Scientific Reports,
Journal Year:
2020,
Volume and Issue:
10(1)
Published: May 29, 2020
Sleep
deprivation
significantly
impairs
a
range
of
cognitive
and
brain
function,
particularly
episodic
memory
the
underlying
hippocampal
function.
However,
it
remains
controversial
whether
one
or
two
nights
recovery
sleep
following
fully
restores
In
this
study,
we
used
functional
magnetic
resonance
imaging
(fMRI)
examined
effects
consecutive
(20-hour
time-in-bed)
on
resting-state
connectivity
deficits
night
total
(TSD)
in
39
healthy
adults
controlled
in-laboratory
protocol.
TSD
reduced
performance
scene
recognition
task,
impaired
to
multiple
prefrontal
default
mode
network
regions,
disrupted
relationships
between
connectivity.
Following
TSD,
restored
baseline
levels,
but
did
not
restore
nor
its
associations
with
These
findings
suggest
that
more
than
are
needed
function
hippocampal-memory
after
loss.
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
Neurobiology of Disease,
Journal Year:
2020,
Volume and Issue:
145, P. 105054 - 105054
Published: Aug. 27, 2020
Here
we
review
the
impact
of
obstructive
sleep
apnea
(OSA)
on
biomarkers
Alzheimer's
disease
(AD)
pathogenesis,
neuroanatomy,
cognition
and
neurophysiology,
present
research
investigating
effects
continuous
positive
airway
pressure
(CPAP)
therapy.
OSA
is
associated
with
an
increase
in
AD
markers
amyloid-β
tau
measured
cerebrospinal
fluid
(CSF),
by
Positron
Emission
Tomography
(PET)
blood
serum.
There
some
evidence
suggesting
CPAP
therapy
normalizes
CSF
but
since
mechanisms
for
production/clearance
humans
are
not
completely
understood,
these
findings
remain
preliminary.
Deficits
cognitive
domains
attention,
vigilance,
memory
executive
functioning
observed
patients
magnitude
impairment
appearing
stronger
younger
people
from
clinical
settings
than
older
community
samples.
Cognition
improves
varying
degrees
after
use,
greatest
effect
seen
attention
middle
age
adults
more
severe
sleepiness.
Paradigms
which
encoding
retrieval
information
separated
periods
or
without
have
been
done
only
rarely,
perhaps
offer
a
better
chance
to
understand
isolated
daytime
testing.
In
cognitively
normal
individuals,
changes
EEG
microstructure
during
sleep,
particularly
slow
oscillations
spindles,
AD,
measures
memory.
Similar
activity
reported
OSA,
such
as
"EEG
slowing"
wake
REM
degradation
NREM
microstructure.
that
partially
reverses
large
longitudinal
studies
demonstrating
this
lacking.
A
diagnostic
definition
relying
solely
Apnea
Hypopnea
Index
(AHI)
does
assist
understanding
high
degree
inter-individual
variation
impairments
related
response
We
conclude
discussing
conceptual
challenges
trial
treatment
prevention,
including
inclusion
criteria
age,
severity,
symptoms,
need
potentially
long
trial,
defining
relevant
primary
outcomes,
treatments
target
optimize
adherence.
Psychophysiology,
Journal Year:
2020,
Volume and Issue:
57(3)
Published: Jan. 12, 2020
Abstract
In
quest
of
new
avenues
to
explain,
predict,
and
treat
pathophysiological
conditions
during
aging,
research
on
sleep
aging
has
flourished.
Despite
the
great
scientific
potential
pinpoint
mechanistic
pathways
between
sleep,
pathology,
only
little
attention
been
paid
suitability
analytic
procedures
applied
study
these
interrelations.
On
basis
electrophysiological
structural
brain
data
healthy
younger
older
adults,
we
identify,
illustrate,
resolve
methodological
core
challenges
in
aging.
We
demonstrate
biases
common
approaches
when
populations.
argue
that
uncovering
age‐dependent
alterations
physiology
requires
development
adjusted
individualized
filter
out
age‐independent
interindividual
differences.
Age‐adapted
are
thus
required
foster
valid
reliable
biomarkers
age‐associated
cognitive
pathologies.
iScience,
Journal Year:
2021,
Volume and Issue:
24(4), P. 102386 - 102386
Published: April 1, 2021
Patients
with
Alzheimer's
disease
(AD)
undergo
a
slowing
of
waking
electroencephalographic
(EEG)
rhythms
since
prodromal
stages,
which
could
be
ascribed
to
poor
sleep
quality.
We
examined
the
relationship
between
wake
and
alterations
by
assessing
EEG
activity
during
(pre-sleep/post-sleep)
wakefulness
in
AD,
mild
cognitive
impairment
(MCI)
healthy
controls.
AD
MCI
show
high
latency
less
slow-wave
sleep.
Reduced
sigma
characterizes
non-rapid
eye
movement
(NREM)
sleep,
reflecting
spindles
loss.
