Journal of Law and Sustainable Development,
Год журнала:
2023,
Номер
11(10), С. e1074 - e1074
Опубликована: Окт. 18, 2023
Introduction:
Physical
exercise
can
activate
important
biochemical
processes
in
the
human
body,
one
of
which
is
a
myokine
called
irisin.
Objective:
This
review
aims
to
identify
effect
on
expression
FNDC5/irisin,
secreted
by
skeletal
muscles
that
produced
response
physical
activity.
hormone
provides
protective
function
central
nervous
system,
specifically
hippocampus.
The
effects
brain
are
well
known,
but
duration,
intensity
and
type
as
underlying
molecular
mechanisms
not
fully
understood.
will
focus
Fibronectin
III
domain-containing
protein
5
(FNDC5)
its
form,
“irisin”
with
mechanism
action
hippocampus
irisin
expression.
Method:
A
literature
search
was
performed
several
databases
(PubMed,
Scopus,
Sciencedirect)
impact
training
irisin,
resulting
17
articles.
Results:
shows
increases
plasma
levels
humans
brains
rats,
including
Discussion;
relationship
between
exercise,
FNDC5
(the
gene
encodes
irisin),
an
area
active
research.
FNDC5/irisin
has
gained
attention
for
potential
role
mediating
some
beneficial
brain,
Conclusion:
Irisin
expressed
result
depends
type,
intensity,
duration
functions
brain.
eNeuro,
Год журнала:
2023,
Номер
10(2), С. ENEURO.0256 - 22.2023
Опубликована: Янв. 25, 2023
Major
depressive
disorder
(MDD)
is
a
major
cause
of
disability
in
adults.
MDD
both
comorbidity
and
risk
factor
for
Alzheimer's
disease
(AD),
regular
physical
exercise
has
been
associated
with
reduced
incidence
severity
AD.
Irisin
an
exercise-induced
myokine
derived
from
proteolytic
processing
fibronectin
type
III
domain-containing
protein
5
(FNDC5).
FNDC5/irisin
the
brains
AD
patients
mouse
models.
However,
whether
brain
expression
altered
depression
remains
elusive.
Here,
we
investigate
changes
Neural Regeneration Research,
Год журнала:
2024,
Номер
20(6), С. 1555 - 1564
Опубликована: Июль 10, 2024
Irisin
is
a
myokine
that
generated
by
cleavage
of
the
membrane
protein
fibronectin
type
III
domain-containing
5
(FNDC5)
in
response
to
physical
exercise.
Studies
reveal
irisin/FNDC5
has
neuroprotective
functions
against
Alzheimer's
disease,
most
common
form
dementia
elderly,
improving
cognitive
function
and
reducing
amyloid-β
tau
pathologies
as
well
neuroinflammation
cell
culture
or
animal
models
disease.
Although
current
ongoing
studies
on
show
promising
results,
further
mechanistic
are
required
clarify
its
potential
meaningful
therapeutic
target
for
alleviating
We
recently
found
irisin
treatment
reduces
pathology
increasing
activity/levels
amyloid-β-degrading
enzyme
neprilysin
secreted
from
astrocytes.
Herein,
we
present
an
overview
irisin/FNDC5's
protective
roles
mechanisms
Frontiers in Endocrinology,
Год журнала:
2023,
Номер
14
Опубликована: Ноя. 24, 2023
Over
the
last
decade,
a
considerable
amount
of
new
data
have
revealed
beneficial
effects
exercise
on
hippocampal
neurogenesis
and
maintenance
or
improvement
cognitive
function.
Investigations
with
animal
models,
as
well
human
studies,
yielded
novel
understanding
mechanisms
through
which
endocrine
signaling
can
stimulate
neurogenesis,
acute
and/or
chronic
levels
these
circulating
hormones.
Considering
aging
decline
specific
factors
that
affect
brain
health,
insights
in
this
area
research
are
particularly
important.
In
review,
we
discuss
how
different
forms
influence
peripheral
production
factors,
particular
emphasis
brain-derived
neurotrophic
factor,
growth
hormone,
insulin-like
factor-1,
ghrelin,
estrogen,
testosterone,
irisin,
vascular
endothelial
erythropoietin,
cortisol.
We
also
describe
responses
to
induce
cellular
changes
increase
improve
Abstract
Background
The
accumulation
of
senescent
microglia
has
been
highlighted
as
a
critical
contributor
to
the
progression
tauopathies.
Irisin,
muscle-derived
hormone
produced
by
proteolytic
cleavage
Fibronectin-domain
III
containing
5
(FNDC5),
mediates
pleiotropic
effects
exercise
on
physical
body.
Herein,
we
investigate
potential
role
irisin
in
microglial
senescence
Methods
To
model
tauopathies
both
vivo
and
vitro,
utilized
P301S
tau
transgenic
mice
K18
fibril-treated
BV2
cells,
respectively.
We
first
examined
expression
phenotypes
Subsequently,
investigated
impact
its
underlying
molecular
mechanisms.
Result
observed
reduction
levels
an
onset
premature
vitro.
Irisin
administration
was
found
counteract
ameliorate
cognitive
decline
mice.
Mechanistically,
effectively
inhibited
stimulating
mitochondrial
transcription
factor
A
(TFAM),
master
regulator
respiratory
chain
biogenesis,
thereby
enhancing
oxidative
phosphorylation
(OXPHOS).
Silencing
TFAM
eliminated
inhibitory
effect
well
restorative
OXPHOS.
