Frontiers in Neuroscience,
Journal Year:
2020,
Volume and Issue:
14
Published: June 30, 2020
Alzheimer’s
disease
(AD)
is
the
major
cause
of
dementia,
characterized
by
presence
amyloid-beta
plaques
and
neurofibrillary
tau
tangles.
Plaques
tangles
are
associated
with
sleep-wake
cycle
disruptions,
including
disruptions
in
non-rapid
eye
movement
(NREM)
slow
wave
sleep.
patients
spend
less
time
NREM
sleep
exhibit
decreased
activity.
Consistent
critical
role
memory
consolidation,
reduced
activity
impaired
consolidation
AD
patients.
The
aberrant
can
be
modeled
transgenic
mouse
models
amyloidosis
tauopathy.
Animal
exhibited
impairments
early
progression,
prior
to
deposition
however
abundant
oligomeric
amyloid-beta.
Optogenetic
rescue
successfully
halted
amyloid
accumulation
restored
intraneuronal
calcium
levels
mice.
On
other
hand,
optogenetic
acceleration
frequency
exacerbated
disrupted
neuronal
homeostasis.
In
this
review,
we
summarize
evidence
mechanisms
underlying
existence
a
positive
feedback
loop
between
amyloid/tau
pathology
that
lead
further
accumulations
AD.
Moreover,
since
occur
plaque
deposition,
provide
an
biomarker
for
disease.
Finally,
propose
therapeutic
targeting
might
effective
treatment
Advanced Materials,
Journal Year:
2021,
Volume and Issue:
33(26)
Published: May 17, 2021
Abstract
Current
therapeutic
strategies
for
Alzheimer's
disease
(AD)
treatments
mainly
focus
on
β‐amyloid
(Aβ)
targeting.
However,
such
have
limited
clinical
outcomes
due
to
the
chronic
and
irreversible
impairment
of
nervous
system
in
late
stage
AD.
Recently,
inflammatory
responses,
manifested
oxidative
stress
glial
cell
activation,
been
reported
as
hallmarks
early
stages
Based
crosstalk
between
response
brain
cells,
a
reactive
oxygen
species
(ROS)‐responsive
dendrimer–peptide
conjugate
(APBP)
is
devised
target
AD
microenvironment
inhibit
responses
at
an
stage.
With
modification
targeting
peptide,
this
nanoconjugate
can
efficiently
deliver
peptides
infected
regions
restore
antioxidant
ability
neurons
by
activating
nuclear
factor
(erythroid‐derived
2)‐like
2
signaling
pathway.
Moreover,
multi‐target
strategy
exhibits
synergistic
function
ROS
scavenging,
promoting
Aβ
phagocytosis,
normalizing
phenotype.
As
result,
reduce
level,
decrease
burden,
alleviate
eventually
enhance
cognitive
functions
APPswe/PSEN1dE9
model
mice.
These
results
indicate
that
APBP
be
promising
candidate
treatment
Advanced Materials,
Journal Year:
2021,
Volume and Issue:
33(13)
Published: Feb. 24, 2021
Abstract
Alzheimer's
disease
(AD)
is
a
common
dementia
that
currently
incurable.
The
existing
treatments
can
only
moderately
relieve
the
symptoms
of
AD
to
slow
down
its
progress.
How
achieve
effective
neural
regeneration
ameliorate
cognitive
impairments
major
challenge
for
current
treatment.
Here,
therapeutic
potential
nanoformulation‐mediated
stem
cell
(NSC)
therapy
capable
simultaneous
Aβ
clearance
and
investigated
in
murine
model.
Genetically
engineered
NSCs
stably
continuously
expressing
neprilysin
(NEP)
are
developed
enhance
degradation
NSC
survival
brain.
A
PBAE‐PLGA‐Ag
2
S‐RA‐siSOX9
(PPAR‐siSOX9)
nanoformulation
with
high
gene/drug
deliverability
synthesized
overcome
microenvironment‐associated
adverse
effects
promote
neuronal
differentiation
NEP‐expressing
NSCs.
For
achieving
accurate
stereotactic
transplantation,
Ag
S
quantum‐dot‐based
fluorescence
imaging
used
guide
transplantation
real
time.
This
strategy
shows
numerous
benefits,
including
efficient
long‐lasting
degradation,
improved
regeneration,
transplantation.
It
shown
single
administration
this
achieves
long‐term
efficacy
(6
months)
respect
memory
reversal
improvement
learning
deficits.
Frontiers in Neuroscience,
Journal Year:
2020,
Volume and Issue:
14
Published: June 30, 2020
Alzheimer’s
disease
(AD)
is
the
major
cause
of
dementia,
characterized
by
presence
amyloid-beta
plaques
and
neurofibrillary
tau
tangles.
Plaques
tangles
are
associated
with
sleep-wake
cycle
disruptions,
including
disruptions
in
non-rapid
eye
movement
(NREM)
slow
wave
sleep.
patients
spend
less
time
NREM
sleep
exhibit
decreased
activity.
Consistent
critical
role
memory
consolidation,
reduced
activity
impaired
consolidation
AD
patients.
The
aberrant
can
be
modeled
transgenic
mouse
models
amyloidosis
tauopathy.
Animal
exhibited
impairments
early
progression,
prior
to
deposition
however
abundant
oligomeric
amyloid-beta.
Optogenetic
rescue
successfully
halted
amyloid
accumulation
restored
intraneuronal
calcium
levels
mice.
On
other
hand,
optogenetic
acceleration
frequency
exacerbated
disrupted
neuronal
homeostasis.
In
this
review,
we
summarize
evidence
mechanisms
underlying
existence
a
positive
feedback
loop
between
amyloid/tau
pathology
that
lead
further
accumulations
AD.
Moreover,
since
occur
plaque
deposition,
provide
an
biomarker
for
disease.
Finally,
propose
therapeutic
targeting
might
effective
treatment
