Schizophrenia Bulletin,
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 13, 2024
The
complex
immune-brain
interactions
and
the
regulatory
role
of
mitochondria
in
immune
response
suggest
that
mitochondrial
damage
reported
schizophrenia
(SZ)
may
be
related
to
abnormalities
observed
brain
functions.
GeroScience,
Год журнала:
2024,
Номер
46(5), С. 4275 - 4314
Опубликована: Апрель 1, 2024
Down
syndrome
(DS)
is
a
genetic
condition
where
the
person
born
with
an
extra
chromosome
21.
DS
associated
accelerated
aging;
people
are
prone
to
age-related
neurological
conditions
including
early-onset
Alzheimer's
disease.
Using
Dp(17)3Yey/
+
mice,
which
overexpresses
portion
of
mouse
17,
encodes
for
transsulfuration
enzyme
cystathionine
β-synthase
(CBS),
we
investigated
functional
role
CBS/hydrogen
sulfide
(H
Molecular Neurodegeneration,
Год журнала:
2025,
Номер
20(1)
Опубликована: Март 4, 2025
The
relationship
between
Alzheimer's
disease
(AD)
and
neuroimmunity
has
gradually
begun
to
be
unveiled.
Emerging
evidence
indicates
that
cyclic
GMP-AMP
synthase
(cGAS)
acts
as
a
cytosolic
DNA
sensor,
recognizing
damage-associated
molecular
patterns
(DAMPs),
inducing
the
innate
immune
response
by
activating
stimulator
of
interferon
genes
(STING).
Dysregulation
this
pathway
culminates
in
AD-related
neuroinflammation
neurodegeneration.
A
substantial
body
mitochondria
are
involved
critical
pathogenic
mechanisms
AD,
whose
damage
leads
release
mitochondrial
(mtDNA)
into
extramitochondrial
space.
This
leaked
mtDNA
serves
DAMP,
various
pattern
recognition
receptors
defense
networks
brain,
including
cGAS-STING
pathway,
ultimately
leading
an
imbalance
homeostasis.
Therefore,
modulation
mtDNA-cGAS-STING
restore
neuroimmune
homeostasis
may
offer
promising
prospects
for
improving
AD
treatment
outcomes.
In
review,
we
focus
on
during
stress
activation
pathway.
Additionally,
delve
research
progress
further
discuss
primary
directions
potential
hurdles
developing
targeted
therapeutic
drugs,
gain
deeper
understanding
pathogenesis
provide
new
approaches
its
therapy.
Cells,
Год журнала:
2025,
Номер
14(3), С. 206 - 206
Опубликована: Янв. 30, 2025
Multiple
sclerosis
(MS)
is
an
inflammatory
autoimmune
disease
of
the
central
nervous
system
(CNS)
linked
to
many
neurological
disabilities.
The
visual
frequently
impaired
in
MS.
In
previous
studies,
we
observed
early
malfunctions
rod
photoreceptor
ribbon
synapses
EAE
mouse
model
MS
that
included
alterations
synaptic
vesicle
cycling
and
disturbances
presynaptic
Ca2+
homeostasis.
Since
these
events
are
highly
energy-demanding,
analyzed
whether
mitochondria,
which
play
a
major
role
energy
metabolism,
might
be
involved
at
stage.
Rod
terminals
contain
single
large
mitochondrion
next
ribbon.
present
study,
expression
functionally
relevant
mitochondrial
proteins
(MIC60,
ATP5B,
COX1,
PINK1,
DRP1)
by
high-resolution
qualitative
quantitative
immunofluorescence
microscopy,
immunogold
electron
microscopy
Western
blot
experiments.
We
decreased
mitochondria
photoreceptors
stage,
suggesting
dysfunctions
important
synapse
pathology.
Interestingly,
were
strongly
compromised
EAE,
whereas
extra-synaptic
inner
segments
remained
unchanged,
demonstrating
functional
heterogeneity
mitochondria.
Abstract
Mitochondria-derived
reactive
oxygen
species
production
at
a
moderate
physiological
level
plays
fundamental
role
in
the
anti-aging
signaling,
due
to
their
action
as
redox-active
sensors
for
maintenance
of
optimal
mitochondrial
balance
between
intracellular
energy
status
and
hormetic
nutrients.
Iron
regulatory
protein
dysregulation,
systematically
increased
iron
levels,
dysfunction,
consequent
oxidative
stress
are
recognized
underlie
pathogenesis
multiple
neurodegenerative
diseases,
such
Parkinson’s
disease
Alzheimer’s
disease.
