Brain Sciences,
Год журнала:
2024,
Номер
14(11), С. 1133 - 1133
Опубликована: Ноя. 10, 2024
Unlike
enriched
environments
for
rodents,
human-built
often
hinder
neuroplasticity
through
sedentary
lifestyles,
to
which
exercise
can
merely
overcome
its
adverse
effects.
This
paper
introduces
"environmental
affordance
physical
activity"
quantify
the
potential
of
spatial
layout
designs
stimulate
activity
and
sustain
neuroplasticity,
mainly
hippocampal
neurogenesis.
Signal Transduction and Targeted Therapy,
Год журнала:
2023,
Номер
8(1)
Опубликована: Окт. 23, 2023
Abstract
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
disorder
characterized
by
the
predominant
impairment
of
neurons
in
hippocampus
and
formation
amyloid
plaques,
hyperphosphorylated
tau
protein,
neurofibrillary
tangles
brain.
The
overexpression
amyloid-β
precursor
protein
(APP)
an
AD
brain
results
binding
APP
intracellular
domain
(AICD)
to
Fe65
via
C-terminal
Fe65-PTB2
interaction,
which
then
triggers
secretion
consequent
pathogenesis
AD.
Apparently,
targeting
interaction
between
can
offer
promising
therapeutic
approach
for
Recently,
exosome,
type
extracellular
vesicle
with
diameter
around
30–200
nm,
has
gained
much
attention
as
potential
delivery
tool
diseases,
including
AD,
due
their
ability
cross
blood–brain
barrier,
efficient
uptake
autologous
cells,
be
surface-modified
target-specific
receptor
ligands.
Here,
engineering
neuron
cell-derived
exosomes
overexpress
Fe65,
enabled
development
novel
exosome-based
targeted
drug
system,
carried
Corynoxine-B
(Cory-B,
autophagy
inducer)
overexpressed-neuron
cells
mice.
Fe65-engineered
HT22
(Fe65-EXO)
loaded
Cory-B
(Fe65-EXO-Cory-B)
hijacked
signaling
blocked
natural
APP,
enabling
APP-targeted
Cory-B.
Notably,
Fe65-EXO-Cory-B
induced
APP-expressing
neuronal
leading
amelioration
cognitive
decline
mice,
demonstrating
effective
intervention
Brain Sciences,
Год журнала:
2023,
Номер
13(12), С. 1610 - 1610
Опубликована: Ноя. 21, 2023
Neuroplasticity
refers
to
the
ability
of
brain
reorganize
and
modify
its
neural
connections
in
response
environmental
stimuli,
experience,
learning,
injury,
disease
processes.
It
encompasses
a
range
mechanisms,
including
changes
synaptic
strength
connectivity,
formation
new
synapses,
alterations
structure
function
neurons,
generation
neurons.
plays
crucial
role
developing
maintaining
function,
learning
memory,
as
well
recovery
from
injury
adaptation
changes.
In
this
review,
we
explore
vast
potential
neuroplasticity
various
aspects
across
lifespan
context
disease.
Changes
aging
significance
cognitive
later
life
will
also
be
reviewed.
Finally,
discuss
common
mechanisms
associated
with
age-related
neurodegenerative
processes
(including
protein
aggregation
accumulation,
mitochondrial
dysfunction,
oxidative
stress,
neuroinflammation)
how
these
can
mitigated,
at
least
partially,
by
non-invasive
non-pharmacologic
lifestyle
interventions
aimed
promoting
harnessing
neuroplasticity.
Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Фев. 2, 2024
Abstract
Neuroinflammation
is
a
pathological
hallmark
of
Alzheimer’s
disease
(AD),
characterized
by
the
stimulation
resident
immune
cells
brain
and
penetration
peripheral
cells.
These
inflammatory
processes
facilitate
deposition
amyloid-beta
(Aβ)
plaques
abnormal
hyperphosphorylation
tau
protein.
Managing
neuroinflammation
to
restore
homeostasis
decrease
neuronal
damage
therapeutic
approach
for
AD.
One
way
achieve
this
through
exercise,
which
can
improve
function
protect
against
neuroinflammation,
oxidative
stress,
synaptic
dysfunction
in
AD
models.
The
neuroprotective
impact
exercise
regulated
various
molecular
factors
that
be
activated
same
as
administration
their
mimetics.
Recent
evidence
has
proven
some
mimetics
effective
alleviating
AD,
and,
additionally,
they
are
helpful
alternative
option
patients
who
unable
perform
regular
physical
manage
neurodegenerative
disorders.
This
review
focuses
on
current
state
knowledge
mimetics,
including
efficacy,
regulatory
mechanisms,
progress,
challenges,
limitations,
future
guidance
application
therapy.
