Neurodegenerative
diseases
are
age-related
disorders
characterized
by
the
cerebral
accumulation
of
amyloidogenic
proteins,
and
cellular
senescence
underlies
their
pathogenesis.
Thus,
it
is
necessary
for
preventing
these
to
remove
toxic
repair
damaged
neurons,
suppress
senescence.
As
a
source
such
prophylactic
agents,
we
selected
zizyphi
spinosi
semen
(ZSS),
medicinal
herb
used
in
traditional
Chinese
medicine.
Oral
administration
ZSS
hot
water
extract
ameliorated
Aβ
tau
pathology
cognitive
impairment
mouse
models
Alzheimer's
disease
frontotemporal
dementia.
Non-extracted
simple
crush
powder
showed
stronger
effects
than
improved
α-synuclein
cognitive/motor
function
Parkinson's
model
mice.
Furthermore,
when
administered
normal
aged
mice,
suppressed
senescence,
reduced
DNA
oxidation,
promoted
brain-derived
neurotrophic
factor
expression
neurogenesis,
enhanced
cognition
levels
similar
those
young
The
quantity
known
active
ingredients
ZSS,
jujuboside
A,
B,
spinosin
was
not
proportional
nootropic
activity
ZSS.
These
results
suggest
that
promising
dietary
material
prevention
neurodegenerative
brain
aging.
Journal of Internal Medicine,
Год журнала:
2024,
Номер
295(5), С. 599 - 619
Опубликована: Март 6, 2024
Abstract
The
older
population
is
increasing
worldwide,
and
life
expectancy
continuously
rising,
predominantly
thanks
to
medical
technological
progress.
Healthspan
refers
the
number
of
years
an
individual
can
live
in
good
health.
From
a
gerontological
viewpoint,
mission
extend
spent
health,
promoting
well‐being
minimizing
impact
aging‐related
diseases
slow
aging
process.
Biologically,
malleable
process
characterized
by
intra‐
inter‐individual
heterogeneous
dynamic
balance
between
accumulating
damage
repair
mechanisms.
Cellular
senescence
key
component
this
process,
with
senescent
cells
different
tissues
organs,
leading
age‐related
disease
susceptibility
over
time.
Removing
from
body
or
slowing
down
burden
rate
has
been
proposed
as
efficient
way
reduce
age‐dependent
deterioration.
In
animal
models,
senotherapeutic
molecules
lifespan
either
senolytic
senomorphic
activity.
Much
research
shows
that
dietary
physical
activity‐driven
lifestyle
interventions
protect
against
senescence.
This
narrative
review
aims
summarize
current
knowledge
on
targeting
risk
models
their
translational
potential
for
humans.
We
focused
studies
have
examined
role
senotherapeutics
modifying
burdens.
concludes
general
discussion
mechanisms
underlying
unique
trajectory
its
implications
future
research.
Frontiers in Cellular Neuroscience,
Год журнала:
2024,
Номер
18
Опубликована: Июль 9, 2024
In
2013,
M.
Lancaster
described
the
first
protocol
to
obtain
human
brain
organoids.
These
organoids,
usually
generated
from
human-induced
pluripotent
stem
cells,
can
mimic
three-dimensional
structure
of
brain.
While
they
recapitulate
salient
developmental
stages
brain,
their
use
investigate
onset
and
mechanisms
neurodegenerative
diseases
still
faces
crucial
limitations.
this
review,
we
aim
highlight
these
limitations,
which
hinder
organoids
becoming
reliable
models
study
such
as
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
amyotrophic
lateral
sclerosis
(ALS).
Specifically,
will
describe
structural
biological
impediments,
including
lack
an
aging
footprint,
angiogenesis,
myelination,
inclusion
functional
immunocompetent
microglia—all
important
factors
in
neurodegeneration
AD,
PD,
ALS.
Additionally,
discuss
technical
limitations
for
monitoring
microanatomy
electrophysiology
parallel,
propose
solutions
overcome
current
thereby
making
a
more
tool
model
neurodegeneration.
Abstract
Neuroinflammation
is
closely
linked
to
aging,
which
damages
the
structure
and
function
of
brain.
It
caused
by
intricate
interactions
immune
cells
in
aged
brain,
such
as
dysregulated
glial
dysfunctional
astrocytes.
Aging-associated
chronic
low
inflammation,
referred
neuroinflammaging,
shows
an
upregulated
proinflammatory
response.
