E3S Web of Conferences,
Год журнала:
2024,
Номер
553, С. 05048 - 05048
Опубликована: Янв. 1, 2024
The
most
prevalent
chronic
disease
among
senior
people,
and
its
prevalence
rises
with
age,
is
Alzheimer’s
(AD).
One
study
predicts
that
the
of
dementia
will
triple
globally
by
2050.
Sleep
disorder
(sleep
disturbance)
a
condition
also
often
occurs
in
elderly
population.
More
than
about
25%~60%
AD
patients
have
sleep
disturbances
or
circadian
rhythm
changes.
But
disorders
during
early
stage
not
been
uniformly
recognized.
Of
stages
AD,
those
experiencing
patients.
Therefore,
this
paper
summarises
conditions
types
first
articles
time
lesions
are
retrieved
analysed.
This
deals
two
pathological
mechanisms
AD:
beta
amyloid
(Aβ)
accumulation
tau
protein
entanglement.
By
describing
effects
western
drugs
Chinese
herbal
medicine,
shows
older
adults
may
suggest
mild
cognitive
impairment
more
attention
needs
to
be
paid
what
current
research
suggests.
Early
can
lead
search
for
accurate
biomarkers
major
driver
development
diagnostics
delay
onset.
Journal of Cellular and Molecular Medicine,
Год журнала:
2024,
Номер
28(10)
Опубликована: Май 1, 2024
Parkinson's
disease
(PD)
is
a
neurodegenerative
disorder
of
the
brain
and
manifested
by
motor
non-motor
symptoms
because
degenerative
changes
in
dopaminergic
neurons
substantia
nigra.
PD
neuropathology
associated
with
mitochondrial
dysfunction,
oxidative
damage
apoptosis.
Thus,
modulation
apoptosis
growth
factors
could
be
novel
boulevard
management
PD.
Brain-derived
neurotrophic
factor
(BDNF)
its
receptor
tropomyosin
kinase
type
B
(TrkB)
are
chiefly
involved
neuropathology.
BDNF
promotes
survival
nigra
enhances
functional
activity
striatal
neurons.
Deficiency
TrkB
triggers
degeneration
accumulation
α-Syn
As
well,
BDNF/TrkB
signalling
reduced
early
phase
Targeting
specific
activators
may
attenuate
this
review
aimed
to
discuss
potential
role
against
In
conclusion,
decreased
linked
severity
long-term
complications.
Activation
Autophagy,
Год журнала:
2023,
Номер
20(2), С. 259 - 274
Опубликована: Сен. 15, 2023
Multiple
sclerosis
(MS)
is
a
chronic
progressive
demyelinating
disease
of
the
central
nervous
system
(CNS)
due
to
an
increase
abnormal
peripherally
auto-reactive
T
lymphocytes
which
elicit
autoimmunity.
The
main
pathophysiology
MS
myelin
sheath
damage
by
immune
cells
and
defect
in
generation
oligodendrocytes.
Macroautophagy/autophagy
critical
degradation
process
that
eliminates
dysfunctional
or
superfluous
cellular
components.
Autophagy
has
property
double-edged
sword
it
may
have
both
beneficial
detrimental
effects
on
neuropathology.
Therefore,
this
review
illustrates
protective
harmful
autophagy
with
regard
disease.
prevents
progression
reducing
oxidative
stress
inflammatory
disorders.
In
contrast,
over-activated
associated
neuropathology
case
use
inhibitors
alleviate
pathogenesis
MS.
Furthermore,
provokes
activation
different
supporting
play
intricate
role
functions
modulation
regulating
cell
proliferation
related
demyelination
remyelination.
enhances
remyelination
increasing
activity
oligodendrocytes,
astrocytes.
However,
induces
activating
microglia
cells.
conclusion,
specific
autophagic
activators
astrocytes,
dendritic
(DCs),
induce
against
Cell Communication and Signaling,
Год журнала:
2024,
Номер
22(1)
Опубликована: Фев. 22, 2024
Abstract
Background
Patients
with
Alzheimer’s
disease
(AD)
are
often
co-morbid
unprovoked
seizures,
making
clinical
diagnosis
and
management
difficult.
Although
it
has
an
important
role
in
both
AD
epilepsy,
abnormal
γ-aminobutyric
acid
(GABA)ergic
transmission
is
recognized
only
as
a
compensative
change
for
glutamatergic
damage.
Neuregulin
1
(NRG1)-ErbB4
signaling
can
promote
GABA
release
suppress
epileptogenesis,
but
its
effects
on
cognition
still
controversial.
Methods
Four-month-old
APPswe/PS1dE9
mice
(APP
mice)
were
used
animal
models
the
early
stage
of
this
study.
Acute/chronic
chemical-kindling
epilepsy
established
pentylenetetrazol.
Electroencephalogram
Racine
scores
performed
to
assess
seizures.
Behavioral
tests
emotion.
Electrophysiology,
western
blot
immunofluorescence
detect
alterations
synapses,
GABAergic
system
components
NRG1-ErbB4
signaling.
Furthermore,
NRG1
was
administrated
intracerebroventricularly
into
APP
then
antiepileptic
cognitive
evaluated.
Results
had
increased
susceptibility
resulting
hippocampal
synaptic
damage
impairment.
Electrophysiological
analysis
revealed
decreased
hippocampus.
This
involved
reduction
number
parvalbumin
interneurons
(PV
+
Ins)
levels
synthesis
transport.
We
also
found
impaired
which
mediated
by
PV
Ins
loss.
And
administration
could
effectively
reduce
seizures
improve
four-month-old
mice.
Conclusion
Our
results
indicated
that
hyperexcitability,
further
excitation/inhibition
imbalance,
promoted
epileptogenesis
AD.
Appropriate
down-regulate
seizure
rescue
function.
study
provided
potential
direction
intervening
co-morbidity
epilepsy.
European journal of medical research,
Год журнала:
2024,
Номер
29(1)
Опубликована: Фев. 9, 2024
Abstract
Multiple
sclerosis
(MS)
is
the
most
frequent
inflammatory
and
demyelinating
disease
of
central
nervous
system
(CNS).
The
underlying
pathophysiology
MS
destruction
myelin
sheath
by
immune
cells.
formation
plaques,
inflammation,
injury
neuronal
characterizes
its
neuropathology.
plaques
are
multiple
focal
regions
demyelination
disseminated
in
brain's
white
matter,
spinal
cords,
deep
grey
cerebral
cortex.
Fenofibrate
a
peroxisome
proliferative
activated
receptor
alpha
(PPAR-α)
that
attenuates
reactions
MS.
inhibits
differentiation
Th17
inhibiting
expression
pro-inflammatory
signaling.
According
to
these
findings,
this
review
intended
illuminate
mechanistic
immunoinflammatory
role
fenofibrate
mitigating
In
conclusion,
can
attenuate
neuropathology
modulating
different
pathways,
including
oxidative
stress,
autophagy,
mitochondrial
dysfunction,
inflammatory-signaling
neuroinflammation.
