Mapping
neurotransmitter
identities
to
neurons
is
key
understanding
information
flow
in
a
nervous
system.
It
also
provides
valuable
entry
points
for
studying
the
development
and
plasticity
of
neuronal
identity
features.
In
Caenorhabditis
elegans
system,
have
been
largely
assigned
by
expression
pattern
analysis
pathway
genes
that
encode
biosynthetic
enzymes
or
transporters.
However,
many
these
assignments
relied
on
multicopy
reporter
transgenes
may
lack
relevant
cis
-regulatory
therefore
not
provide
an
accurate
picture
usage.
We
analyzed
patterns
16
CRISPR/Cas9-engineered
knock-in
strains
all
main
types
neurotransmitters
C.
(glutamate,
acetylcholine,
GABA,
serotonin,
dopamine,
tyramine,
octopamine)
both
hermaphrodite
male.
Our
reveals
novel
sites
systems
within
glia,
as
well
non-neural
cells,
most
notably
gonadal
cells.
The
resulting
atlas
defines
be
exclusively
neuropeptidergic,
substantially
expands
repertoire
capable
co-transmitting
multiple
neurotransmitters,
identifies
monoaminergic
uptake.
Furthermore,
we
observed
unusual
co-expression
synthesis
genes,
suggesting
existence
transmitters.
results
what
constitutes
extensive
whole-animal-wide
map
usage
date,
paving
way
better
communication
specification
.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Feb. 16, 2024
Abstract
The
human
gastrointestinal
tract
is
populated
with
a
diverse
microbial
community.
vast
genetic
and
metabolic
potential
of
the
gut
microbiome
underpins
its
ubiquity
in
nearly
every
aspect
biology,
including
health
maintenance,
development,
aging,
disease.
advent
new
sequencing
technologies
culture-independent
methods
has
allowed
researchers
to
move
beyond
correlative
studies
toward
mechanistic
explorations
shed
light
on
microbiome–host
interactions.
Evidence
unveiled
bidirectional
communication
between
central
nervous
system,
referred
as
“microbiota–gut–brain
axis”.
microbiota–gut–brain
axis
represents
an
important
regulator
glial
functions,
making
it
actionable
target
ameliorate
development
progression
neurodegenerative
diseases.
In
this
review,
we
discuss
mechanisms
As
provides
essential
cues
microglia,
astrocytes,
oligodendrocytes,
examine
communications
microbiota
these
cells
during
healthy
states
Subsequently,
diseases
using
metabolite-centric
approach,
while
also
examining
role
microbiota-related
neurotransmitters
hormones.
Next,
targeting
intestinal
barrier,
blood–brain
meninges,
peripheral
immune
system
counteract
dysfunction
neurodegeneration.
Finally,
conclude
by
assessing
pre-clinical
clinical
evidence
probiotics,
prebiotics,
fecal
transplantation
A
thorough
comprehension
will
foster
effective
therapeutic
interventions
for
management
Advanced Materials,
Journal Year:
2024,
Volume and Issue:
36(26)
Published: April 7, 2024
Abstract
Brain
disorders
represent
a
significant
challenge
in
medical
science
due
to
the
formidable
blood–brain
barrier
(BBB),
which
severely
limits
penetration
of
conventional
therapeutics,
hindering
effective
treatment
strategies.
This
review
delves
into
innovative
realm
biomimetic
nanodelivery
systems,
including
stem
cell‐derived
nanoghosts,
tumor
cell
membrane‐coated
nanoparticles,
and
erythrocyte
membrane‐based
carriers,
highlighting
their
potential
circumvent
BBB's
restrictions.
By
mimicking
native
properties,
these
nanocarriers
emerge
as
promising
solution
for
enhancing
drug
delivery
brain,
offering
strategic
advantage
overcoming
barrier's
selective
permeability.