Central
pathogenesis,
Nrf2
signaling
dysfunction
occurs
with
disruption
metabolic
homeostasis.
We
highlight
potential
therapeutic
importance
nutritional
polyphenols
substantive
regulators
pathway.
Here,
we
discuss
common
mechanisms
targeting
Nrf2/vitagene
pathway,
novel
strategies
minimize
consequences
neuroinflammation,
generally
associated
cognitive
demonstrate
its
key
neuroprotective
anti-neuroinflammatory
properties,
summarizing
pharmacotherapeutic
aspects
relevant
brain
pathophysiology.
Brain,
Год журнала:
2024,
Номер
147(8), С. 2691 - 2705
Опубликована: Июль 5, 2024
Early
pathological
upregulation
of
adenosine
A2A
receptors
(A2ARs),
one
the
caffeine
targets,
by
neurons
is
thought
to
be
involved
in
development
synaptic
and
memory
deficits
Alzheimer's
disease
(AD)
but
mechanisms
remain
ill-defined.
To
tackle
this
question,
we
promoted
a
neuronal
A2AR
hippocampus
APP/PS1
mice
developing
AD-like
amyloidogenesis.
Our
findings
revealed
that
early
presence
an
ongoing
amyloid
pathology
exacerbates
impairments
mice.
These
behavioural
changes
were
not
linked
major
change
rather
associated
with
increased
phosphorylated
tau
at
neuritic
plaques.
Moreover,
proteomic
transcriptomic
analyses
coupled
quantitative
immunofluorescence
studies
indicated
receptor
both
non-neuronal
autonomous
alterations,
i.e.
enhanced
neuroinflammatory
response
also
loss
excitatory
synapses
impaired
mitochondrial
function,
presumably
accounting
for
detrimental
effect
on
memory.
Overall,
our
results
provide
compelling
evidence
dysfunction,
as
seen
brain
patients,
contributes
amyloid-related
pathogenesis
underscores
potential
relevant
therapeutic
target
mitigating
cognitive
neurodegenerative
disorder.
Reproductive Biology and Endocrinology,
Год журнала:
2024,
Номер
22(1)
Опубликована: Июнь 7, 2024
Abstract
Fatigue,
an
increasingly
acknowledged
symptom
in
various
chronic
diseases,
has
garnered
heightened
attention,
during
the
medical
era
of
bio-psycho-social
model.
Its
persistence
not
only
significantly
compromises
individual’s
quality
life
but
also
correlates
with
organ
damage.
Surprisingly,
intricate
relationship
between
fatigue
and
female
reproductive
health,
specifically
infertility,
remains
largely
unexplored.
Our
exploration
into
existing
body
evidence
establishes
a
compelling
link
uterine
ovarian
as
well
conditions
associated
such
rheumatism.
This
observation
suggests
potentially
pivotal
role
influencing
overall
fertility.
Furthermore,
we
propose
hypothetical
mechanism
elucidating
impact
on
infertility
from
multiple
perspectives,
postulating
that
neuroendocrine,
neurotransmitter,
inflammatory
immune,
mitochondrial
dysfunction
resulting
its
co-factors
may
further
contribute
to
endocrine
disorders,
menstrual
irregularities,
sexual
dysfunction,
ultimately
leading
infertility.
In
addition
providing
this
comprehensive
theoretical
framework,
summarize
anti-fatigue
strategies
accentuate
current
knowledge
gaps.
By
doing
so,
our
aim
is
offer
novel
insights,
stimulate
research,
advance
understanding
crucial
interplay
health.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
177, С. 117011 - 117011
Опубликована: Июнь 24, 2024
Microglia
are
essential
for
maintaining
homeostasis
and
responding
to
pathological
events
in
the
central
nervous
system
(CNS).
Their
dynamic
multidimensional
states
different
environments
pivotal
factors
various
CNS
disorders.
However,
therapeutic
modulation
of
microglial
is
challenging
due
intricate
balance
these
cells
maintain
environment
blood-brain
barrier's
restriction
drug
delivery.
Nanomedicine
presents
a
promising
avenue
addressing
challenges,
offering
method
targeted
efficient
states.
This
review
covers
challenges
faced
potential
use
nanoparticle-based
delivery
systems.
We
provide
an
in-depth
examination
nanoparticle
applications
modulating
range
disorders,
encompassing
neurodegenerative
autoimmune
diseases,
infections,
traumatic
injuries,
stroke,
tumors,
chronic
pain,
psychiatric
conditions.
highlights
recent
advancements
future
prospects
nanomedicine
modulation,
paving
way
research
clinical
interventions