Frontiers in Psychiatry,
Год журнала:
2023,
Номер
14
Опубликована: Май 2, 2023
Background
The
incidence
of
sleep
disorders
in
children
with
autism
spectrum
disorder
(ASD)
is
very
high.
Sleep
can
exacerbate
the
development
ASD
and
impose
a
heavy
burden
on
families
society.
pathological
mechanism
complex,
but
gene
mutations
neural
abnormalities
may
be
involved.
Methods
In
this
review,
we
examined
literature
addressing
genetic
mechanisms
ASD.
databases
PubMed
Scopus
were
searched
for
eligible
studies
published
between
2013
2023.
Results
Prolonged
awakenings
caused
by
following
processes.
Mutations
MECP2,
VGAT
SLC6A1
genes
decrease
GABA
inhibition
neurons
locus
coeruleus,
leading
to
hyperactivity
noradrenergic
prolonged
HRH1,
HRH2
,
HRH3
heighten
expression
histamine
receptors
posterior
hypothalamus,
potentially
intensifying
histamine’s
ability
promote
arousal.
KCNQ3
PCDH10
cause
atypical
modulation
amygdala
impact
orexinergic
neurons,
causing
hyperexcitability
hypothalamic
orexin
system.
AHI1
ARHGEF10
UBE3A
SLC6A3
affect
dopamine
synthesis,
catabolism,
reuptake
processes,
which
elevate
concentrations
midbrain.
Secondly,
non-rapid
eye
movement
closely
related
lack
butyric
acid,
iron
deficiency
dysfunction
thalamic
reticular
nucleus
induced
PTCHD1
alterations.
Thirdly,
HTR2A,
SLC6A4
MAOA,
MAOB
TPH2
VMATs
SHANK3,
CADPS2
induce
structural
functional
dorsal
raphe
(DRN)
amygdala,
disturb
REM
sleep.
addition,
melatonin
levels
ASMT
MTNR1A
MTNR1B
mutations,
along
basal
forebrain
cholinergic
lead
abnormal
sleep–wake
rhythm
transitions.
Conclusion
Our
review
revealed
that
circuits
are
strongly
correlated
Exploring
underlying
pathology
significant
further
therapy.
Molecular Neurodegeneration,
Год журнала:
2023,
Номер
18(1)
Опубликована: Апрель 21, 2023
Abstract
Failed
proteostasis
is
a
well-documented
feature
of
Alzheimer’s
disease,
particularly,
reduced
protein
degradation
and
clearance.
However,
the
contribution
failed
to
neuronal
circuit
dysfunction
an
emerging
concept
in
neurodegenerative
research
will
prove
critical
understanding
cognitive
decline.
Our
objective
convey
disease
progression
with
growing
evidence
for
bidirectional
relationship
sleep
disruption
failure.
Proteostasis
tauopathy
disrupts
neurons
that
regulate
sleep–wake
cycle,
which
presents
behavior
as
impaired
slow
wave
rapid
eye
movement
patterns.
Subsequent
loss
further
impairs
Sleep
defined
seen
early
many
disorders
contributes
memory
impairments
disease.
Canonical
pathological
hallmarks,
β-amyloid,
tau,
directly
disrupt
sleep,
neurodegeneration
locus
coeruleus,
hippocampal
hypothalamic
from
tau
proteinopathy
causes
circuitry
sleep.
Acting
positive-feedback-loop,
circadian
rhythm
then
increase
spread
β-amyloid
through
proteasome,
autophagy,
unfolded
response
glymphatic
This
phenomenon
extends
beyond
interactions
impairment
homeostasis
TDP-43,
α-synuclein,
FUS,
huntingtin
proteins,
implicating
important
consideration
array
diseases
cases
mixed
neuropathology.
Critically,
dynamics
this
interaction
environment
are
not
fully
elucidated
deserving
discussion
research.
Finally,
we
propose
sleep-enhancing
therapeutics
potential
interventions
promoting
healthy
proteostasis,
including
clearance,
mechanistically
linking
these
processes.
With
clinical
preclinical
research,
dynamic
diagnostic
therapeutic
framework,
informing
precise
single-
combinatorial-treatments
other
brain
disorders.
Graphical
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
174, С. 116547 - 116547
Опубликована: Апрель 9, 2024
Several
studies
have
found
that
sleep
deprivation
(SD)
can
lead
to
neuronal
ferroptosis
and
affect
hippocampal
function.
However,
there
are
currently
no
effective
interventions.
Vitamin
B6
is
a
co-factor
for
key
enzymes
in
the
transsulfuration
pathway
which
critical
maintaining
cell
growth
presence
of
cysteine
deprivation.
The
results
showed
SD
inhibited
cystine-glutamate
antiporter
light
chain
subunit
xCT
protein
expression
caused
deficiency,
reduced
synthesis
glutathione
(GSH)
trigger
ferroptosis.
Nissl
staining
further
revealed
significant
loss
shrinkage
CA1
CA3
regions
hippocampus
mice.
Typical
ferroptotic
indicators
characterized
by
lipid
peroxidation
iron
accumulation
were
after
As
expected,
vitamin
could
alleviate
upregulating
cystathionine
beta-synthase
(CBS)
pathway,
thereby
replenishing
intracellular
deficient
GSH
restoring
GPX4.
Similar
anti-ferroptotic
effects
demonstrated
HT-22
cells
treated
with
activator
erastin.
Furthermore,
had
inhibitory
effect
on
erastin-induced
CBS-knockout
HT22
cells.
Our
findings
suggested
chronic
disrupting
cyst(e)ine/GSH/GPX4
axis.
alleviated
deprivation-induced
enhancing
CBS
pathway.
