The Crucial Role of the Blood–Brain Barrier in Neurodegenerative Diseases: Mechanisms of Disruption and Therapeutic Implications
Journal of Clinical Medicine,
Год журнала:
2025,
Номер
14(2), С. 386 - 386
Опубликована: Янв. 9, 2025
The
blood-brain
barrier
(BBB)
is
a
crucial
structure
that
maintains
brain
homeostasis
by
regulating
the
entry
of
molecules
and
cells
from
bloodstream
into
central
nervous
system
(CNS).
Neurodegenerative
diseases
such
as
Alzheimer's
Parkinson's
disease,
well
ischemic
stroke,
compromise
integrity
BBB.
This
leads
to
increased
permeability
infiltration
harmful
substances,
thereby
accelerating
neurodegeneration.
In
this
review,
we
explore
mechanisms
underlying
BBB
disruption,
including
oxidative
stress,
neuroinflammation,
vascular
dysfunction,
loss
tight
junction
integrity,
in
patients
with
neurodegenerative
diseases.
We
discuss
how
breakdown
contributes
neurotoxicity,
abnormal
accumulation
pathological
proteins,
all
which
exacerbate
neuronal
damage
facilitate
disease
progression.
Furthermore,
potential
therapeutic
strategies
aimed
at
preserving
or
restoring
function,
anti-inflammatory
treatments,
antioxidant
therapies,
approaches
enhance
integrity.
Given
role
neurodegeneration,
maintaining
its
represents
promising
approach
slow
prevent
progression
Язык: Английский
La maladie de Parkinson : de la génétique aux thérapies ciblées
Comptes Rendus Biologies,
Год журнала:
2025,
Номер
348(G1), С. 21 - 33
Опубликована: Фев. 13, 2025
La
maladie
de
Parkinson
(MP)
est
une
multifactorielle
impliquant
des
facteurs
génétiques
et
environnementaux.
Cependant,
l'âge
début,
l'étendue
lésions
la
rapidité
progression
peuvent
varier
façon
considérable,
ce
qui
conduit
à
s'interroger
sur
l'unicité
MP.
L'identification
formes
monogéniques,
dont
certaines
semblent
impliquer
mécanismes
différents,
renforce
l'hypothèse
distinctes
partagent
présence
d'un
syndrome
parkinsonien.
Alors
que
le
gène
SNCA
fût
premier
identifié
dans
les
rares,
variants
pathogènes
gènes
GBA1
LRRK2
représentent
causes
ou
risque
MP
plus
communs,
PRKN
souvent
impliqué
autosomiques
récessives
Les
patients
présentant
SNCA,
GBA1,
diffèrent
par
leurs
caractéristiques
cliniques,
anatomopathologiques
biochimiques.
Ainsi,
ces
quatre
associés
sont
intérêt
tout
particulier
pour
développement
thérapeutiques
spécifiques,
d'autant
approches
actuelles
restent
symptomatiques.
essais
cliniques
fondés
nature
du
débutent.
Dans
cette
revue,
nous
présentons
principales
physiopathologiques
avant
discuter
nouvelles
ciblent
spécifiquement.
Parkinson's
disease
(PD)
is
a
multifactorial
disorder
involving
various
biological
pathways.
However,
it
more
accurate
not
to
define
PD
as
unique
entity,
but
rather
mixture
of
several
diseases
with
similar
phenotypes.
Attempts
classify
subtypes
based
on
the
clinical
phenotype
or
biomarkers
were
tried.
Nonetheless,
for
subset
individuals,
classification
implied
gene
appears
be
most
practical.
Although
was
first
identified
in
rare
patients,
pathogenic
and
are
common
genetic
risk
factors
PD,
frequent
autosomal
recessive
PD.
Patients
show
clinical,
anatomopathological
biochemical
aspects.
Therefore,
these
four
genes
associated
particular
interest
development
targeted
therapies.
This
fact
reinforced
by
reality
that
current
approaches
only
symptomatic,
no
curative
treatment
available
today.
A
number
trials
aiming
slow
stop
running,
involved.
In
this
review,
we
will
discuss
therapeutic
targeting
PRKN.
Peripheral Inflammation and Insulin Resistance: Their Impact on Blood–Brain Barrier Integrity and Glia Activation in Alzheimer’s Disease
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(9), С. 4209 - 4209
Опубликована: Апрель 29, 2025
Alzheimer’s
disease
(AD)
is
a
progressive
neurodegenerative
disorder
characterized
by
cognitive
decline,
memory
impairment,
and
synaptic
dysfunction.
The
accumulation
of
amyloid
beta
(Aβ)
plaques
hyperphosphorylated
tau
protein
leads
to
neuronal
dysfunction,
neuroinflammation,
glial
cell
activation.
Emerging
evidence
suggests
that
peripheral
insulin
resistance
chronic
inflammation,
often
associated
with
type
2
diabetes
(T2D)
obesity,
promote
increased
proinflammatory
cytokines,
oxidative
stress,
immune
infiltration.
These
conditions
further
damage
the
blood–brain
barrier
(BBB)
integrity
neurotoxicity
This
induces
neuroinflammation
impaired
signaling,
reducing
glucose
metabolism
exacerbating
Aβ
hyperphosphorylation.
Indeed,
epidemiological
studies
have
linked
T2D
obesity
an
risk
developing
AD,
reinforcing
connection
between
metabolic
disorders
neurodegeneration.
review
explores
relationships
resistance,
BBB
highlighting
their
role
in
activation
exacerbation
AD
pathology.
Язык: Английский