Biomedicines,
Год журнала:
2022,
Номер
10(5), С. 1206 - 1206
Опубликована: Май 23, 2022
Astrocytes
are
essential
for
normal
brain
development
and
functioning.
They
respond
to
injury
disease
through
a
process
referred
as
reactive
astrogliosis,
where
the
reactivity
is
highly
heterogenous
context-dependent.
Reactive
astrocytes
active
contributors
pathology
can
exert
beneficial,
detrimental,
or
mixed
effects
following
insults.
Transforming
growth
factor-β
(TGF-β)
has
been
identified
one
of
key
factors
regulating
astrocyte
reactivity.
The
genetic
pharmacological
manipulation
TGF-β
signaling
pathway
in
animal
models
central
nervous
system
(CNS)
alters
pathological
functional
outcomes.
This
review
aims
provide
recent
understanding
regarding
injury,
aging,
neurodegeneration.
Further,
it
explores
how
modulates
function
context
CNS
injury.
The Annual Review of Pharmacology and Toxicology,
Год журнала:
2021,
Номер
62(1), С. 255 - 277
Опубликована: Окт. 12, 2021
Neurodegenerative
diseases
are
characterized
by
the
loss
of
homeostatic
functions
that
control
redox
and
energy
metabolism,
neuroinflammation,
proteostasis.
The
transcription
factor
nuclear
erythroid
2–related
2
(NRF2)
is
a
master
controller
these
functions,
its
overall
activity
compromised
during
aging
in
diseases.
However,
NRF2
can
be
activated
pharmacologically
now
being
considered
common
therapeutic
target.
Many
gaps
still
exist
our
knowledge
specific
role
plays
specialized
brain
cell
or
how
cells
respond
to
hallmarks
This
review
discusses
relevance
several
hallmark
features
neurodegenerative
current
status
pharmacological
activators
might
pass
through
blood-brain
barrier
provide
disease-modifying
effect.
Brain Plasticity,
Год журнала:
2022,
Номер
8(1), С. 97 - 119
Опубликована: Сен. 30, 2022
The
birth,
maturation,
and
integration
of
new
neurons
in
the
adult
hippocampus
regulates
specific
learning
memory
processes,
responses
to
stress,
antidepressant
treatment
efficacy.
This
process
hippocampal
neurogenesis
is
sensitive
environmental
stimuli,
including
peripheral
signals
from
certain
cytokines,
hormones,
metabolites,
which
can
promote
or
hinder
production
survival
neurons.
trillions
microorganisms
resident
gastrointestinal
tract,
collectively
known
as
gut
microbiota,
also
demonstrate
ability
modulate
neurogenesis.
In
doing
so,
microbiota-gut-brain
axis
influence
brain
functions
regulated
by
Unlike
hippocampus,
microbiota
highly
accessible
direct
interventions,
such
prebiotics,
probiotics,
antibiotics,
be
manipulated
lifestyle
choices
diet.
Therefore,
understanding
pathways
shapes
may
reveal
novel
targets
for
non-invasive
therapeutics
treat
disorders
alterations
have
been
implicated.
review
first
outlines
factors
both
microbiome
neurogenesis,
with
cognizance
that
these
effects
might
happen
either
independently
due
microbiota-driven
mechanisms.
We
then
highlight
approaches
investigating
regulation
axis.
Finally,
we
summarize
current
evidence
demonstrating
microbiota's
mechanisms
driven
through
immune
pathways,
microbial
endocrine
signalling,
nervous
system,
postulate
implications
disease
onset
treatment.
Neural Regeneration Research,
Год журнала:
2023,
Номер
19(3), С. 619 - 628
Опубликована: Июль 28, 2023
Abstract
Recent
studies
have
demonstrated
that
neuroplasticity,
such
as
synaptic
plasticity
and
neurogenesis,
exists
throughout
the
normal
lifespan
but
declines
with
age
is
significantly
impaired
in
individuals
Alzheimer’s
disease.
Hence,
promoting
neuroplasticity
may
represent
an
effective
strategy
which
disease
can
be
alleviated.
Due
to
their
significant
ability
self-renew,
differentiate,
migrate,
neural
stem
cells
play
essential
role
reversing
neuronal
damage,
reducing
pathology
of
disease,
including
amyloid-β,
tau
protein,
neuroinflammation,
secreting
neurotrophic
factors
growth
are
related
plasticity.
These
events
promote
neurogenesis
repair
microenvironment
mammalian
brain.
Consequently,
considered
a
potential
regenerative
therapy
improve
other
neurodegenerative
diseases.
In
this
review,
we
discuss
how
regulate
optimize
effects
enhance
for
treating
clinic.