Autophagy
senescence
play
crucial
roles
moderators
aging
neuroinflammatory
responses.
The
neuroimmune
system,
dystrophic
cells,
release
factors
alter
blood-brain
barrier,
causing
a
landscape.
Chronic
inflammation
combined
with
deteriorating
neurons
exacerbate
neurological
disorders
decline
cognitive
function.
This
review
highlights
neuroinflammaging
mechanism
associated
interplay
central
nervous
system
cellular
senescence,
autophagy
regulation
brain's
under
conditions.
Moreover,
microglia
peripheral
process
brain
have
also
been
discussed.
Determining
treatment
targets
comprehending
mechanisms
that
influence
necessary
decrease
neuroinflammation.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(19), С. 10757 - 10757
Опубликована: Окт. 6, 2024
With
the
aging
of
global
population,
neurodegenerative
diseases
are
emerging
as
a
major
public
health
issue.
The
adoption
less
sedentary
lifestyle
has
been
shown
to
have
beneficial
effect
on
cognitive
decline,
but
molecular
mechanisms
responsible
clear.
Here
we
provide
detailed
analysis
complex
molecular,
cellular,
and
systemic
underlying
age-related
decline
how
choices
influence
these
processes.
A
review
evidence
from
animal
models,
human
studies,
postmortem
analyses
emphasizes
importance
integrating
physical
exercise
with
cognitive,
multisensory,
motor
stimulation
part
multifaceted
approach
mitigating
decline.
We
highlight
potential
non-pharmacological
interventions
address
key
hallmarks,
such
genomic
instability,
telomere
attrition,
neuroinflammation,
underscore
need
for
comprehensive
personalized
strategies
promote
resilience
healthy
aging.
Diabetic Medicine,
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 5, 2024
Abstract
Aim
Among
people
with
diabetes
those
chronic
kidney
disease
(CKD)
have
a
reduced
life
expectancy
increased
risk
of
cardiovascular
(CVD)
major
contributor
to
morbidity
and
mortality.
CKD
related
is
growing
worldwide
one
the
leading
causes
failure
globally.
Diabetes
associated
accelerated
vascular
ageing
mechanisms
mediators
that
drive
progression
CVD
in
may
help
provide
insights
into
pathophysiology
cardio‐renal
complications
guide
treatment
interventions
diabetes.
Methods
We
conducted
narrative
review
literature
using
PubMed
for
English
language
articles
contained
keywords
diabetes,
or
diabetic
disease,
ageing,
cellular
senescence,
arterial
stiffness,
Klotho
sirtuins,
sodium‐glucose
co‐transporter‐2
(SGLT‐2)
inhibitors,
renin
angiotensin
aldosterone
system
(RAAS)
glucagon‐like
peptide‐1
(GLP‐1)
receptor
agonists.
Results
Progressive
driven
part
by
multiple
processes
such
as
inflammation,
oxidative
stress
circulating
uremic
toxins.
This
phenotype
contributes
endothelial
dysfunction,
cognitive
decline
muscle
wasting,
thereby
elevating
mortality
individuals
CKD.
Deficiency
kidney‐derived
anti‐ageing
hormone
sirtuin
levels
play
pivotal
roles
these
pathways.
Dietary,
lifestyle
pharmacological
targeting
reduce
The
current
standard
care
pillars
RAAS
SGLT‐2
inhibitors
GLP‐1
agonists
all
influence
pathways
involved
ageing.
Conclusions
A
multifactorial
intervention
prevent
development
traditional
factors
well
novel
agents
beneficial
effects
can
extend
lifespan
Brain Sciences,
Год журнала:
2024,
Номер
14(11), С. 1101 - 1101
Опубликована: Окт. 30, 2024
Obesity,
type
2
diabetes
(T2D),
and
Alzheimer's
disease
(AD)
are
pathologies
that
affect
millions
of
people
worldwide.
They
have
no
effective
therapy
difficult
to
prevent
control
when
they
develop.
It
has
been
known
for
many
years
these
diseases
pathogenic
aspects
in
common.
We
highlight
this
review
neuroglial
cells
(astroglia,
oligodendroglia,
microglia)
play
a
vital
role
the
origin,
clinical-pathological
development,
course
brain
neurodegeneration.
Moreover,
we
include
new
results
T2D-AD
mouse
model
(APP+PS1
mice
on
high-calorie
diet)
investigating.
