukin-1 Receptor-Associated Kinase-3 Aggravates Neuroinflammatory Injury After Intracerebral Hemorrhage via Activation NF-κB/IL-17A Pathway in Mice
Journal of Inflammation Research,
Journal Year:
2025,
Volume and Issue:
Volume 18, P. 1167 - 1189
Published: Jan. 1, 2025
Neuroinflammatory
reactions
are
crucial
factors
in
secondary
brain
damage
following
intracerebral
hemorrhage
(ICH).
Although
previous
studies
have
shown
that
IRAK3
is
involved
immune
responses,
the
potential
effects
of
on
ICH
remain
unclear.
Collagenase
IV-induced
mouse
model.
Western
blotting
was
used
to
determine
expression
at
different
time
points
ICH.
Immunofluorescence
investigate
cellular
localization
IRAK3.
The
model
treated
with
recombinant
human
(rh-IRAK3)
or
siRNA
via
an
intracerebroventricular
injection.
effect
mice
assessed
by
and
short-term
long-term
neurological
function
evaluation.
RNA-seq
performed
explore
mechanism
which
promotes
inflammation
after
mechanisms
neuroinflammation
will
be
further
investigated
blotting,
qRT-PCR
immunofluorescence.
Recombinant
IL-17A
connection
between
NF-κB/IL-17A
signaling
pathway
vivo
vitro
experiments.
increased,
peaking
24
h,
followed
a
subsequent
decrease
mainly
expressed
microglia.
analysis
revealed
1,797
differentially
genes
around
perihematomal
tissue
treatment,
multiple
inflammatory
pathways
being
downregulated.
Rh-IRAK3
treatment
resulted
upregulation
levels
cytokines
exacerbated
deficits.
Furthermore,
markedly
decreased
microglial
activation
pathway.
response
vitro;
however,
knockdown
reversed
this
process.
aggravates
activating
pathway,
thereby
exacerbating
deficits
Therefore,
inhibition
may
promising
approach
for
treating
Language: Английский
Advancements in the investigation of gut microbiota-based strategies for stroke prevention and treatment
Min Wang,
No information about this author
Yan Liu,
No information about this author
Li Zhong
No information about this author
et al.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 4, 2025
Stroke
represents
a
predominant
cause
of
mortality
and
disability
on
global
scale,
impacting
millions
annually
exerting
considerable
strain
healthcare
systems.
The
incidence
stroke
exhibits
regional
variability,
with
ischemic
accounting
for
the
majority
occurrences.
Post-stroke
complications,
such
as
cognitive
impairment,
motor
dysfunction,
recurrent
stroke,
profoundly
affect
patients’
quality
life.
Recent
advancements
have
elucidated
microbiota-gut-brain
axis
(MGBA),
underscoring
complex
interplay
between
gut
health
brain
function.
Dysbiosis,
characterized
by
an
imbalance
in
microbiota,
is
significantly
linked
to
elevated
risk
unfavorable
outcomes.
MGBA
plays
crucial
role
modulating
immune
function,
neurotransmitter
levels,
metabolic
byproducts,
which
may
intensify
neuroinflammation
impair
cerebral
health.
This
review
elucidates
pathophysiology
explores
potential
gut-targeted
therapeutic
strategies
reduce
promote
recovery,
including
probiotics,
prebiotics,
pharmacological
interventions,
dietary
modifications.
However,
current
prevention
treatment
based
intestinal
flora
still
face
many
problems,
large
difference
individual
flora,
stability
efficacy,
long-term
safety
need
be
considered.
Further
research
needs
strengthened
its
better
application
clinical
practice.
Language: Английский
Melatonin Promotes Cerebral Angiogenesis in Ischemic Mice via BMP6/Smad1/5/9 Pathway
Linlin Li,
No information about this author
Yujia Yuan,
No information about this author
Cong Zhang
No information about this author
et al.
