Journal of Neuroscience,
Год журнала:
2018,
Номер
38(12), С. 2911 - 2919
Опубликована: Март 21, 2018
Microglia
are
emerging
as
key
players
in
neurodegenerative
diseases,
such
Alzheimer's
disease
(AD).
Thus
far,
microglia
have
rather
been
known
modulator
of
neurodegeneration
with
functions
limited
to
neuroinflammation
and
release
neurotoxic
molecules.
However,
several
recent
studies
demonstrated
a
direct
role
"neuro"
degeneration
observed
AD
by
promoting
phagocytosis
neuronal,
particular,
synaptic
structures.
While
some
the
address
involvement
β-amyloid
peptides
process,
also
indicate
that
this
could
occur
independent
amyloid,
further
elevating
importance
AD.
Here
we
review
these
speculate
about
possible
cellular
mechanisms,
how
they
be
regulated
risk
genes
sleep.
Finally,
deliberate
on
avenues
for
targeting
microglia-mediated
synapse
loss
therapy
prevention.Dual
Perspectives
Companion
Paper:
Disease
Sleep-Wake
Disturbances:
Amyloid,
Astrocytes,
Animal
Models
William
M.
Vanderheyden,
Miranda
Lim,
Erik
S.
Musiek,
Jason
R.
Gerstner.
JAMA Neurology,
Год журнала:
2014,
Номер
71(12), С. 1498 - 1498
Опубликована: Окт. 15, 2014
Importance
Nocturnal
sleep
disruption
develops
in
Alzheimer
disease
(AD)
owing
to
the
derangement
of
sleep-wake
cycle
regulation
pathways.
Orexin
contributes
by
increasing
arousal
levels
and
maintaining
wakefulness.
Objectives
To
study
cerebrospinal
fluid
orexin
patients
with
AD,
evaluate
relationship
degree
dementia
AD
biomarkers
(tau
proteins
β-amyloid
1-42),
analyze
potentially
related
architecture
changes
measured
polysomnography.
Design,
Setting,
Participants
We
conducted
a
case-control
from
August
1,
2012,
through
May
31,
2013.
included
48
drug-naive
referred
Neurological
Clinic
University
Hospital
Rome
Tor
Vergata.
Based
on
Mini-Mental
State
Examination
score,
21
were
mild
group
(score,
≥21),
whereas
27
moderate
severe
<21).
The
control
consisted
29
nondemented
participants
similar
age
sex.
Exposure
Laboratory
assessment
orexin,
tau
proteins,
1-42
polysomnographic
variables.
Main
Outcomes
Measures
Levels
1-42;
macrostructural
variables
nocturnal
(total
time,
efficiency,
onset
rapid
eye
movement
[REM]
latencies,
non-REM
REM
stages,
wakefulness
after
onset);
scores.
Results
Patients
presented
higher
mean
(SD)
compared
controls
(154.36
[28.16]
vs
131.03
[26.55];P
<
.01)
more
impaired
respect
AD.
On
other
hand,
global
group,
positively
correlated
total
protein
(r
=
0.32;P
.03)
strictly
impairment.
Finally,
cognitive
impairment,
as
Examination,
was
structure
deterioration.
Conclusions
Relevance
Our
results
demonstrate
that,
increased
are
parallel
deterioration,
which
appears
be
associated
decline.
Therefore,
orexinergic
system
seems
dysregulated
its
output
function
appear
overexpressed
along
progression
neurodegenerative
process.
This
overexpression
may
result
an
imbalance
neurotransmitter
networks
regulating
wake-sleep
toward
promoting
Journal of Neuroscience,
Год журнала:
2018,
Номер
38(12), С. 2911 - 2919
Опубликована: Март 21, 2018
Microglia
are
emerging
as
key
players
in
neurodegenerative
diseases,
such
Alzheimer's
disease
(AD).
Thus
far,
microglia
have
rather
been
known
modulator
of
neurodegeneration
with
functions
limited
to
neuroinflammation
and
release
neurotoxic
molecules.
However,
several
recent
studies
demonstrated
a
direct
role
"neuro"
degeneration
observed
AD
by
promoting
phagocytosis
neuronal,
particular,
synaptic
structures.
While
some
the
address
involvement
β-amyloid
peptides
process,
also
indicate
that
this
could
occur
independent
amyloid,
further
elevating
importance
AD.
Here
we
review
these
speculate
about
possible
cellular
mechanisms,
how
they
be
regulated
risk
genes
sleep.
Finally,
deliberate
on
avenues
for
targeting
microglia-mediated
synapse
loss
therapy
prevention.Dual
Perspectives
Companion
Paper:
Disease
Sleep-Wake
Disturbances:
Amyloid,
Astrocytes,
Animal
Models
William
M.
Vanderheyden,
Miranda
Lim,
Erik
S.
Musiek,
Jason
R.
Gerstner.
