Revista Salud Bosque,
Год журнала:
2022,
Номер
14(2)
Опубликована: Авг. 23, 2022
La
comprensión
de
las
causas,
desarrollo
y
tratamiento
la
enfermedad
Huntington
representan
un
reto
para
el
personal
médico,
porque
requiere
una
adecuada
interpretación
del
plano
genético,
histológico
fisiopatológico
sistema
nervioso.
Entender
a
esta
neurodegenerativa
no
solo
como
proceso
resultado
alteración
genética,
sino
complejo
modificado
en
red,
características
morfológicas
fisiológicas
diferentes
poblaciones
celulares,
permitirían
generar
abordaje
puntual
patología.
El
siguiente
articulo
describe
celulares
metabólicas
más
relevantes
buscando
brindar
al
lector
reconociendo
integral
enfermedad.
Frontiers in Cellular Neuroscience,
Год журнала:
2025,
Номер
19
Опубликована: Фев. 11, 2025
Neurodegenerative
diseases,
such
as
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
Multiple
Sclerosis
(MS),
and
Huntington’s
(HD),
although
distinct
in
their
clinical
manifestations,
share
a
common
hallmark:
disrupted
neuroinflammatory
environment
orchestrated
by
dysregulation
of
neuroglial
intercellular
communication.
Neuroglial
crosstalk
is
physiologically
ensured
extracellular
mediators
the
activity
connexins
(Cxs),
forming
proteins
gap
junctions
(Gjs)
hemichannels
(HCs),
which
maintain
intracellular
homeostasis.
However,
accumulating
evidence
suggests
that
Cxs
can
also
act
pathological
pore
conditions,
thereby
contributing
to
neurodegenerative
phenomena
synaptic
dysfunction,
oxidative
stress,
ultimately
cell
death.
This
review
explores
mechanistic
insights
Cxs-mediated
communication
progression
diseases
discusses
therapeutic
potential
targeting
restore
cellular
Biomolecules,
Год журнала:
2024,
Номер
14(10), С. 1204 - 1204
Опубликована: Сен. 25, 2024
Astrocytes
are
one
of
the
key
glial
types
central
nervous
system
(CNS),
accounting
for
over
20%
total
cells
in
brain.
Extensive
evidence
has
established
their
indispensable
functions
maintenance
CNS
homeostasis,
as
well
broad
involvement
neurological
conditions.
In
particular,
astrocytes
can
participate
various
neuroinflammatory
processes,
e.g.,
releasing
a
repertoire
cytokines
and
chemokines
or
specific
neurotrophic
factors,
which
result
both
beneficial
detrimental
effects.
It
become
increasingly
clear
that
such
astrocyte-mediated
neuroinflammation,
together
with
its
complex
crosstalk
other
immune
cells,
designates
neuronal
survival
functional
integrity
neurocircuits,
thus
critically
contributing
to
disease
onset
progression.
this
review,
we
focus
on
current
knowledge
responses
astrocytes,
summarizing
common
features
Moreover,
highlight
several
vital
questions
future
research
promise
novel
insights
into
diagnostic
therapeutic
strategies
against
those
debilitating
diseases.
Early-life
stress
can
have
lifelong
consequences,
enhancing
susceptibility
and
resulting
in
behavioural
cognitive
deficits.
While
the
effects
of
early-life
on
neuronal
function
been
well-described,
we
still
know
very
little
about
contribution
non-neuronal
brain
cells.
Investigating
complex
interactions
between
distinct
cell
types
is
critical
to
fully
understand
how
cellular
changes
manifest
as
deficits
following
stress.
Here,
using
male
female
mice
report
that
induces
anxiety-like
behaviour
fear
generalisation
an
amygdala-dependent
learning
memory
task.
These
were
associated
with
impaired
synaptic
plasticity,
increased
neural
excitability,
astrocyte
hypofunction.
Genetic
perturbation
amygdala
by
either
reducing
calcium
activity
or
network
was
sufficient
replicate
cellular,
synaptic,
Our
data
reveal
a
role
astrocytes
tuning
emotionally
salient
provide
mechanistic
links
stress,
hypofunction,
Early-life
stress
can
have
lifelong
consequences,
enhancing
susceptibility
and
resulting
in
behavioural
cognitive
deficits.
While
the
effects
of
early-life
on
neuronal
function
been
well-described,
we
still
know
very
little
about
contribution
non-neuronal
brain
cells.
