Radiation,
Journal Year:
2024,
Volume and Issue:
4(2), P. 125 - 141
Published: May 8, 2024
For
patients
with
recurrent
brain
metastases,
there
is
an
urgent
need
for
a
more
effective
and
less
toxic
treatment
approach.
Accumulating
evidence
has
shown
that
spatially
fractionated
radiation
therapy
(SFRT)
able
to
provide
significantly
higher
therapeutic
ratio
lower
toxicity
compared
conventional
using
uniform
dose.
The
purpose
of
this
study
was
explore
the
potential
low
benefit
mini-beam
radiotherapy
(MBRT),
form
SFRT,
whole-brain
re-irradiation
in
healthy
mouse
model.
Animals
first
received
initial
25
Gy
irradiation.
Five
weeks
later,
they
were
randomized
into
three
groups
receive
different
treatments
as
follows:
(1)
irradiation
at
Gy;
(2)
MBRT
volume-averaged
dose
(106.1/8.8
peak/valley
dose,
Gy-MBRT);
(3)
43
(182.5/15.1
Gy-MBRT).
Animal
survival
changes
body
weight
monitored
signs
toxicity.
Brains
harvested
5
after
histologic
evaluation
immunostaining.
showed
Gy-MBRT
resulted
loss
than
re-irradiation.
Mice
group
had
level
CD11b-stained
microglia
but
also
maintained
Ki67-stained
proliferative
progenitor
cells
mice
group.
However,
high-dose
severe
low-dose
groups,
indicating
dose-dependent
Our
demonstrates
appropriate
Future
studies
investigating
use
metastases
are
warranted.
Medicina,
Journal Year:
2024,
Volume and Issue:
60(4), P. 653 - 653
Published: April 18, 2024
Radioactivity
is
a
process
in
which
the
nuclei
of
unstable
atoms
spontaneously
decay,
producing
other
and
releasing
energy
form
ionizing
radiation
alpha
(α)
beta
(β)
particles
as
well
emission
gamma
(γ)
electromagnetic
waves.
People
may
be
exposed
to
various
forms,
casualties
nuclear
accidents,
workers
power
plants,
or
while
working
using
different
sources
medicine
health
care.
Acute
syndrome
(ARS)
occurs
subjects
very
high
dose
short
period
time.
Each
has
unique
pathophysiological
effect.
Unfortunately,
higher
organisms—human
beings—in
course
evolution
have
not
acquired
receptors
for
direct
“capture”
energy,
transferred
at
level
DNA,
cells,
tissues,
organs.
Radiation
biological
systems
depends
on
amount
absorbed
its
spatial
distribution,
particularly
depending
linear
transfer
(LET).
Photon
with
low
LET
leads
homogeneous
deposition
entire
tissue
volume.
On
hand,
produces
fast
Bragg
peak,
generates
input
dose,
whereby
penetration
depth
into
increases
energy.
The
consequences
are
mutations,
apoptosis,
development
cancer,
cell
death.
most
sensitive
cells
those
that
divide
intensively—bone
marrow
digestive
tract
reproductive
skin
cells.
care
system
public
should
raise
awareness
radiation.
Therefore,
our
aim
identify
ARS
taking
account
damage
respiratory
system,
nervous
hematopoietic
gastrointestinal
tract,
skin.
Neurosciences,
Journal Year:
2025,
Volume and Issue:
30(1), P. 5 - 19
Published: Jan. 1, 2025
The
hippocampus,
noted
as
(HC),
plays
a
crucial
role
in
the
processes
of
learning,
memory
formation,
and
spatial
navigation.
Recent
research
reveals
that
this
brain
region
can
undergo
structural
functional
changes
due
to
environmental
exposures,
including
stress,
noise
pollution,
sleep
deprivation,
microgravity.
This
review
synthesizes
findings
from
animal
human
studies,
emphasizing
HC's
plasticity
response
these
factors.
