Diabetes,
Journal Year:
2024,
Volume and Issue:
73(9), P. 1513 - 1526
Published: June 13, 2024
Diabetic
encephalopathy
(DE)
is
a
severe
complication
of
the
central
nervous
system
associated
with
diabetes.
In
this
study,
we
investigated
regulatory
role
mammalian
target
rapamycin
(mTOR)
on
nuclear
factor
κB
(NF-κB)
in
mice
DE,
and
neuroprotective
effect
therapeutic
mechanisms
luteolin,
natural
flavonoid
compound
anti-inflammatory,
antioxidant,
properties.
The
results
indicated
that
treatment
luteolin
improved
degree
cognitive
impairment
DE.
It
also
decreased
levels
phosphorylated
mTOR,
NF-κB,
histone
deacetylase
2
(HDAC2)
increased
expression
brain-derived
neurotrophic
synaptic-related
proteins.
Furthermore,
protein-protein
interaction
Gene
Ontology
analysis
revealed
was
involved
network
HDAC2
through
mTOR/NF-κB
signaling
cascade.
Our
bioinformatics
molecular
docking
may
directly
HDAC2,
as
an
inhibitor,
to
alleviate
complementing
inhibition.
Analysis
luteolin's
proteins
their
interactions
suggest
cognition.
conclusion,
tau
hyperphosphorylation
are
regulated
by
cascade
found
reverse
these
effects,
demonstrating
its
protective
Current Neurovascular Research,
Journal Year:
2023,
Volume and Issue:
20(3), P. 314 - 333
Published: July 25, 2023
Disorders
of
metabolism
affect
multiple
systems
throughout
the
body
but
may
have
greatest
impact
on
both
central
and
peripheral
nervous
systems.
Currently
available
treatments
behavior
changes
for
disorders
that
include
diabetes
mellitus
(DM)
system
diseases
are
limited
cannot
reverse
disease
burden.
Greater
access
to
healthcare
a
longer
lifespan
led
an
increased
prevalence
metabolic
neurodegenerative
disorders.
In
light
these
challenges,
innovative
studies
into
underlying
pathways
offer
new
treatment
perspectives
Alzheimer's
Disease,
Parkinson's
Huntington's
Disease.
Metabolic
intimately
tied
can
lead
debilitating
outcomes,
such
as
multi-nervous
disease,
susceptibility
viral
pathogens,
long-term
cognitive
disability.
Novel
strategies
robustly
address
involve
careful
consideration
cellular
metabolism,
programmed
cell
death
pathways,
mechanistic
target
rapamycin
(mTOR)
its
associated
mTOR
Complex
1
(mTORC1),
2
(mTORC2),
AMP-activated
protein
kinase
(AMPK),
growth
factor
signaling,
risk
factors
apolipoprotein
E
(APOE-ε4)
gene.
Yet,
complex
necessitate
comprehensive
understanding
achieve
clinical
outcomes
susceptibility,
onset,
progression.
Neuroscience & Biobehavioral Reviews,
Journal Year:
2024,
Volume and Issue:
162, P. 105724 - 105724
Published: May 16, 2024
Alzheimer's
disease
(AD)
is
prevalent
around
the
world,
yet
our
understanding
of
still
very
limited.
Recent
work
suggests
that
cornerstone
AD
may
include
inflammation
accompanies
it.
Failure
a
normal
pro-inflammatory
immune
response
to
resolve
lead
persistent
central
contributes
unsuccessful
clearance
amyloid-beta
plaques
as
they
form,
neuronal
death,
and
ultimately
cognitive
decline.
Individual
metabolic,
dietary
(lipid)
profiles
can
differentially
regulate
this
inflammatory
process
with
aging,
obesity,
poor
diet,
early
life
stress
other
factors
contributing
greater
risk
developing
AD.
Here,
we
integrate
evidence
for
interface
between
these
factors,
how
contribute
brain
milieu.
In
particular,
discuss
importance
appropriate
polyunsaturated
fatty
acids
(PUFA)
in
diet
metabolism
specialised
pro-resolving
mediators
(SPMs);
raising
possibility
strategies
improve
outlook.
Signal Transduction and Targeted Therapy,
Journal Year:
2025,
Volume and Issue:
10(1)
Published: March 10, 2025
Abstract
In
the
context
of
global
ageing,
prevalence
neurodegenerative
diseases
and
dementia,
such
as
Alzheimer’s
disease
(AD),
is
increasing.
However,
current
symptomatic
disease-modifying
therapies
have
achieved
limited
benefits
for
in
clinical
settings.
Halting
progress
neurodegeneration
cognitive
decline
or
even
improving
impaired
cognition
function
are
clinically
meaningful
goals
treatments
diseases.
Ageing
primary
risk
factor
their
associated
comorbidities,
vascular
pathologies,
elderly
individuals.
Thus,
we
aim
to
elucidate
role
ageing
from
perspective
a
complex
system,
which
brain
core
peripheral
organs
tissues
form
holistic
network
support
functions.
During
progressive
deterioration
structure
entire
body
hampers
its
active
adaptive
responses
various
stimuli,
thereby
rendering
individuals
more
vulnerable
Consequently,
propose
that
prevention
treatment
should
be
grounded
antiageing
rejuvenation
means
complemented
by
interventions
targeting
disease-specific
pathogenic
events.
