Alzheimer s Research & Therapy,
Journal Year:
2024,
Volume and Issue:
16(1)
Published: May 21, 2024
Abstract
Systemic
inflammation
and
neuroinflammation
affect
the
natural
course
of
sporadic
form
Alzheimer’s
disease
(AD),
as
supported
by
epidemiological
preclinical
data,
several
studies
indicate
a
higher
prevalence
AD
in
patients
with
inflammatory
bowel
disease.
In
this
study,
we
explored
whether
colitis
induced
dextran
sulfate
sodium
(DSS)
young,
presymptomatic/preplaque
mice
worsens
and/or
anticipates
age-dependent
cognitive
impairment
Tg2576,
widely
used
mouse
model
AD.
We
demonstrated
that
DSS
young
Tg2576
onset
age
learning
memory
deficit
Morris
water
maze
test.
To
explore
potential
mechanisms
behind
acceleration
decline
colitis,
focused
on
gut
microbiota,
systemic
markers.
observed
Firmicutes/Bacteroidetes
ratio
change
animals
comparable
to
elderly
mice,
suggesting
accelerated
microbiota
aging
not
C57BL6
mice.
also
substantial
differences
between
WT
neuroinflammation-related
parameters
early
3
months
age,
well
before
plaque
deposition,
picture
which
evolved
rapidly
(between
5.5
age)
contrast
littermates
treated
DSS.
detail,
following
induction
exhibited
contrasting
features
expression
level
inflammation-evoked
astrocyte-associated
genes
hippocampus.
No
changes
microglial
occurred
hippocampus
experimental
groups,
whereas
reduced
glial
fibrillary
acidic
protein
immunoreactivity
was
vs.
This
finding
may
reflect
an
atrophic,
“loss-of-function”
profile,
further
exacerbated
where
decreased
GFAP
mRNA
detected.
conclusion,
suggest
as-yet
unidentified
peripheral
mediators
evoked
involving
gut-brain
axis
emphasize
astrocyte
profile
present
leading
impaired
synaptic
morphological
functional
integrity
very
sign
Translational Neurodegeneration,
Journal Year:
2025,
Volume and Issue:
14(1)
Published: April 3, 2025
Neurodegenerative
diseases
(NDDs)
such
as
Alzheimer's
and
Parkinson's
disease
are
increasing
globally
represent
a
significant
cause
of
age-related
death
in
the
population.
Recent
studies
emphasize
strong
association
between
environmental
stressors,
particularly
dietary
factors,
brain
health
neurodegeneration
unsatisfactory
outcomes.
Despite
ongoing
efforts,
efficiency
current
treatments
for
NDDs
remains
wanting.
Considering
this,
nootropic
foods
with
neuroprotective
effects
high
interest
part
possible
long-term
therapeutic
strategy
to
improve
alleviate
NDDs.
However,
since
it
is
new
emerging
area
food
neuroscience,
there
limited
information
on
mechanisms
challenges
consider
this
be
successful
intervention.
Here,
we
seek
address
these
gaps
by
presenting
comprehensive
review
pathways
or
including
mutual
interactions
governing
metabolism,
linkages
NDDs,
intake,
properties
foods.
We
also
discuss
in-depth
intervention
compounds
patterns
providing
detailed
exploration
their
action.
Additionally,
analyze
demand,
challenges,
future
directions
development
targeting
Journal of Alzheimer s Disease,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 18, 2024
Several
studies
indicate
that
the
development
of
Alzheimer's
disease
(AD)
has
strong
interactions
with
immune
mechanisms
within
brain,
indicating
a
close
association
between
inflammation
in
central
nervous
system
and
progression
neurodegeneration.
Despite
considerable
progress
understanding
inflammatory
aspects
AD,
several
them
remain
unresolved.
Pro-inflammatory
cytokines
microglia
are
pivotal
components
cascade.
Among
these,
role
interleukin-8
(IL-8)
neurodegeneration
seems
complex
multifaceted,
involving
inflammation,
neurotoxicity,
blood-brain
barrier
disruption,
oxidative
stress,
is
still
poorly
characterized.
We
conducted
review
to
describe
evidence
IL-8
involvement
AD.
cytokine
known
for
its
proinflammatory
properties
typically
produced
by
macrophages,
predominantly
functions
as
chemotactic
signal
attracting
neutrophils
inflamed
sites
bloodstream.
Interestingly,
also
present
where
it
primarily
released
response
signals.
