Reviews in Medical Virology,
Journal Year:
2024,
Volume and Issue:
34(5)
Published: Sept. 1, 2024
ABSTRACT
Neurotropic
viruses
have
been
implicated
in
altering
the
central
nervous
system
microenvironment
and
promoting
brain
metastasis
of
breast
cancer
through
complex
interactions
involving
viral
entry
mechanisms,
modulation
blood–brain
barrier,
immune
evasion,
alteration
tumour
microenvironment.
This
narrative
review
explores
molecular
mechanisms
by
which
neurotropic
such
as
Herpes
Simplex
Virus,
Human
Immunodeficiency
Japanese
Encephalitis
Rabies
Virus
facilitate
metastasis,
focusing
on
their
ability
to
disrupt
barrier
integrity,
modulate
responses,
create
a
permissive
environment
for
metastatic
cell
survival
growth
within
system.
Current
therapeutic
implications
challenges
targeting
prevent
or
treat
are
discussed,
highlighting
need
innovative
strategies
multidisciplinary
approaches
virology,
oncology,
immunology.
Neuroglia,
Journal Year:
2025,
Volume and Issue:
6(1), P. 4 - 4
Published: Jan. 6, 2025
Overexposure
of
humans
to
heavy
metals
and
essential
poses
a
significant
risk
for
the
development
neurological
neurodevelopmental
disorders.
The
mechanisms
through
which
these
exert
their
effects
include
generation
reactive
oxygen
species,
mitochondrial
dysfunction,
activation
inflammatory
pathways,
disruption
cellular
signaling.
function
glial
cells
in
brain
maintenance
homeostasis
cannot
be
overlooked.
are
particularly
susceptible
metal-induced
neurotoxicity.
Accumulation
promotes
microglial
activation,
triggering
responses
that
can
coincide
with
other
neurotoxicity,
inducing
alteration
synaptic
transmission,
cognitive
deficit,
neuronal
damage.
In
this
review,
we
highlighted
role
dysfunction
some
selected
neurodegenerative
diseases
We
further
dive
into
how
exposure
such
as
nickel,
manganese,
methyl
mercury,
cadmium,
iron,
arsenic,
lead
affect
functions
microglia,
astrocytes,
oligodendrocytes
they
on
relation
Potential
therapeutic
interventions
use
new
improved
chelating
agents
antioxidant
therapies
might
approach
alleviating
perturbations.
Brain Sciences,
Journal Year:
2024,
Volume and Issue:
14(4), P. 331 - 331
Published: March 29, 2024
Glioblastoma
multiforme
(GBM)
stands
out
as
the
most
tremendous
brain
tumor,
constituting
60%
of
primary
cancers,
accompanied
by
dismal
survival
rates.
Despite
advancements
in
research,
therapeutic
options
remain
limited
to
chemotherapy
and
surgery.
GBM
molecular
heterogeneity,
intricate
interaction
with
tumor
microenvironment
(TME),
non-selective
treatments
contribute
neoplastic
relapse.
Diagnostic
challenges
arise
from
advanced-stage
detection,
necessitating
exploration
novel
biomarkers
for
early
diagnosis.
Using
data
literature
a
bioinformatic
tool,
current
manuscript
delineates
interplay
between
human
GBM,
astrocytes,
myeloid
cells,
underscoring
selected
protein
pathways
belonging
astroglia
lineage,
which
can
be
considered
targeted
therapies.
Moreover,
pivotal
role
extracellular
vesicles
(EVs)
orchestrating
favorable
cancer
progression
is
highlighted,
suggesting
their
utility
identifying
Pharmacological Research,
Journal Year:
2024,
Volume and Issue:
205, P. 107255 - 107255
Published: June 12, 2024
Research
has
shown
that
a
significant
portion
of
cancer
patients
experience
depressive
symptoms,
often
accompanied
by
neuroendocrine
hormone
imbalances.
Depression
is
frequently
associated
with
decreased
levels
serotonin
the
alternate
name
5-hydroxytryptamine
(5-HT),
leading
to
common
use
selective
reuptake
inhibitors
(SSRIs)
as
antidepressants.
However,
role
in
tumor
regulation
remains
unclear,
its
expression
displaying
varied
effects
across
different
types
tumors.
Tumor
initiation
and
progression
are
closely
intertwined
immune
function
human
body.
Neuroimmunity,
an
interdisciplinary
subject,
played
unique
study
relationship
between
psychosocial
factors
tumors
their
mechanisms
recent
years.
This
article
offers
comprehensive
review
serotonin's
regulatory
roles
onset
progression,
well
impacts
on
cells
microenvironment.
The
aim
stimulate
further
research
discover
novel
targets
for
treatment.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(1), P. 216 - 216
Published: Jan. 16, 2025
Background:
Brain
cancers
represent
a
formidable
oncological
challenge
characterized
by
their
aggressive
nature
and
resistance
to
conventional
therapeutic
interventions.
The
tumor
microenvironment
has
emerged
as
critical
determinant
of
progression
treatment
efficacy.
Within
this
complex
ecosystem,
microglia
macrophages
play
fundamental
roles,
forming
intricate
networks
with
peripheral
immune
cell
populations,
particularly
T
cells.
precise
mechanisms
underlying
microglial
interactions
cells
contributions
immunosuppression
remain
incompletely
understood.
Methods:
This
review
comprehensively
examines
the
cellular
dialogue
between
in
two
prominent
brain
malignancies:
primary
glioblastoma
secondary
metastases.
Results:
Through
comprehensive
current
scientific
literature,
we
explore
nuanced
through
which
microglial-T
modulate
growth
responses.
Conclusions:
Our
analysis
seeks
unravel
communication
pathways
that
potentially
underpin
progression,
ultimate
goal
illuminating
novel
strategies
for
cancer
intervention.