Investigating
complex
interactions
between
distinct
cell
types
is
critical
to
fully
understand
how
cellular
changes
manifest
as
deficits
following
stress.
Here,
using
male
female
mice
report
that
induces
anxiety-like
behaviour
fear
generalisation
an
amygdala-dependent
learning
memory
task.
These
were
associated
with
impaired
synaptic
plasticity,
increased
neural
excitability,
astrocyte
hypofunction.
Genetic
perturbation
amygdala
by
either
reducing
calcium
activity
or
network
was
sufficient
replicate
cellular,
synaptic,
Our
data
reveal
a
role
astrocytes
tuning
emotionally
salient
provide
mechanistic
links
stress,
hypofunction,
Early-life
stress
can
have
lifelong
consequences,
enhancing
susceptibility
and
resulting
in
behavioural
cognitive
deficits.
While
the
effects
of
early-life
on
neuronal
function
been
well-described,
we
still
know
very
little
about
contribution
non-neuronal
brain
cells.
Investigating
complex
interactions
between
distinct
cell
types
is
critical
to
fully
understand
how
cellular
changes
manifest
as
deficits
following
stress.
Here,
using
male
female
mice
report
that
induces
anxiety-like
behaviour
fear
generalisation
an
amygdala-dependent
learning
memory
task.
These
were
associated
with
impaired
synaptic
plasticity,
increased
neural
excitability,
astrocyte
hypofunction.
Genetic
perturbation
amygdala
by
either
reducing
calcium
activity
or
network
was
sufficient
replicate
cellular,
synaptic,
Our
data
reveal
a
role
astrocytes
tuning
emotionally
salient
provide
mechanistic
links
stress,
hypofunction,
Early-life
stress
can
have
lifelong
consequences,
enhancing
susceptibility
and
resulting
in
behavioral
cognitive
deficits.
While
the
effects
of
early-life
on
neuronal
function
been
well-described,
we
still
know
very
little
about
contribution
non-neuronal
brain
cells.
Investigating
complex
interactions
between
distinct
cell
types
is
critical
to
fully
understand
how
cellular
changes
manifest
as
deficits
following
stress.
Here,
using
male
female
mice
report
that
induces
anxiety-like
behavior
fear
generalisation
an
amygdala-dependent
learning
memory
task.
These
were
associated
with
impaired
synaptic
plasticity,
increased
neural
excitability,
astrocyte
dysfunction.
Genetic
perturbation
amygdala
by
either
silencing
these
cells
or
reducing
network
was
sufficient
replicate
cellular,
synaptic,
data
provide
mechanistic
links
Our
reveal
a
role
astrocytes
tuning
emotionally
salient
dysfunction
generalisation.
Further
understanding
are
affected
might
offer
new
insights
into
long-term
impact
affective
states.
Life,
Год журнала:
2023,
Номер
13(10), С. 2038 - 2038
Опубликована: Окт. 11, 2023
The
human
brain
is
composed
of
nearly
one
hundred
billion
neurons
and
an
equal
number
glial
cells,
including
macroglia,
i.e.,
astrocytes
oligodendrocytes,
microglia,
the
resident
immune
cells
brain.
In
last
few
decades,
compelling
evidence
has
revealed
that
are
far
more
active
complex
than
previously
thought.
particular,
astrocytes,
most
abundant
cell
population,
not
only
take
part
in
development,
metabolism,
defense
against
pathogens
insults,
but
they
also
affect
sensory,
motor,
cognitive
functions
by
constantly
modulating
synaptic
activity.
Not
surprisingly,
actively
involved
neurodegenerative
diseases
(NDs)
other
neurological
disorders
like
tumors,
which
rapidly
become
reactive
mediate
neuroinflammation.
Reactive
acquire
or
lose
specific
differently
modulate
disease
progression
symptoms,
impairments.
Astrocytes
express
several
types
ion
channels,
K+,
Na+,
Ca2+
transient
receptor
potential
channels
(TRP),
aquaporins,
mechanoreceptors,
anion
whose
properties
partially
understood,
particularly
small
processes
contact
synapses.
addition,
ionotropic
receptors
for
neurotransmitters.
Here,
we
provide
extensive
up-to-date
review
roles
astrocyte
physiology
pathology.
As
examples
two
different
pathologies,
focus
on
Alzheimer’s
(AD),
diffuse
disorders,
glioblastoma
(GBM),
common
tumor.
Understanding
how
participate
NDs
tumors
necessary
developing
new
therapeutic
tools
these
increasingly
conditions.