This
aims
provide
comprehensive
overview
structure,
function,
regulatory
relevant
AD
pathology.
Alzheimer s & Dementia,
Journal Year:
2023,
Volume and Issue:
20(1), P. 494 - 510
Published: Sept. 11, 2023
Abstract
INTRODUCTION
Anesthesia
often
exacerbates
memory
recall
difficulties
in
individuals
with
Alzheimer's
disease
(AD),
but
the
underlying
mechanisms
remain
unclear.
METHODS
We
used
vivo
Ca
2+
imaging,
viral‐based
circuit
tracing,
and
chemogenetic
approaches
to
investigate
anesthesia‐induced
remote
impairment
mouse
models
of
presymptomatic
AD.
RESULTS
Our
study
identified
pyramidal
neuron
hyperactivity
anterior
cingulate
cortex
(ACC)
as
a
significant
contributor
impairment.
This
ACC
hyperactivation
arises
from
disinhibition
local
inhibitory
circuits
increased
excitatory
inputs
hippocampal
CA1
region.
Inhibiting
CA1‐ACC
improved
after
anesthesia.
Moreover,
anesthesia
led
tau
phosphorylation
hippocampus,
inhibiting
this
hyperphosphorylation
prevented
subsequent
DISCUSSION
Hippocampal‐cortical
plays
role
Targeting
shows
promise
therapeutic
strategy
mitigate
neural
network
dysfunction
retrograde
amnesia
Signa Vitae,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Jan. 1, 2024
Postoperative
neurocognitive
impairments
following
surgery
are
a
growing
concern,
especially
in
the
elderly
population,
since
it
is
associated
with
significantly
increased
risk
of
morbi-mortality
postoperative
period.
Among
them,
delirium
or
early
cognitive
decline
further
prolonged
dysfunction
and
may
quicken
long-term
impairment
(POCD).
The
current
knowledge
regarding
preventive
strategies
for
not
focused
anymore
only
on
pharmacological
behavioral
management
period,
but
also
supports
preoperative
training
programs.
Since
evaluation
proactive
interventions
to
optimize
surgical
patient
outcomes
rather
impossible
emergency
setting,
what
appropriate
that
can
be
implemented
day-to-day
practice?
In
this
review,
we
try
highlight
most
recent
experimental
clinical
strategies,
outline
relevant
recommendations
clinicial
practicioners
based
available
data.
Alzheimer s Research & Therapy,
Journal Year:
2024,
Volume and Issue:
16(1)
Published: May 21, 2024
Abstract
Systemic
inflammation
and
neuroinflammation
affect
the
natural
course
of
sporadic
form
Alzheimer’s
disease
(AD),
as
supported
by
epidemiological
preclinical
data,
several
studies
indicate
a
higher
prevalence
AD
in
patients
with
inflammatory
bowel
disease.
In
this
study,
we
explored
whether
colitis
induced
dextran
sulfate
sodium
(DSS)
young,
presymptomatic/preplaque
mice
worsens
and/or
anticipates
age-dependent
cognitive
impairment
Tg2576,
widely
used
mouse
model
AD.
We
demonstrated
that
DSS
young
Tg2576
onset
age
learning
memory
deficit
Morris
water
maze
test.
To
explore
potential
mechanisms
behind
acceleration
decline
colitis,
focused
on
gut
microbiota,
systemic
markers.
observed
Firmicutes/Bacteroidetes
ratio
change
animals
comparable
to
elderly
mice,
suggesting
accelerated
microbiota
aging
not
C57BL6
mice.
also
substantial
differences
between
WT
neuroinflammation-related
parameters
early
3
months
age,
well
before
plaque
deposition,
picture
which
evolved
rapidly
(between
5.5
age)
contrast
littermates
treated
DSS.
detail,
following
induction
exhibited
contrasting
features
expression
level
inflammation-evoked
astrocyte-associated
genes
hippocampus.
No
changes
microglial
occurred
hippocampus
experimental
groups,
whereas
reduced
glial
fibrillary
acidic
protein
immunoreactivity
was
vs.
This
finding
may
reflect
an
atrophic,
“loss-of-function”
profile,
further
exacerbated
where
decreased
GFAP
mRNA
detected.
conclusion,
suggest
as-yet
unidentified
peripheral
mediators
evoked
involving
gut-brain
axis
emphasize
astrocyte
profile
present
leading
impaired
synaptic
morphological
functional
integrity
very
sign