Clinical Science,
Journal Year:
2023,
Volume and Issue:
137(6), P. 401 - 414
Published: March 1, 2023
Sepsis
is
a
life-threatening
organ
dysfunction
triggered
by
dysregulated
host
immune
response
to
eliminate
an
infection.
After
the
activated,
complex,
dynamic,
and
time-dependent
process
triggered.
This
promotes
production
of
inflammatory
mediators,
including
acute-phase
proteins,
complement
system
cytokines,
chemokines,
antimicrobial
peptides,
which
are
required
initiate
environment
for
eliminating
invading
pathogen.
The
physiological
this
sepsis-induced
systemic
inflammation
can
affect
blood-brain
barrier
(BBB)
function;
subsequently,
endothelial
cells
produce
matrix
metalloproteinases
(MMPs)
that
degrade
tight
junction
(TJ)
proteins
decrease
BBB
function.
resulting
permeability
allows
peripheral
from
bloodstream
enter
brain,
then
release
range
mediators
activate
glial
cells.
activated
microglia
astrocytes
reactive
oxygen
species
(ROS),
neurochemicals,
mitochondrial
neuronal
damage,
exacerbate
milieu
in
brain.
These
changes
trigger
sepsis-associated
encephalopathy
(SAE),
has
potential
increase
cognitive
deterioration
susceptibility
decline
later
life.
Journal of Neuroinflammation,
Journal Year:
2022,
Volume and Issue:
19(1)
Published: April 29, 2022
Abstract
Sepsis
is
a
life-threatening
organ
dysfunction
caused
by
dysregulated
host
response
to
infection.
causes
cerebral
in
the
short
and
long
term
induces
disruption
of
blood–brain
barrier
(BBB),
neuroinflammation,
hypoperfusion,
accumulation
amyloid
β
(Aβ)
tau
protein
brain.
White
matter
changes
brain
atrophy
can
be
detected
using
imaging,
but
unfortunately,
there
no
specific
treatment
that
directly
addresses
underlying
mechanisms
cognitive
impairments
sepsis.
Here,
we
review
sepsis-associated
injury,
with
focus
on
BBB
Aβ
We
also
describe
neurological
manifestations
imaging
findings
finally,
propose
potential
therapeutic
strategies
for
acute
long-term
associated
In
phase
sepsis,
suggest
antibiotics
(such
as
rifampicin),
targeting
proinflammatory
cytokines,
preventing
ischemic
injuries
hypoperfusion.
late
dysfunction,
phosphorylation,
glycogen
synthase
kinase-3
beta
(GSK3β),
receptor
advanced
glycation
end
products
(RAGE).
These
proposed
are
meant
bring
new
mechanism-based
directions
future
basic
clinical
research
aimed
at
or
ameliorating
patients
Redox Biology,
Journal Year:
2023,
Volume and Issue:
63, P. 102745 - 102745
Published: May 13, 2023
Sepsis-associated
encephalopathy
(SAE)
is
one
of
the
common
serious
complications
in
sepsis,
and
pathogenesis
SAE
remains
unclear.
Sirtuin
1
(SIRT1)
has
been
reported
to
be
downregulated
hippocampus
SIRT1
agonists
can
attenuated
cognitive
dysfunction
septic
mice.
Nicotinamide
adenine
dinucleotide
(NAD+)
a
key
substrate
maintain
deacetylation
activity
SIRT1.
As
an
intermediate
NAD+,
β-Nicotinamide
Mononucleotide
(NMN)
promising
treating
neurodegenerative
diseases
cerebral
ischemic
injury.
Thus
we
sought
investigate
potential
role
NMN
treatment.
The
model
was
established
by
cecal
ligation
puncture
(CLP)
vivo,
neuroinflammation
with
LPS-treated
BV-2
cells
vitro.
Memory
impairment
assessed
Morris
water
maze
fear
conditioning
tests.
result,
levels
PGC-1α
were
significantly
reduced
mice,
while
acetylation
total
lysine,
phosphorylation
P38
P65
enhanced.
All
these
changes
induced
sepsis
inverted
NMN.
Treating
resulted
improved
behavior
performance
tests
maze.
Apoptosis,
inflammatory
oxidative
responses
mice
after
administration.
These
protective
effect
against
memory
dysfunction,
injuries
reversed
inhibitor,
EX-527.
Similarly,
LPS-induced
activation
NMN,
EX-527
or
knockdown
could
reverse
such
In
conclusion,
sepsis-induced
region
NAD+/SIRT1
pathway
might
involved
mechanisms
effect.
Epilepsia,
Journal Year:
2020,
Volume and Issue:
61(8)
Published: June 27, 2020
Neurological
manifestations
of
coronavirus
disease
19
(COVID-19)
such
as
encephalitis
and
seizures
have
been
reported
increasingly,
but
our
understanding
COVID-19-related
brain
injury
is
still
limited.
