Mechanisms of radiation‐induced tissue damage and response
MedComm,
Год журнала:
2024,
Номер
5(10)
Опубликована: Сен. 20, 2024
Radiation-induced
tissue
injury
(RITI)
is
the
most
common
complication
in
clinical
tumor
radiotherapy.
Due
to
heterogeneity
response
of
different
tissues
radiation
(IR),
radiotherapy
will
cause
types
and
degrees
RITI,
which
greatly
limits
application
Efforts
are
continuously
ongoing
elucidate
molecular
mechanism
RITI
develop
corresponding
prevention
treatment
drugs
for
RITI.
Single-cell
sequencing
(Sc-seq)
has
emerged
as
a
powerful
tool
uncovering
mechanisms
identifying
potential
targets
by
enhancing
our
understanding
complex
intercellular
relationships,
facilitating
identification
novel
cell
phenotypes,
allowing
assessment
spatiotemporal
developmental
trajectories.
Based
on
comprehensive
review
we
analyzed
regulatory
networks
combination
with
Sc-seq
summarized
targeted
intervention
pathways
therapeutic
Deciphering
diverse
underlying
can
shed
light
its
pathogenesis
unveil
new
avenues
potentially
facilitate
repair
or
regeneration
currently
irreversible
Furthermore,
discuss
how
personalized
strategies
based
offer
promise
mitigating
Язык: Английский
New Multiomic Studies Shed Light on Cellular Diversity and Neuronal Susceptibility in Parkinson's Disease
Movement Disorders,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 15, 2025
Parkinson's
disease
is
a
complex
neurodegenerative
disorder
characterized
by
degeneration
of
dopaminergic
neurons,
with
patients
manifesting
varying
motor
and
nonmotor
symptoms.
Previous
studies
using
single-cell
RNA
sequencing
in
rodent
models
humans
have
identified
distinct
heterogeneity
neurons
glial
cells
differential
vulnerability.
Recent
increasingly
leveraged
multiomics
approaches,
including
spatial
transcriptomics,
epigenomics,
proteomics,
the
study
disease,
providing
new
insights
into
pathogenic
mechanisms.
Continued
advancements
experimental
technologies
sophisticated
computational
tools
will
be
essential
uncovering
network
neuronal
vulnerability
prioritizing
modifiers
for
novel
therapeutics
development.
©
2025
International
Parkinson
Movement
Disorder
Society.
Язык: Английский
Sp3 ameliorated experimental autoimmune encephalomyelitis by triggering Socs3 in Th17 cells
Journal of Advanced Research,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Chromatin accessibility provides a window into the genetic etiology of human brain disease
Trends in Genetics,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Genomic and Transcriptomic Approaches Advance the Diagnosis and Prognosis of Neurodegenerative Diseases
Genes,
Год журнала:
2025,
Номер
16(2), С. 135 - 135
Опубликована: Янв. 24, 2025
Neurodegenerative
diseases,
such
as
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
Huntington’s
(HD),
and
amyotrophic
lateral
sclerosis
(ALS),
represent
a
growing
societal
challenge
due
to
their
irreversible
progression
significant
impact
on
patients,
caregivers,
healthcare
systems.
Despite
advances
in
clinical
imaging-based
diagnostics,
these
diseases
are
often
detected
at
advanced
stages,
limiting
the
effectiveness
of
therapeutic
interventions.
Recent
breakthroughs
genomic
transcriptomic
technologies,
including
whole-genome
sequencing,
single-cell
RNA
sequencing
(scRNA-seq),
CRISPR-based
screens,
have
revolutionized
field,
offering
new
avenues
for
early
diagnosis
personalized
prognosis.
Genomic
approaches
elucidated
disease-specific
genetic
risk
factors
molecular
pathways,
while
studies
identified
stage-specific
biomarkers
that
correlate
with
severity.
Furthermore,
genome-wide
association
(GWAS),
polygenic
scores
(PRS),
spatial
transcriptomics
enabling
stratification
patients
based
profiles
prognostic
trajectories.
Advances
functional
genomics
uncovered
actionable
targets,
ATXN2
ALS
TREM2
AD,
paving
way
tailored
strategies.
achievements,
challenges
remain
translating
discoveries
into
practice
heterogeneity
complexity
neurodegenerative
pathophysiology.
Future
integration
technologies
holds
promise
transforming
diagnostic
paradigms,
hope
improved
patient
outcomes
precision
medicine
approaches.
Язык: Английский
Mechanisms driving epigenetic and transcriptional responses of microglia in a neurodegenerative lysosomal storage disorder model
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 14, 2024
Lysosomal
dysfunction
is
causally
linked
to
neurodegeneration
in
many
lysosomal
storage
disorders
(LSDs)
and
associated
with
various
age-related
neurodegenerative
diseases
Язык: Английский
Synaptic vesicle endocytosis deficits underlie GBA-linked cognitive dysfunction in Parkinson’s disease and Dementia with Lewy bodies
Research Square (Research Square),
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 27, 2024
GBA
is
the
major
risk
gene
for
Parkinson's
disease
(PD)
and
Dementia
with
Lewy
Bodies
(DLB),
two
common
α-synucleinopathies
cognitive
deficits.
We
investigated
role
of
mutant
in
decline
by
utilizing
Gba
(L444P)
mutant,
SNCA
transgenic
(tg),
Gba-SNCA
double
mice.
Notably,
mice
showed
early
deficits
but
lacked
PD-like
motor
or
α-synuclein
pathology.
Conversely,
tg
displayed
age-related
deficits,
without
abnormalities.
exhibited
both
exacerbated
accompanied
greater
cortical
phospho-α-synuclein
pathology,
especially
layer
5
neurons.
Single-nucleus
RNA
sequencing
cortex
uncovered
synaptic
vesicle
(SV)
endocytosis
defects
excitatory
neurons
mice,
via
robust
downregulation
genes
regulating
SV
cycle
synapse
assembly.
Immunohistochemistry
electron
microscopy
validated
these
findings.
Our
results
indicate
that
mutations,
while
exacerbating
pre-existing
aggregation
contribute
to
through
α-synuclein-independent
mechanisms,
involving
dysfunction
endocytosis.
Язык: Английский
Synaptic vesicle endocytosis deficits underlie GBA-linked cognitive dysfunction in Parkinson′s disease and Dementia with Lewy bodies
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 23, 2024
Abstract
GBA
is
the
major
risk
gene
for
Parkinson’s
disease
(PD)
and
Dementia
with
Lewy
Bodies
(DLB),
two
common
α-synucleinopathies
cognitive
deficits.
We
investigated
role
of
mutant
in
decline
by
utilizing
Gba
(L444P)
mutant,
SNCA
transgenic
(tg),
Gba-SNCA
double
mice.
Notably,
mice
showed
early
deficits
but
lacked
PD-like
motor
or
α-synuclein
pathology.
Conversely,
tg
displayed
age-related
deficits,
without
abnormalities.
exhibited
both
exacerbated
accompanied
greater
cortical
phospho-α-synuclein
pathology,
especially
layer
5
neurons.
Single-nucleus
RNA
sequencing
cortex
uncovered
synaptic
vesicle
(SV)
endocytosis
defects
excitatory
neurons
mice,
via
robust
downregulation
genes
regulating
SV
cycle
synapse
assembly.
Immunohistochemistry
electron
microscopy
validated
these
findings.
Our
results
indicate
that
mutations,
while
exacerbating
pre-existing
aggregation
contribute
to
through
α-synuclein-independent
mechanisms,
involving
dysfunction
endocytosis.
Язык: Английский