Experimental Gerontology,
Journal Year:
2023,
Volume and Issue:
182, P. 112309 - 112309
Published: Oct. 1, 2023
Neuronal
hyperactivity
is
a
key
abnormality
in
early
stage
Alzheimer's
disease
(AD).
Medial
entorhinal
cortex
(mEC)
plays
vital
role
memory
function
and
affected
AD.
Growing
evidence
indicates
benefits
of
regular
exercise
on
cognitive
humans
with
AD,
although,
the
underlying
mechanisms
are
not
clear.
Therefore,
this
study
was
designed
to
test
effects
16
weeks
treadmill
spatial
learning
cellular
6-month-old
3xTg-AD
mice.
Whole-cell
patch
clamp
used
examine
neuronal
intrinsic
excitability,
spontaneous
excitatory
postsynaptic
currents
(sEPSCs)
inhibitory
(sIPSCs)
mEC
layer
II/III
pyramidal
neurons
following
groups:
wild
type
(WT
+
sham),
(AD+sham),
WT
receiving
Ex),
AD
(AD+Ex).
We
found
that
at
behavioral
level,
decreased
working
errors
radial
arm
maze
(RAM)
At
we
prevented
abnormal
increase
neuron
input
resistance
action
potential
firing
mice
compared
sham
AD+Ex
mice;
further,
sEPSC
amplitude
frequency
were
normal
but
overactive
AD+sham;
additionally,
GABAergic
inhibition
reduced
AD+sham.
In
conclusion,
our
results
indicate
improves
prevents
network
hyperexcitability
by
reducing
excitability
normalizing
synaptic
transmission
Frontiers in Aging Neuroscience,
Journal Year:
2024,
Volume and Issue:
16
Published: Dec. 18, 2024
Anxiety
and
depression-like
symptoms
occur
in
the
early
stages
of
Alzheimer's
disease.
Hippocampal
Sirtuin
1
(SIRT1)
signaling
mediates
anxiety-
behavior.
Exercise
training
improves
anxiety
behavior
various
disease
models,
such
as
rat
chronic
restraint
stress
model,
model
posttraumatic
disorder,
fetal
alcohol
spectrum
disorders.
Here,
we
aimed
to
investigate
whether
exercise
ameliorates
depression
like
behaviors
APP/PS1
mice
explore
potential
mechanisms.
Frontiers in Molecular Neuroscience,
Journal Year:
2024,
Volume and Issue:
17
Published: June 26, 2024
Neuropathic
pain
is
a
type
of
chronic
caused
by
an
injury
or
somatosensory
nervous
system
disease.
Drugs
and
exercise
could
effectively
relieve
neuropathic
pain,
but
no
treatment
can
completely
stop
pain.
The
integration
into
management
has
attracted
considerable
interest
in
recent
years,
treadmill
training
the
most
used
among
therapies.
be
treated
if
its
mechanism
clarified.
In
association
between
neuroinflammation
been
explored.
Neuroinflammation
trigger
proinflammatory
cytokines,
activate
microglia,
inhibit
descending
modulatory
systems,
promote
overexpression
brain-derived
neurotrophic
factor,
which
lead
to
generation
hypersensitivity.
Treadmill
alleviate
mainly
regulating
neuroinflammation,
including
inhibiting
activity
pro-inflammatory
factors
over
activation
microglia
dorsal
horn,
expression
mu
opioid
receptor
rostral
ventromedial
medulla
levels
γ-aminobutyric
acid
factor.
This
article
reviews
summarizes
research
on
effect
role
regulation
explore
benefits
for
treatment.
Experimental Gerontology,
Journal Year:
2023,
Volume and Issue:
182, P. 112309 - 112309
Published: Oct. 1, 2023
Neuronal
hyperactivity
is
a
key
abnormality
in
early
stage
Alzheimer's
disease
(AD).
Medial
entorhinal
cortex
(mEC)
plays
vital
role
memory
function
and
affected
AD.
Growing
evidence
indicates
benefits
of
regular
exercise
on
cognitive
humans
with
AD,
although,
the
underlying
mechanisms
are
not
clear.
Therefore,
this
study
was
designed
to
test
effects
16
weeks
treadmill
spatial
learning
cellular
6-month-old
3xTg-AD
mice.
Whole-cell
patch
clamp
used
examine
neuronal
intrinsic
excitability,
spontaneous
excitatory
postsynaptic
currents
(sEPSCs)
inhibitory
(sIPSCs)
mEC
layer
II/III
pyramidal
neurons
following
groups:
wild
type
(WT
+
sham),
(AD+sham),
WT
receiving
Ex),
AD
(AD+Ex).
We
found
that
at
behavioral
level,
decreased
working
errors
radial
arm
maze
(RAM)
At
we
prevented
abnormal
increase
neuron
input
resistance
action
potential
firing
mice
compared
sham
AD+Ex
mice;
further,
sEPSC
amplitude
frequency
were
normal
but
overactive
AD+sham;
additionally,
GABAergic
inhibition
reduced
AD+sham.
In
conclusion,
our
results
indicate
improves
prevents
network
hyperexcitability
by
reducing
excitability
normalizing
synaptic
transmission