The
unique
benefits
leveraging
membranes
from
various
sources
is
evaluated
advanced
technologies
fabricating
membrane‐encapsulated
nanoparticles
capable
masquerading
endogenous
cells
are
examined.
enables
targeted
broad
spectrum
therapeutic
agents,
ranging
small
molecule
drugs
proteins,
thereby
providing
an
approach
neurocare.
Further,
contrasts
capabilities
limitations
with
traditional
methods,
underlining
enable
targeted,
sustained,
minimally
invasive
modalities.
concluded
perspective
on
clinical
translation
underscoring
transformative
impact
landscape
intractable
brain
diseases.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
25(1), P. 360 - 360
Published: Dec. 26, 2023
Parkinson’s
disease
(PD)
is
a
complex
neurodegenerative
characterized
by
the
progressive
loss
of
dopaminergic
neurons
in
substantia
nigra
and
widespread
accumulation
alpha-synuclein
(αSyn)
protein
aggregates.
αSyn
aggregation
disrupts
critical
cellular
processes,
including
synaptic
function,
mitochondrial
integrity,
proteostasis,
which
culminate
neuronal
cell
death.
Importantly,
pathology
extends
beyond
neurons—it
also
encompasses
spreading
throughout
environment
internalization
microglia
astrocytes.
Once
internalized,
glia
can
act
as
neuroprotective
scavengers,
limit
spread
αSyn.
However,
they
become
reactive,
thereby
contributing
to
neuroinflammation
progression
PD.
Recent
advances
research
have
enabled
molecular
diagnosis
PD
accelerated
development
targeted
therapies.
Nevertheless,
despite
more
than
two
decades
research,
mechanisms,
induction
damage
remain
incompletely
understood.
Unraveling
interplay
between
αSyn,
neurons,
may
provide
insights
into
initiation
progression,
bring
us
closer
exploring
new
effective
therapeutic
strategies.
Herein,
we
an
overview
recent
studies
emphasizing
multifaceted
nature
its
impact
on
both
neuron
glial
damage.
Trends in Neurosciences,
Journal Year:
2024,
Volume and Issue:
47(4), P. 289 - 302
Published: March 22, 2024
Selective
vulnerability
of
specific
brain
regions
and
cell
populations
is
a
hallmark
neurodegenerative
disorders.
Mechanisms
selective
involve
neuronal
heterogeneity,
functional
specializations,
differential
sensitivities
to
stressors
pathogenic
factors.
In
this
review
we
discuss
the
growing
body
literature
suggesting
that,
like
neurons,
astrocytes
are
heterogeneous
specialized,
respond
integrate
diverse
inputs,
induce
effects
on
function.
disease,
undergo
specific,
context-dependent
changes
that
promote
different
trajectories
outcomes.
We
propose
contribute
through
maladaptive
transitions
context-divergent
phenotypes
impair
functions.
Further
studies
multifaceted
roles
in
disease
may
provide
new
therapeutic
approaches
enhance
resilience
against
Molecular Neurobiology,
Journal Year:
2024,
Volume and Issue:
61(8), P. 5628 - 5645
Published: Jan. 13, 2024
Exercise
has
been
recognized
as
a
beneficial
factor
for
cognitive
health,
particularly
in
relation
to
the
hippocampus,
vital
brain
region
responsible
learning
and
memory.
Previous
research
demonstrated
that
exercise-mediated
improvement
of
memory
humans
rodents
correlates
with
increased
adult
neurogenesis
processes
related
enhanced
synaptic
plasticity.
Nevertheless,
underlying
molecular
mechanisms
are
not
fully
understood.
With
aim
further
elucidate
these
mechanisms,
we
provide
comprehensive
dataset
mouse
hippocampal
transcriptome
at
single-cell
level
after
4
weeks
voluntary
wheel-running.
Our
analysis
provides
number
interesting
observations.
For
example,
results
suggest
exercise
affects
by
accelerating
maturation
subpopulation
Prdm16-expressing
neurons.