Frontiers in Human Neuroscience,
Год журнала:
2023,
Номер
17
Опубликована: Июль 26, 2023
This
paper
explores
memory
from
a
cognitive
neuroscience
perspective
and
examines
associated
neural
mechanisms.
It
the
different
types
of
memory:
working,
declarative,
non-declarative,
brain
regions
involved
in
each
type.
The
highlights
role
regions,
such
as
prefrontal
cortex
working
hippocampus
declarative
memory.
also
mechanisms
that
underlie
formation
consolidation
memory,
including
importance
sleep
linking
new
memories
to
existing
schemata.
two
processes:
cellular
system
consolidation.
Cellular
is
process
stabilizing
information
by
strengthening
synaptic
connections.
System
models
suggest
are
initially
stored
gradually
consolidated
into
neocortex
over
time.
involves
hippocampal-neocortical
binding
incorporating
newly
acquired
medial
temporal
lobe
its
involvement
autobiographical
Further,
discusses
relationship
between
episodic
semantic
hippocampus.
Finally,
underscores
need
for
further
research
neurobiological
underlying
non-declarative
particularly
conditioning.
Overall,
provides
comprehensive
overview
processes
Neuroscience & Biobehavioral Reviews,
Год журнала:
2023,
Номер
155, С. 105465 - 105465
Опубликована: Ноя. 15, 2023
Wakefulness,
non-rapid
eye-movement
(NREM)
and
rapid
(REM)
sleep
differ
from
each
other
along
three
dimensions:
behavioral,
phenomenological,
physiological.
Although
these
dimensions
often
fluctuate
in
step,
they
can
also
dissociate.
The
current
paradigm
that
views
as
made
of
global
NREM
REM
states
fail
to
account
for
dissociations.
This
conundrum
be
dissolved
by
stressing
the
existence
significance
local
regulation
sleep.
We
will
review
evidence
animals
humans,
healthy
pathological
brains,
showing
different
forms
consequences
on
behavior,
cognition,
subjective
experience.
Altogether,
we
argue
notion
provides
a
unified
host
phenomena:
dreaming
sleep,
parasomnias,
intrasleep
responsiveness,
inattention
mind
wandering
wakefulness.
Yet,
physiological
origins
or
its
putative
functions
remain
unclear.
Exploring
further
could
provide
unique
novel
perspective
how
why
Frontiers in Systems Neuroscience,
Год журнала:
2023,
Номер
17
Опубликована: Март 23, 2023
There
is
a
growing
appreciation
for
the
cerebellum
beyond
its
role
in
motor
function
and
accumulating
evidence
that
hippocampus
interact
across
range
of
brain
states
behaviors.
Acute
chronic
manipulations,
simultaneous
recordings,
imaging
studies
together
indicate
coordinated
coactivation
bidirectional
functional
connectivity
relevant
various
physiological
functions,
including
spatiotemporal
processing.
This
likely
supported
by
multiple
circuit
paths.
It
also
important
temporal
lobe
epilepsy:
impacted
seizures
epilepsy,
modulation
cerebellar
circuitry
can
be
an
effective
strategy
to
inhibit
hippocampal
seizures.
review
highlights
some
recent
key
hippobellum
literature.
Nature Communications,
Год журнала:
2023,
Номер
14(1)
Опубликована: Июль 3, 2023
Abstract
Rapid-eye-movement
(REM)
sleep
is
a
distinct
behavioral
state
associated
with
vivid
dreaming
and
memory
processing.
Phasic
bursts
of
electrical
activity,
measurable
as
spike-like
pontine
(P)-waves,
are
hallmark
REM
implicated
in
consolidation.
However,
the
brainstem
circuits
regulating
P-waves,
their
interactions
generating
sleep,
remain
largely
unknown.
Here,
we
show
that
an
excitatory
population
dorsomedial
medulla
(dmM)
neurons
expressing
corticotropin-releasing-hormone
(CRH)
regulates
both
P-waves
mice.
Calcium
imaging
showed
dmM
CRH
selectively
activated
during
recruited
opto-
chemogenetic
experiments
revealed
this
promotes
sleep.
Chemogenetic
manipulation
also
induced
prolonged
changes
P-wave
frequency,
while
brief
optogenetic
activation
reliably
triggered
along
transiently
accelerated
theta
oscillations
electroencephalogram
(EEG).
Together,
these
findings
anatomically
functionally
delineate
common
medullary
hub
for
regulation
P-waves.
Neuroscience & Biobehavioral Reviews,
Год журнала:
2024,
Номер
159, С. 105574 - 105574
Опубликована: Фев. 6, 2024
The
quest
to
understand
the
memory
engram
has
intrigued
humans
for
centuries.
Recent
technological
advances,
including
genetic
labelling,
imaging,
optogenetic
and
chemogenetic
techniques,
have
propelled
field
of
research
forward.
These
tools
enabled
researchers
create
erase
components.
While
these
innovative
techniques
yielded
invaluable
insights,
they
often
focus
on
specific
elements
trace.
Genetic
labelling
may
rely
a
particular
immediate
early
gene
as
marker
activity,
optogenetics
activate
or
inhibit
one
type
neuron,
imaging
capture
activity
snapshots
in
given
brain
region
at
times.
Yet,
memories
are
multifaceted,
involving
diverse
arrays
neuronal
subpopulations,
circuits,
regions
that
work
concert
create,
store,
retrieve
information.
Consideration
contributions
both
excitatory
inhibitory
neurons,
micro
macro
circuits
across
regions,
dynamic
nature
active
ensembles,
representational
drift
is
crucial
comprehensive
understanding
complex
memory.