Molecular Neurobiology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 25, 2025
Angiogenesis
facilitates
the
reinstatement
of
blood
supply
to
cerebral
tissues
after
stroke
by
reconstructing
vascular
network,
thereby
rescuing
penumbra
region
and
restoring
neural
functions.
Melatonin
can
modulate
angiogenesis
under
a
variety
biological
disease-related
states,
bone
morphogenetic
protein
6
(BMP6)
targets
regulators
associated
with
angiogenesis.
The
specific
functions
melatonin
BMP6
in
following
infarction,
along
potential
intrinsic
regulatory
interactions
between
them,
are
currently
unclear
need
further
investigation.
was
given
mice
from
1st
day
through
28th
post
permanent
distal
middle
artery
occlusion
(dMCAO).
Our
research
revealed
that
enhanced
neurological
performance
decreased
size
brain
infarction.
Additionally,
it
boosted
circulation
fostered
area.
Meanwhile,
facilitated
endothelial
cells
migration
tube
formation
oxygen-glucose
deprivation
(OGD).
promoted
expression
its
downstream
targets,
Smad1/5/9,
as
well
factors
Vascular
Endothelial
Growth
Factor
(VEGF)
Angiopoietin-1
(Ang1)
vivo
vitro,
which
counteracted
or
partially
inhibited
suppression
expression.
provides
strong
evidence
promotes
infarction
BMP6/Smad1/5/9
signaling
pathway,
supporting
restoration
function.
Language: Английский
Dual role for pannexin 1 at synapses: regulating functional and morphological plasticity
The Journal of Physiology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 12, 2024
Abstract
Pannexin
1
(PANX1)
is
an
ion
and
metabolite
membrane
channel
scaffold
protein
enriched
in
synaptic
compartments
of
neurons
the
central
nervous
system.
In
addition
to
a
well‐established
link
between
PANX1
plasticity,
we
recently
identified
role
for
regulation
dendritic
spine
stability.
Notably,
its
interacting
proteins
are
linked
neurological
conditions
involving
loss.
Understanding
dual
function
morphology
may
help
shed
light
on
these
links.
We
explore
potential
mechanisms,
including
PANX1's
interactions
with
postsynaptic
receptors
cytoskeleton
regulating
proteins.
Finally,
contextualize
within
diseases
synapse
dysfunction.
image
Language: Английский
Prognostic serum biomarkers of synaptic, neuronal and glial injury in patients with acute ischemic stroke of the anterior circulation
European Journal of Neurology,
Journal Year:
2024,
Volume and Issue:
32(1)
Published: Dec. 23, 2024
Abstract
Background
We
aimed
to
investigate
the
prognostic
role
of
β‐synuclein
in
comparison
that
neurofilament
light
chain
(NfL)
and
glial
fibrillary
acidic
protein
(GFAP)
for
predicting
functional
outcome
after
acute
ischemic
stroke
(AIS).
Methods
measured
serum
concentrations
β‐synuclein,
NfL
GFAP
24
h
hospital
admission
213
consecutive
patients
with
moderate‐to‐severe
AIS.
investigated
association
between
biomarkers
radiological/clinical
characteristics,
3‐months
mortality
on
modified
Rankin
Scale
(mRS).
Results
In
AIS
[mean
age:
76.1
(±12.5)
years,
53.1%
males,
median
NIHSS
score
admission:
13
(IQR:
9–17)],
higher
levels
were
associated
scores
lower
Alberta
Stroke
Program
CT
Score
(ASPECTS)
points
admission.
Serum
was
significantly
correlated
(rho
=
0.715,
p
<
0.001)
0.684,
0.001).
The
inclusion
improved
accuracy
prediction
models
without
overall
(AUC:
0.836
vs.
0.752,
mRS
3–6
0–2
0.812
0.624,
Combination
and/or
showed
a
similar
accuracy.
Conclusions
may
be
used
assess
synaptic
damage/dysfunction
predict
clinical
outcomes
Language: Английский