Ageing Research Reviews,
Год журнала:
2021,
Номер
72, С. 101464 - 101464
Опубликована: Сен. 20, 2021
Alzheimer's
disease
(AD)
is
a
complex
neurodegenerative
in
the
elderly
and
most
common
cause
of
human
dementia.
AD
characterized
by
accumulation
abnormal
protein
aggregates
including
amyloid
plaques
(composed
beta-amyloid
(Aβ)
peptides)
neurofibrillary
tangles
(formed
hyper-phosphorylated
tau
protein).
Synaptic
plasticity,
neuroinflammation,
calcium
signaling
etc.
also
show
dysfunction
patients.
Autophagy
an
evolutionarily
conserved
lysosome-dependent
cellular
event
eukaryotes.
It
closely
linked
to
modulation
metabolism,
through
which
damaged
organelles
mis-folded
proteins
are
degraded
then
recycled
maintain
homeostasis.
Accumulating
evidence
has
shown
that
impaired
autophagy
contributes
pathogenesis.
In
present
review,
we
highlight
role
autophagy,
bulk
selective
regulating
metabolic
circuits
We
discuss
potential
future
perspectives
autophagy-inducing
strategies
therapeutics.
Molecular Neurodegeneration,
Год журнала:
2020,
Номер
15(1)
Опубликована: Май 29, 2020
Abstract
Alzheimer’s
disease
(AD)
is
one
of
the
most
prevalent
neurodegenerative
diseases,
characterized
by
impaired
cognitive
function
due
to
progressive
loss
neurons
in
brain.
Under
microscope,
neuronal
accumulation
abnormal
tau
proteins
and
amyloid
plaques
are
two
pathological
hallmarks
affected
brain
regions.
Although
detailed
mechanism
pathogenesis
AD
still
elusive,
a
large
body
evidence
suggests
that
damaged
mitochondria
likely
play
fundamental
roles
AD.
It
believed
healthy
pool
not
only
supports
activity
providing
enough
energy
supply
other
related
mitochondrial
functions
neurons,
but
also
guards
minimizing
oxidative
damage.
In
this
regard,
exploration
multitude
mechanisms
altered
constitutes
novel
promising
therapeutic
targets
for
disease.
review,
we
will
summarize
recent
progress
underscores
essential
role
dysfunction
discuss
underlying
with
focus
on
structural
functional
integrity
including
biogenesis
dynamics,
axonal
transport,
ER-mitochondria
interaction,
mitophagy
proteostasis.
Signal Transduction and Targeted Therapy,
Год журнала:
2022,
Номер
7(1)
Опубликована: Дек. 16, 2022
Aging
is
a
gradual
and
irreversible
pathophysiological
process.
It
presents
with
declines
in
tissue
cell
functions
significant
increases
the
risks
of
various
aging-related
diseases,
including
neurodegenerative
cardiovascular
metabolic
musculoskeletal
immune
system
diseases.
Although
development
modern
medicine
has
promoted
human
health
greatly
extended
life
expectancy,
aging
society,
variety
chronic
diseases
have
gradually
become
most
important
causes
disability
death
elderly
individuals.
Current
research
on
focuses
elucidating
how
endogenous
exogenous
stresses
(such
as
genomic
instability,
telomere
dysfunction,
epigenetic
alterations,
loss
proteostasis,
compromise
autophagy,
mitochondrial
cellular
senescence,
stem
exhaustion,
altered
intercellular
communication,
deregulated
nutrient
sensing)
participate
regulation
aging.
Furthermore,
thorough
pathogenesis
to
identify
interventions
that
promote
longevity
caloric
restriction,
microbiota
transplantation,
nutritional
intervention)
clinical
treatment
methods
for
(depletion
senescent
cells,
therapy,
antioxidative
anti-inflammatory
treatments,
hormone
replacement
therapy)
could
decrease
incidence
turn
healthy
longevity.
Molecular Neurodegeneration,
Год журнала:
2020,
Номер
15(1)
Опубликована: Июль 16, 2020
Abstract
Alzheimer’s
disease
(AD)
is
the
most
common
neurodegenerative
disorder
seen
in
age-dependent
dementia.
There
currently
no
effective
treatment
for
AD,
which
may
be
attributed
part
to
lack
of
a
clear
underlying
mechanism.
Studies
within
last
few
decades
provide
growing
evidence
central
role
amyloid
β
(Aβ)
and
tau,
as
well
glial
contributions
various
molecular
cellular
pathways
AD
pathogenesis.
Herein,
we
review
recent
progress
with
respect
Aβ-
tau-associated
mechanisms,
discuss
dysfunction
emphasis
on
neuronal
receptors
that
mediate
Aβ-induced
toxicity.
We
also
other
critical
factors
affect
pathogenesis,
including
genetics,
aging,
variables
related
environment,
lifestyle
habits,
describe
potential
apolipoprotein
E
(APOE),
viral
bacterial
infection,
sleep,
microbiota.
Although
have
gained
much
towards
understanding
aspects
this
devastating
disorder,
greater
commitment
research
mechanism,
diagnostics
will
needed
future
research.
Signal Transduction and Targeted Therapy,
Год журнала:
2019,
Номер
4(1)
Опубликована: Авг. 23, 2019
Abstract
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
characterized
by
progressive
memory
loss
along
with
neuropsychiatric
symptoms
and
decline
in
activities
of
daily
life.
Its
main
pathological
features
are
cerebral
atrophy,
amyloid
plaques,
neurofibrillary
tangles
the
brains
patients.
There
various
descriptive
hypotheses
regarding
causes
AD,
including
cholinergic
hypothesis,
tau
propagation
mitochondrial
cascade
calcium
homeostasis
neurovascular
inflammatory
metal
ion
lymphatic
system
hypothesis.
However,
ultimate
etiology
AD
remains
obscure.
In
this
review,
we
discuss
related
clinical
trials.
Wealthy
puzzles
lessons
have
made
it
possible
to
develop
explanatory
theories
identify
potential
strategies
for
therapeutic
interventions
AD.
The
combination
hypometabolism
autophagy
deficiency
likely
be
causative
factor
We
further
propose
that
fluoxetine,
selective
serotonin
reuptake
inhibitor,
has
treat