Furthermore,
SIRT1/PGC1α
signaling
pathway
appeared
be
implicated
irisin-mediated
upregulation
TFAM.
Conclusion
Taken
together,
our
study
revealed
that
mitigated
via
TFAM-driven
suggesting
promising
new
avenue
for
therapeutic
strategies
targeting
Communications Biology,
Год журнала:
2023,
Номер
6(1)
Опубликована: Ноя. 7, 2023
Abstract
The
proteasome
plays
key
roles
in
synaptic
plasticity
and
memory
by
regulating
protein
turnover,
quality
control,
elimination
of
oxidized/misfolded
proteins.
Here,
we
investigate
function
localization
at
synapses
Alzheimer’s
disease
(AD)
post-mortem
brain
tissue
experimental
models.
We
found
a
marked
increase
ubiquitinylated
proteins
AD
hippocampi
compared
to
controls.
Using
several
models,
show
that
amyloid-β
oligomers
(AβOs)
inhibit
activity
trigger
reduction
content.
further
inhibition
specifically
hippocampal
fractions
derived
from
APPswePS1ΔE9
mice.
Reduced
instigated
AβOs
is
corrected
treatment
with
rolipram,
phosphodiesterase-4
inhibitor,
Results
dynein
blocks
AβO-induced
dendritic
content
neurons.
Finally,
induces
AD-like
pathological
features,
including
reactive
oxygen
species
spine
loss
neurons,
mRNA
translation,
impairment
suggest
may
contribute
deficits
AD.
Brain Communications,
Год журнала:
2023,
Номер
5(4)
Опубликована: Янв. 1, 2023
Abstract
Fibronectin
type
III
domain–containing
protein
5
(FNDC5)
and
its
derived
hormone,
irisin,
have
been
associated
with
metabolic
control
in
humans,
described
FNDC5
single
nucleotide
polymorphisms
being
linked
to
obesity
syndrome.
Decreased
brain
FNDC5/irisin
has
reported
subjects
dementia
due
Alzheimer’s
disease.
Since
impaired
glucose
metabolism
develops
ageing
is
prominent
disease,
here,
we
examined
associations
of
a
polymorphism
the
gene
(rs1746661)
amyloid-β
deposition
cohort
240
cognitively
unimpaired
485
elderly
individuals
from
Disease
Neuroimaging
Initiative.
In
harbouring
rs1746661(T)
allele,
observed
regional
reduction
low
memory-linked
regions
increased
PET
load.
No
differences
cognition
or
levels
cerebrospinal
fluid
amyloid-β42,
phosphorylated
tau
total
were
between
allele
carriers
non-carriers.
Our
results
indicate
that
genetic
variant
suggest
may
participate
regulation
vulnerable
disease
pathophysiology.
Understanding
variants
metabolism-linked
genes
signatures
contribute
elucidating
modulators
humans.
Scientific Reports,
Год журнала:
2023,
Номер
13(1)
Опубликована: Окт. 30, 2023
Abstract
Angelman
syndrome
(AS)
is
a
rare
neurogenetic
disorder
caused
by
UBE3A
deficiency
and
characterized
severe
developmental
delay,
cognitive
impairment,
motor
dysfunction.
In
the
present
study,
we
performed
RNA-seq
on
hippocampal
samples
from
both
wildtype
(WT)
AS
male
mice,
with
or
without
contextual
fear
memory
recall.
There
were
281
recall-associated
differentially
expressed
genes
(DEGs)
in
WT
mice
268
DEGs
129
shared
two
genotypes.
Gene
ontology
analysis
showed
that
extracellular
matrix
stimulation-induced
response
prominently
enriched
while
nuclear
acid
metabolism
tissue
development
highly
those
mice.
Further
analyses
belonged
to
genes.
Unique
recall
biological
processes
critical
for
synaptic
plasticity
learning
memory,
including
network
clustered
around
fibronectin
1
collagens.
contrast,
AS-specific
not
any
known
pathways.
These
results
suggest
altering
transcriptome,
fails
recruit
memory-associated
transcriptional
programs,
which
could
be
responsible
impairment
PLoS ONE,
Год журнала:
2024,
Номер
19(3), С. e0300888 - e0300888
Опубликована: Март 21, 2024
Neuronal
death
could
be
responsible
for
the
cognitive
impairments
found
in
astronauts
exposed
to
spaceflight,
highlighting
need
identify
potential
countermeasures
ensure
neuronal
health
microgravity
conditions.
Therefore,
differentiated
HT22
cells
were
simulated
by
random
positioning
machine
(RPM)
48
h,
treating
them
with
a
single
administration
of
Trolox,
recombinant
irisin
(r-Irisin)
or
both.
Particularly,
we
investigated
cell
viability
MTS
assay,
Trypan
Blue
staining
and
western
blotting
analysis
Akt
B-cell
lymphoma
2
(Bcl-2),
intracellular
increase
reactive
oxygen
species
(ROS)
fluorescent
probe
NADPH
oxidase
4
(NOX4)
expression,
as
well
expression
brain-derived
neurotrophic
factor
(BDNF),
major
neurotrophin
neurogenesis
synaptic
plasticity.
Although
both
Trolox
r-Irisin
manifested
protective
effect
on
health,
combined
treatment
produced
best
results,
significant
improvement
all
parameters
examined.
In
conclusion,
further
studies
are
needed
evaluate
such
combination
counteracting
weightlessness-induced
death,
other
strategies
safeguard
spaceflight.