Cancers,
Journal Year:
2025,
Volume and Issue:
17(2), P. 298 - 298
Published: Jan. 17, 2025
Gatekeeper
or
accomplice?
That
is
the
paradoxical
role
of
blood-brain
barrier
(BBB)
in
developing
brain
metastasis
(BM).
BM
occurs
when
cancerous
cells
from
primary
cancer
elsewhere
body
gain
ability
to
metastasize
and
invade
parenchyma
despite
formidable
defense
BBB.
These
metastatic
manipulate
BBB's
components,
changing
them
gatekeepers
accomplices
that
aid
their
progression
into
tissue.
This
dual
BBB-as
both
a
protective
system
potential
facilitator
cells-highlights
its
complexity.
Even
with
therapy
such
as
chemotherapy,
usually
recurs
due
BBB
limiting
crossing
drugs
via
efflux
transporters;
therefore,
treatment
efficacy
limited.
The
pathophysiology
also
complex,
our
understanding
interplay
between
components
still
needs
be
improved.
However,
advancements
clinical
research
are
helping
bridge
knowledge
gap,
which
essential
for
effective
therapy.
By
targeting
neurovascular
unit
polarization
microglia,
astrocytes,
pericytes,
by
utilizing
technological
tools
like
focused
ultrasound
transiently
disrupt
therapeutic
nanoparticles
improve
drug
delivery
efficiency
tissue,
we
can
better
address
this
pathology.
narrative
review
delves
latest
literature
analyze
manifestation
explores
avenues
BBB-tumor
cell
interaction.
Cancer Science,
Journal Year:
2024,
Volume and Issue:
115(9), P. 2871 - 2878
Published: July 11, 2024
Abstract
Cancer
brain
metastasis
has
a
poor
prognosis,
is
commonly
observed
in
clinical
practice,
and
the
number
of
cases
increasing
as
overall
cancer
survival
improves.
However,
experiments
mouse
models
have
shown
that
itself
an
inefficient
process.
One
reason
for
this
inefficiency
microenvironment,
which
differs
significantly
from
other
organs,
making
it
difficult
cells
to
adapt.
The
microenvironment
consists
unique
resident
cell
types
such
neurons,
oligodendrocytes,
astrocytes,
microglia.
Accumulating
evidence
over
past
decades
suggests
interactions
between
glial
can
positively
or
negatively
influence
development
metastasis.
Nevertheless,
elucidating
complex
remains
challenging,
part
due
limitations
existing
experimental
culture.
In
review,
we
first
provide
overview
culture
methods
then
examine
recent
discoveries
regarding
metastatic
surrounding
cells,
with
special
focus
on
astrocytes
Finally,
discuss
future
perspectives
understanding
multifaceted
treatment
tumors.
Frontiers in Oncology,
Journal Year:
2024,
Volume and Issue:
14
Published: Aug. 12, 2024
Breast
cancer
is
the
leading
diagnosed
in
women
globally,
with
brain
metastasis
emerging
as
a
major
cause
of
death,
particularly
human
epidermal
growth
factor
receptor
2
positive
and
triple-negative
breast
subtypes.
Comprehensive
understanding
molecular
foundations
central
nervous
system
metastases
imperative
for
evolution
efficacious
treatment
strategies.
Lipocalin-2
(LCN2),
secreted
iron
transport
protein
multiple
functions,
has
been
linked
to
progression
(BCBM).
In
primary
tumors,
LCN2
promotes
proliferation
angiogenesis
cells,
triggers
epithelial-mesenchymal
transition,
interacts
matrix
metalloproteinase-9,
thereby
facilitating
reorganization
extracellular
enhancing
cell
invasion
migration.
microenvironment,
undermines
blood-brain
barrier
facilitates
tumor
seeding
by
modulating
behavior
key
cellular
components.
summary,
this
review
meticulously
examines
fuel
role
BCBM
cascade,
investigates
potential
mechanisms
involved.
It
highlights
both
therapeutic
target
biomarker,
indicating
that
interventions
targeting
may
offer
improved
outcomes
patients
afflicted
BCBM.
Alzheimer s & Dementia,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 6, 2024
Abstract
Recent
research
highlights
the
critical
role
of
inflammation
in
accelerating
amyloid
beta
and
phosphorylated
tubulin‐associated
protein
tau
cascade
Alzheimer's
disease
(AD)
progression.
Emerging
evidence
suggests
that
exercise
influences
AD
by
modulating
inflammatory
responses.
We
conducted
a
comprehensive
search
across
multiple
online
databases.
Our
approach
focused
on
previous
recent
studies
exploring
links
among
inflammation,
AD,
effects
exercise,
specifically
targeting
articles
books
published
English.
pointed
out
extends
from
periphery
to
central
nervous
system,
facilitated
macrophage/microglial
NLRP3
(nucleotide‐binding
domain,
leucine
rich–containing
family,
pyrin
domain–containing
3)
inflammasome
signaling,
which
exacerbates
classical
mechanisms.
Moreover,
we
provided
further
insights
into
modulation
signaling
through
exerkines,
may
contribute
mitigating
development.
These
deepen
our
understanding
mechanisms
offer
potential
for
identifying
key
therapeutic
targets
biomarkers
crucial
effective
management
treatment.
Highlights
Inflammation
is
potentially
linked
acceleration
pathogenesis,
including
pathways
involving
tau,
mediated
pro‐inflammatory
cytokines.
Inflammation,
initiated
nucleotide‐binding
3
(NLRP3)
pathway
within
M1‐type
macrophages/microglia,
neuroinflammation
Exercise
has
reduce
development
influencing
via
exerkines.