It
examines
volume,
architecture,
neurogenesis,
synaptic
plasticity,
gene
expression
highlights
critical
periods
vulnerability
influences
impacting
cognition
behavior.
also
investigates
underlying
mechanisms
such
glucocorticoid
signaling,
epigenetic
alterations,
neural
circuit
adaptations.
Understanding
how
HC
reacts
various
exposures
is
vital
for
developing
strategies
enhance
cognitive
resilience
mitigate
negative
effects
on
region.
Further
needed
identify
protective
risk
factors
create
effective
interventions.
Materials Today Bio,
Journal Year:
2025,
Volume and Issue:
31, P. 101568 - 101568
Published: Feb. 11, 2025
Acute
exposure
to
high-dose
radiation
during
head
and
neck
tumors
radiotherapy
can
result
in
radiation-induced
brain
injury
(RIBI),
characterized
by
neurocognitive
deficits,
dementia,
epilepsy.
Asparagine
endopeptidase
(AEP),
a
cysteine
proteinase,
is
effective
preventing
neurodegenerative
diseases
RIBI.
However,
the
limited
permeability
of
selective
AEP
inhibitor
(AEPI)
delivery
reduces
its
effectiveness
This
study
constructed
nose-to-brain
platform
for
AEPI
encapsulating
it
liposomes
that
are
surface
modified
with
rabies
virus
glycoprotein
(RVG29),
creating
RVG29-AEPI
liposomes.
These
demonstrated
efficient
cellular
uptake
blood-brain
barrier
penetration
vitro
vivo.
effectively
shielded
DNA
from
damage
resulted
more
reactive
oxygen
species
removal
than
primary
neurons
microglial
cells.
Notably,
treatment
(10
mg/kg
AEPI)
was
highly
systemically
safe
significantly
reduced
injury.
Behavioral
tests
liposomes-treated
mice
had
less
motor
dysfunction.
Moreover,
prevented
neuronal
microglia
cell
activation
under
photon
modern
proton
irradiation.
findings
demonstrate
potential
medication
radioprotection,
indicating
viable
technique
enormous
clinical
translation.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: April 3, 2024
Abstract
Cranial
irradiation
causes
cognitive
deficits
that
are
in
part
mediated
by
microglia,
the
resident
immune
cells
of
brain.
Microglia
highly
reactive,
exhibiting
changes
shape
and
morphology
depending
on
function
they
performing.
Additionally,
microglia
processes
make
dynamic,
physical
contacts
with
different
components
their
environment
to
monitor
functional
state
brain
promote
plasticity.
Though
evidence
suggests
radiation
perturbs
homeostatic
functions,
it
is
unknown
how
cranial
impacts
dynamic
behavior
over
time.
Here,
we
paired
vivo
two-photon
microscopy
a
transgenic
mouse
model
labels
cortical
follow
these
determine
change
time
irradiated
mice
control
littermates.
We
show
single
dose
10
Gy
disrupts
dynamics
during
1-month
course.
found
lasting
loss
microglial
following
irradiation,
coupled
modest
dysregulation
soma
displacement
at
earlier
timepoints.
The
homogeneous
distribution
was
maintained,
suggesting
rearrange
themselves
account
for
cell
maintain
territorial
organization
irradiation.
Furthermore,
reduced
coverage
parenchyma
surveillance
capacity,
without
overtly
changing
morphology.
Our
results
demonstrate
can
induce
could
influence
neurological
health.
These
set
foundation
future
work
examining
complex
cellular
which
contribute
manifestation
deficits.
Frontiers in Public Health,
Journal Year:
2024,
Volume and Issue:
12
Published: May 22, 2024
Background
Owing
to
the
long
penetration
depth
of
gamma
(γ)-rays,
individuals
working
in
ionizing
radiation
environments
are
chronically
exposed
low-dose
γ-radiation,
resulting
cognitive
changes.
