Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: June 5, 2024
Abstract
Background
Mounting
evidence
links
glucose
intolerance
and
diabetes
as
aspects
of
metabolic
dysregulation
that
are
associated
with
an
increased
risk
developing
dementia.
Inflammation
inflammasome
activation
have
emerged
a
potential
link
between
these
disparate
pathologies.
As
diet
is
key
factor
in
both
the
development
disorders
inflammation,
we
hypothesize
long
term
changes
dietary
factors
can
influence
nervous
system
function
by
regulating
activity
this
phenotype
would
be
sex-dependent,
sex
hormones
known
to
regulate
metabolism
immune
processes.
Methods
5-week-old
male
female
transgenic
mice
expressing
caspase-1
bioluminescent
reporter
underwent
cranial
window
surgeries
were
fed
control
(65%
complex
carbohydrates,
15%
fat),
high
glycemic
index
carbohydrates
from
sucrose,
or
ketogenic
(1%
79%
fat)
6
26
weeks
age.
Glucose
regulation
was
assessed
tolerance
test
following
4-h
morning
fast.
Bioluminescence
brain
quantified
using
IVIS
vivo
imaging.
Blood
cytokine
levels
measured
bead
array.
16S
ribosomal
RNA
gene
amplicon
sequencing
mouse
feces
performed
assess
alterations
gut
microbiome.
Behavior
also
evaluated.
Results
The
caused
weight
gain
mice.
In
mice,
led
biosensor
over
course
study,
while
females
drove
increase
compared
their
respective
controls.
These
correlated
inflammatory
cytokines
present
serum
emergence
anxiety-like
behavior.
microbiome
composition
differed
significantly
diets;
however
no
significant
diet,
tolerance,
signal
established.
Conclusions
Our
findings
suggest
composition,
specifically
source
quantity
has
sex-specific
effects
on
central
This
manifested
anxiety
future
studies
needed
determine
if
linked
composition.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
25(1), P. 124 - 124
Published: Dec. 21, 2023
Ketone
bodies
(KBs),
such
as
acetoacetate
and
β-hydroxybutyrate,
serve
crucial
alternative
energy
sources
during
glucose
deficiency.
KBs,
generated
through
ketogenesis
in
the
liver,
are
metabolized
into
acetyl-CoA
extrahepatic
tissues,
entering
tricarboxylic
acid
cycle
electron
transport
chain
for
ATP
production.
Reduced
metabolism
mitochondrial
dysfunction
correlate
with
increased
neuronal
death
brain
damage
cerebral
ischemia
neurodegeneration.
Both
KBs
ketogenic
diet
(KD)
demonstrate
neuroprotective
effects
by
orchestrating
various
cellular
processes
metabolic
signaling
functions.
They
enhance
function,
mitigate
oxidative
stress
apoptosis,
regulate
epigenetic
post-translational
modifications
of
histones
non-histone
proteins.
Additionally,
KD
contribute
to
reducing
neuroinflammation
modulating
autophagy,
neurotransmission
systems,
gut
microbiome.
This
review
aims
explore
current
understanding
molecular
mechanisms
underpinning
against
neurodegenerative
diseases,
including
Alzheimer’s
disease
Parkinson’s
disease.
ACS Chemical Neuroscience,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 9, 2025
Epilepsy
is
a
chronic
neurological
disorder
caused
by
abnormal
discharges
of
neurons
in
the
brain,
which
seriously
affects
quality
life
patients.
Although
there
are
various
drug
treatments
available,
many
epilepsy
patients
still
experience
seizures
with
effect
drugs
and
develop
refractory
epilepsy.
The
ketogenic
diet
can
treat
drug-refractory
regulating
body's
metabolism
enhance
improving
their
cognition,
behavior,
sleep
quality.
However,
no
unified
conclusion
on
mechanism
through
plays
therapeutic
role
This
article
provides
review
possible
mechanisms
how
exerts
protective
Frontiers in Nutrition,
Journal Year:
2024,
Volume and Issue:
11
Published: March 21, 2024
Metabolic
dysfunction-associated
fatty
liver
disease
(MAFLD)
is
the
most
common
chronic
disease.
Ketogenic
diet
(KD),
a
with
very
low
intake
in
carbohydrates,
gained
popularity
as
weight-loss
approach.
However,
mice
models,
it
has
been
reported
that
an
excess
exposition
of
dietary
fat
induces
hepatic
insulin
resistance
and
steatosis.
data
published
inconsistent.
Herein,
we
investigated
mouse
model,
metabolic
effects
KD
its
contribution
to
pathogenesis
NALFD.
Mice
were
exposed
or
CHOW
for
12
weeks
while
third
group
was
also
then
switched
4
determine
if
can
rescue
phenotype.
We
evaluated
treatments
on
distribution,
glucose,
homeostasis
well
fed
developed
glucose
intolerance
but
not
accompanied
by
increase
inflammation.
KD-fed
showed
accumulation
white
adipose
tissue
liver.
This
effect
could
be
explained
uptake
no
changes
catabolism
leading
MAFLD.
Interestingly,
able
phenotype
switching
diet.
Our
studies
demonstrate
even
develop
steatosis
after
KD,
they
do
more
importantly,
reversed
from
CHOW.
Immunological Reviews,
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 11, 2024
Summary
Alzheimer's
disease
(AD)
is
a
degenerative
brain
disorder
and
the
most
common
form
of
dementia.
AD
pathology
characterized
by
senile
plaques
neurofibrillary
tangles
(NFTs)
composed
amyloid‐β
(Aβ)
hyperphosphorylated
tau,
respectively.
Neuroinflammation
has
been
shown
to
drive
Aβ
tau
pathology,
with
evidence
suggesting
nod‐like
receptor
family
pyrin
domain
containing
3
(NLRP3)
inflammasome
as
key
pathway
in
pathogenesis.
NLRP3
activation
microglia,
primary
immune
effector
cells
brain,
results
caspase‐1
secretion
IL‐1β
IL‐18.
Recent
studies
have
demonstrated
dramatic
interplay
between
metabolic
state
functions
cells.
Microglial
metabolism
particular
interest,
ketone
bodies
(acetone,
acetoacetate
(AcAc),
β‐hydroxybutyrate
(BHB))
serve
an
alternative
energy
source
when
glucose
utilization
compromised
patients
AD.
Furthermore,
reduced
cerebral
concomitant
increased
BHB
levels
inhibit
activation.
Here,
we
review
role
microglial
body
We
also
highlight
inhibition
several
therapies
promising
new
treatment
strategy
for
Food & Function,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 1, 2025
HCD
mitigates
brain
damage,
oxidative
stress,
and
inflammation
in
hypoxic
mice,
enhancing
neuronal
survival.
It
also
modulates
the
gut
microbiota,
suggesting
that
“microbiota–gut–brain”
axis
acts
as
a
pathway
for
cognitive
benefits
of
an
HCD.