The
REM
MCI,
strong
correlations
among
two
phenomena
suggesting
common
neuropathological
mechanisms.
Evening-to-morning
variations
revealed
gradual
disappearance
overnight
changes
delta
activity,
indicating
progressive
decay
restorative
functions
on
diurnal
that
correlates
high-frequency
AD.
Our
findings
support
linkage
alterations,
importance
sleep-related
processes
progression.
Drug Design Development and Therapy,
Journal Year:
2021,
Volume and Issue:
Volume 15, P. 2013 - 2024
Published: May 1, 2021
Recent
evidence
has
highlighted
the
anti-inflammatory
properties
of
constituent
Green
Tea
Polyphenols
(GTP),
epigallocatechin-3-gallate
(EGCG)
which
been
suggested
to
exert
a
neuroprotective
effect
on
Alzheimer's
disease
(AD).
The
current
study
aimed
elucidate
EGCG
memory
function
in
rats
with
AD.AD
rat
models
were
initially
established
through
an
injection
Aβ
25-35
solution,
followed
by
gavage
at
varying
doses
determine
learning
and
cognitive
deficits
AD.
Morris
water
maze
test
was
conducted
evaluate
spatial
rats.
Immunohistochemistry
Western
blot
analysis
performed
identify
Tau
phosphorylation.
expression
β-site
amyloid
precursor
protein-cleaving
enzyme
1
(BACE1)
mRNA
protein
hippocampus
measured
reverse
transcription
quantitative
polymerase
chain
reaction
(RT-qPCR)
analysis.
Acetylcholinesterase
(AchE)
activity,
Aβ1-42
Ach
content
all
detected
using
enzyme-linked
immunosorbent
assay
(ELISA).EGCG
intervention
brought
about
decrease
escape
latency
period
while
increasing
time
target
quadrant
among
AD
decreased
hyperphosphorylation
hippocampus.
BACE1
activity
as
well
suppressed
EGCG.
Moreover,
promoted
diminishing
AchE.The
demonstrates
that
may
diminish
protein,
downregulate
improve
antioxidant
system
JAMA Network Open,
Journal Year:
2021,
Volume and Issue:
4(7), P. e2117573 - e2117573
Published: July 23, 2021
Importance
Disrupted
sleep
commonly
occurs
with
progressing
neurodegenerative
disease.
Large,
well-characterized
neuroimaging
studies
of
cognitively
unimpaired
adults
are
warranted
to
clarify
the
magnitude
and
onset
association
between
emerging
β-amyloid
(Aβ)
pathology.
Objective
To
evaluate
associations
daytime
nighttime
duration
regional
Aβ
pathology
in
older
adults.
Design,
Setting,
Participants
In
this
cross-sectional
study,
screening
data
were
collected
April
1,
2014,
December
31,
2017,
from
healthy,
65
85
years
age
who
underwent
florbetapir
F
18
positron
emission
tomography
(PET),
hadAPOEgenotype
information,
scored
25
30
on
Mini-Mental
State
Examination,
had
a
Clinical
Dementia
Rating
0
for
Anti-Amyloid
Treatment
Asymptomatic
Alzheimer
Disease
(A4)
Study.
Data
analysis
was
performed
2019,
May
10,
2021.
Exposures
Self-reported
duration.
Main
Outcomes
Measures
Regional
pathology,
measured
by
PET
standardized
uptake
value
ratio.
increased
risk
deposition
reduced
occurred
early,
before
cognitive
impairment
or
significant
deposition.
may
be
an
early
accumulation
did
not
appear
corrective
loss
sleep,
demonstrating
circadian
rhythm
dependence
preventing
accumulation.
Treatments
that
improve
reduce
aid
delaying
dysfunction
JAMA Neurology,
Journal Year:
2023,
Volume and Issue:
80(12), P. 1326 - 1326
Published: Oct. 30, 2023
Slow-wave
sleep
(SWS)
supports
the
aging
brain
in
many
ways,
including
facilitating
glymphatic
clearance
of
proteins
that
aggregate
Alzheimer
disease.
However,
role
SWS
development
dementia
remains
equivocal.
BMC Medicine,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: May 3, 2023
Alzheimer's
disease
(AD)
pathology
impairs
cognitive
function.
Yet
some
individuals
with
high
amounts
of
AD
suffer
marked
memory
impairment,
while
others
the
same
degree
burden
show
little
impairment.
Why
is
this?
One
proposed
explanation
reserve
i.e.,
factors
that
confer
resilience
against,
or
compensation
for
effects
pathology.
Deep
NREM
slow
wave
sleep
(SWS)
recognized
to
enhance
functions
learning
and
in
healthy
older
adults.
However,
quality
SWS
(NREM
activity,
SWA)
represents
a
novel
factor
adults
pathology,
thereby
providing
against
dysfunction
otherwise
caused
by
burden,
remains
unknown.