This
integrated
approach
promising
strategy
effectively
prevent,
pause
slow
down
progression
Alzheimer s & Dementia,
Journal Year:
2023,
Volume and Issue:
20(2), P. 1334 - 1349
Published: Nov. 20, 2023
Abstract
INTRODUCTION
The
molecular
mechanisms
that
contribute
to
sex
differences,
in
particular
female
predominance,
Alzheimer's
disease
(AD)
prevalence,
symptomology,
and
pathology,
are
incompletely
understood.
METHODS
To
address
this
problem,
we
investigated
cellular
metabolism
immune
responses
(“immunometabolism
endophenotype”)
across
AD
individuals
as
a
function
of
with
diverse
clinical
diagnosis
cognitive
status
at
death
(cogdx),
Braak
staging,
Consortium
Establish
Registry
for
(CERAD)
scores
using
human
cortex
metabolomics
transcriptomics
data
from
the
Religious
Orders
Study
/
Memory
Aging
Project
(ROSMAP)
cohort.
RESULTS
We
identified
sex‐specific
metabolites,
metabolic
genes,
pathways
associated
progression.
female‐specific
elevation
glycerophosphorylcholine
N‐acetylglutamate,
which
inflammatory
metabolites
involved
interleukin
(IL)‐17
signaling,
C‐type
lectin
receptor,
interferon
Toll‐like
receptor
pathways.
pinpointed
distinct
microglia‐specific
immunometabolism
endophenotypes
(i.e.,
lipid‐
amino
acid‐specific
IL‐10
IL‐17
signaling
pathways)
between
male
subjects.
In
addition,
subjects
showed
evidence
diminished
excitatory
neuron
microglia
communications
via
glutamate‐mediated
immunometabolism.
DISCUSSION
Our
results
point
new
understanding
basis
predominance
AD,
warrant
future
independent
validations
ethnically
patient
cohorts
establish
likely
causal
relationship
microglial
differences
AD.
Highlights
Sex‐specific
gene
networks
pathways,
pathogenesis
Female
exhibit
characterized
by
decreased
glutamate
elevated
interleukin‐10
pathway
activity.
shift
cell‐cell
neurons
astrocyte.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(7), P. 3866 - 3866
Published: March 30, 2024
For
much
of
human
evolution,
the
average
lifespan
was
<40
years,
due
in
part
to
disease,
infant
mortality,
predators,
food
insecurity,
and,
for
females,
complications
childbirth.
Thus,
many
females
did
not
reach
age
menopause
(45–50
years
age)
and
it
is
mainly
past
several
hundred
that
has
been
extended
>75
primarily
public
health
advances,
medical
interventions,
antibiotics,
nutrition.
Therefore,
underlying
biological
mechanisms
responsible
disease
risk
following
must
have
evolved
during
complex
processes
leading
Homo
sapiens
serve
functions
pre-menopausal
state.
Furthermore,
as
a
primary
function
survival
species
effective
reproduction,
likely
most
advantages
having
such
post-menopausal
risks
relate
reproduction
ability
address
environmental
stresses.
This
opinion/perspective
will
be
discussed
context
how
could
enhance
with
improved
offspring,
perhaps
why
are
preserved.
Not
all
exhibit
this
set
diseases,
those
who
do
develop
diseases
conditions.
The
state
operate
unified
complex,
but
independent
variables,
potential
some
overlap.
there
would
heterogeneity
if
factors
essential
reproductive
also
concept
sets
reversible
epigenetic
changes
associated
puberty,
pregnancy,
lactation
offered
explain
observations
regarding
distribution
conditions
their
roles
reproduction.
While
involvement
an
system
dynamic
“modification-demodification-remodification”
paradigm
contributing
hypothesis
at
point,
validation
lead
better
understanding
commonalities
may
future
interventions
control
after
menopause.
Cell Biochemistry and Function,
Journal Year:
2024,
Volume and Issue:
42(8)
Published: Dec. 1, 2024
Alzheimer's
disease
(AD),
one
of
the
most
prevalent
neurodegenerative
responsible
for
60%-80%
dementia
cases
globally.
The
is
more
among
elder
females.
Female
reproductive
hormones
are
found
to
be
essential
cellular
activities
in
brain.
physiological
role
neurotrophins
and
sex
hippocampal
region
during
neurogenesis
neuron
differentiation
was
studied
as
well.
In
addition
triggering
pathways,
estrogen
progesterone
carry
out
a
number
biological
processes
that
lead
neuroprotection.
They
might
have
an
impact
on
learning
memory.
One
estrogen's
modest
antioxidant
properties
its
direct
scavenging
free
radicals.
neurotrophic
effect
can
explained
by
their
ability
rise
expression
brain-derived
factor
(BDNF)
mRNA.
Additionally,
they
degrade
beta-amyloid
stop
inflammation,
apoptotic
neuronal
cell
death,
tau
protein
phosphorylation.
To
enhance
neuroprotective
action,
various
cross-talking
pathways
cells
mediated
estrogen,
progesterone,
BDNF
receptors.
This
include
signaling
mitogen-activated
kinase/extracellular
regulated
kinase,
phosphatidylinositol
3-kinase/protein
kinase
B,
phospholipase/protein
C.
Clinical
research
establish
significance
these
substances
fragmented,
despite
publications
claiming
lower
prevalence
AD
when
medication
started
before
menopause.
review
article
emphasizes
update
AD.