Herein
we
describe
prefrontal
involvement
in
a
patient
with
COVID-19
who
presented
prior
anosmia,
raising
the
question
potential
trans-olfactory
bulb
invasion.
Gastroenterology Research and Practice,
Journal Year:
2021,
Volume and Issue:
2021, P. 1 - 20
Published: Jan. 16, 2021
Gut
dysbacteriosis
is
closely
related
to
various
intestinal
and
extraintestinal
diseases.
Fecal
microbiota
transplantation
(FMT)
a
biological
therapy
that
entails
transferring
the
gut
from
healthy
individuals
patients
in
order
reconstruct
microflora
latter.
It
has
been
proved
be
an
effective
treatment
for
recurrent
Clostridium
difficile
infection.
Studies
show
plays
important
role
pathophysiology
of
neurological
psychiatric
disorders
through
microbiota-gut-brain
axis.
Therefore,
reconstruction
promising
new
strategy
treating
cerebral
We
have
reviewed
latest
research
on
different
nervous
system
diseases
as
well
FMT
context
its
application
neurological,
psychiatric,
other
system-related
(Parkinson's
disease,
Alzheimer's
multiple
sclerosis,
epilepsy,
autism
spectrum
disorder,
bipolar
hepatic
encephalopathy,
neuropathic
pain,
etc.).
Brain,
Journal Year:
2022,
Volume and Issue:
145(11), P. 4097 - 4107
Published: Sept. 6, 2022
COVID-19
is
associated
with
neurological
complications
including
stroke,
delirium
and
encephalitis.
Furthermore,
a
post-viral
syndrome
dominated
by
neuropsychiatric
symptoms
common,
seemingly
unrelated
to
severity.
The
true
frequency
underlying
mechanisms
of
injury
are
unknown,
but
exaggerated
host
inflammatory
responses
appear
be
key
driver
We
investigated
the
dynamics
of,
relationship
between,
serum
markers
brain
[neurofilament
light
(NfL),
glial
fibrillary
acidic
protein
(GFAP)
total
tau]
dysregulated
response
(autoantibody
production
cytokine
profiles)
in
175
patients
admitted
45
influenza.
During
hospitalization,
sera
from
demonstrated
elevations
NfL
GFAP
severity-dependent
manner,
evidence
ongoing
active
at
follow-up
4
months
later.
These
biomarkers
were
pro-inflammatory
cytokines
presence
autoantibodies
large
number
different
antigens.
Autoantibodies
commonly
seen
against
lung
surfactant
proteins
also
such
as
myelin
glycoprotein.
Commensurate
findings
influenza
cohort.
A
distinct
process
characterized
elevation
tau
was
follow-up,
which
appeared
independent
initial
disease
severity
not
immune
unlike
GFAP.
results
demonstrate
that
common
consequence
both
influenza,
therefore
likely
feature
severe
viral
infection
more
broadly.
occurs
context
dysregulation
innate
adaptive
responses,
no
single
pathogenic
mechanism
clearly
responsible.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: July 26, 2022
Sepsis-associated
encephalopathy
(SAE)
is
a
cognitive
impairment
associated
with
sepsis
that
occurs
in
the
absence
of
direct
infection
central
nervous
system
or
structural
brain
damage.
Microglia
are
thought
to
be
macrophages
system,
devouring
bits
neuronal
cells
and
dead
brain.
They
activated
various
ways,
microglia-mediated
neuroinflammation
characteristic
diseases,
including
SAE.
Here,
we
systematically
described
pathogenesis
SAE
demonstrated
microglia
closely
related
occurrence
development
Furthermore,
comprehensively
discussed
function
phenotype
summarized
their
activation
mechanism
role
pathogenesis.
Finally,
this
review
summarizes
recent
studies
on
treating
by
blocking
microglial
toxic
factors
produced
after
activation.
We
suggest
targeting
may
putative
treatment
for
Pharmaceuticals,
Journal Year:
2021,
Volume and Issue:
14(5), P. 416 - 416
Published: May 1, 2021
Frequently
underestimated,
encephalopathy
or
delirium
are
common
neurological
manifestations
associated
with
sepsis.
Brain
dysfunction
occurs
in
up
to
80%
of
cases
and
is
directly
increased
mortality
long-term
neurocognitive
consequences.
Although
the
central
nervous
system
(CNS)
has
been
classically
viewed
as
an
immune-privileged
system,
neuroinflammation
emerging
a
mechanism
brain
Microglial
cells
major
players
this
setting.
Here,
we
aimed
discuss
current
knowledge
on
how
affected
by
peripheral
immune
activation
sepsis
role
microglia
these
processes.
This
review
focused
molecular
pathways
microglial
activity
sepsis,
its
regulatory
mechanisms,
their
interaction
other
CNS
cells,
especially
neuronal
circuits.