Dose
rate
significantly
affects
radiation-induced
biological
effects;
however,
its
role
chronic
γ-irradiation-induced
impairment
remains
unclear.
We
aimed
investigate
whether
γ-irradiation
at
low-dose-rate
(LDR)
could
induce
and
compare
alteration
caused
by
LDR
high-dose-rate
(HDR).
Methods
The
rats
were
a
6
mGy/h
HDR
20
for
30
days
(5
h/day).
Functional
imaging
was
performed
assess
brain
inflammation
blood–brain
barrier
(BBB)
destruction
rats.
Histological
immunofluorescence
analyses
used
reveal
neuron
damage
activation
microglia
astrocytes
hippocampus.
RNA
sequencing
conducted
changes
gene
expression
Results
group
exhibited
more
persistent
than
those
group.
Furthermore,
irradiated
showed
compromised
BBB.
Histologically,
number
hippocampal
neurons
comparable
but
markedly
decreased
HDR.
Additionally,
activated
M1-like
A1-like
observed
hippocampus
group;
only
Mechanistically,
PI3K–Akt
signaling
pathway
contributed
different
function
change
between
Conclusion
Compared
with
HDR,
induced
severe
which
might
involve
PI3K/Akt
pathway.
Abstract
Background
Radiation‐induced
brain
injury
is
a
neurological
condition
resulting
from
radiotherapy
for
malignant
tumors,
with
its
underlying
pathogenesis
still
not
fully
understood.
Current
hypotheses
suggest
that
immune
cells,
particularly
the
excessive
activation
of
microglia
in
central
nervous
system
and
migration
peripheral
cells
into
brain,
play
critical
role
initiating
progressing
injury.
This
review
aimed
to
summarize
latest
advances
cellular
molecular
mechanisms
therapeutic
potential
radiation‐induced
Methods
article
critically
examines
recent
developments
understanding
It
elucidates
associated
explores
novel
research
pathways
options
managing
this
condition.
Results
Post‐irradiation,
activated
release
numerous
inflammatory
factors,
exacerbating
neuroinflammation
facilitating
onset
progression
damage.
Therefore,
controlling
microglial
suppressing
secretion
related
factors
crucial
preventing
While
primary
factor
neuroinflammation,
precise
by
which
radiation
prompts
remain
elusive.
Multiple
signaling
likely
contribute
Conclusions
The
intricate
microenvironment
underscore
roles
progression.
By
investigating
interplay
among
microglia,
neurons,
astrocytes,
strategies
emerge
mitigate
activation,
reduce
agents,
impede
entry
brain.
Discover Oncology,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Aug. 22, 2024
Radiation-induced
brain
injury
(RIBI)
is
a
debilitating
sequela
after
cranial
radiotherapy.
Research
on
the
topic
of
RIBI
has
gradually
entered
public
eye,
with
more
innovations
and
applications
evidence-based
research
biological
mechanism
in
field
that.
This
was
first
bibliometric
analysis
RIBI,
assessing
related
to
radiation
articles
that
were
published
during
1998–2023,
provide
an
emerging
theoretical
basis
for
future
development
RIBI.
Literature
obtained
from
Web
Science
Core
Collection
(WOSCC)
its
inception
December
31,
2023.
The
column
publications,
author
details,
affiliated
institutions
countries,
publication
year,
keywords
also
recorded.
A
total
2543
journal
selected.
annual
publications
fluctuated
within
certain
range.
Journal
Neuro-oncology
most
Radiation
Oncology
impactful
one.
LIMOLI
CL
prolific
37
shared
highest
h-index
BARNETT
GH.
top
one
country
USA
University
California
System,
respectively.
Clusters
co-keywords
demonstrated
temporal
trends
this
primarily
focused
imaging
examination
therapy
study
collects,
visualizes,
analyzes
literature
over
last
25
years
map
process,
frontiers
hotspots,
cutting-edge
directions
clinical
practice
mechanisms