Moreover,
uncover
existence
an
intricate
crosstalk
among
multiple
signaling
pathways
such
NF-κB,
Wnt/β-catenin,
Notch,
retinoic
acid
(RA)
altered
upon
specific
cluster
excitatory
neurons
within
Cornu
Ammonis
(CA)
hippocampus.
In
conclusion,
our
study
important
resource
sheds
light
on
changes
induced
These
findings
have
implications
developing
targeted
interventions
aimed
optimizing
health
preventing
age-related
decline.
Frontiers in Neurology,
Journal Year:
2024,
Volume and Issue:
15
Published: Feb. 8, 2024
Alzheimer’s
disease
(AD)
and
dementia
with
Lewy
bodies
(DLB)
stand
as
the
prevailing
sources
of
neurodegenerative
dementia,
impacting
over
55
million
individuals
across
globe.
Patients
AD
DLB
exhibit
a
higher
prevalence
epileptic
activity
compared
to
those
other
forms
dementia.
Seizures
can
accompany
in
early
stages,
associated
contribute
cognitive
symptoms
exacerbate
decline.
Aberrant
neuronal
may
be
caused
by
several
mechanisms
that
are
not
yet
understood.
Hyperexcitability
could
biomarker
for
detection
or
before
onset
In
this
review,
we
compare
contrast
network
hyperexcitability
DLB.
We
examine
contributions
genetic
risk
factors,
Ca
2+
dysregulation,
glutamate,
AMPA
NMDA
receptors,
mTOR,
pathological
amyloid
beta,
tau
α-synuclein,
altered
microglial
astrocytic
activity,
impaired
inhibitory
interneuron
function.
By
gaining
deeper
understanding
molecular
cause
hyperexcitability,
might
uncover
therapeutic
approaches
effectively
ease
slow
down
advancement
Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
11
Published: Jan. 18, 2024
Extracellular
ATP
and
adenosine
are
neuromodulators
that
regulate
numerous
neuronal
functions
in
the
brain.
Neuronal
activity
brain
insults
such
as
ischemic
traumatic
injury
upregulate
these
neuromodulators,
which
exert
their
effects
by
activating
purinergic
receptors.
In
addition,
extracellular
ATP/adenosine
signaling
plays
a
pivotal
role
pathogenesis
of
neurological
diseases.
Virtually
every
cell
type
contributes
to
elevation
ATP/adenosine,
various
mechanisms
underlying
this
increase
have
been
proposed.
is
thought
be
mainly
produced
via
degradation
ATP.
However,
also
released
from
neurons
glia
Therefore,
regulation
physiological
pathophysiological
conditions
likely
far
more
complex
than
previously
thought.
To
elucidate
levels,
accurate
methods
assessing
spatiotemporal
dynamics
needed.
Several
novel
techniques
for
acquiring
information
on
including
fluorescent
sensors,
developed
started
reveal
release,
uptake
ATP/adenosine.
Here,
we
review
analyzing
well
current
state
knowledge
We
focus
used
cooperatively
produce
activity-dependent
its
significance
Aging and Disease,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Jan. 1, 2024
Post-stroke
depression
(PSD)
is
a
complex
mood
disorder
that
emerges
in
individuals
following
stroke,
characterized
by
the
development
of
depressive
symptoms.
The
pathogensis
PSD
diverse,
with
inflammation
playing
vital
role
its
onset
and
progression.
Emerging
evidence
suggests
microglial
activation,
astrocyte
responses,
nuclear
factor
κB(NF-κB)
signaling,
dysregulation
hypothalamic
pituitary
adrenal
(HPA)
axis,
alterations
brain-derived
neurotrophic
(BDNF)
expression,
neurotransmitter
imbalances,
adenosine
triphosphate
(ATP)
receptors
oxidative
stress
are
intricately
linked
to
pathogenesis
PSD.
involvement
inflammatory
cytokines
these
processes
highlights
significance
pathway.
Integrating
hypotheses,
mechanism
offers
novel
perspective
expand
therapeutic
strategies
for
