Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Июль 29, 2024
Abstract
Traumatic
brain
injury
(TBI)
remains
a
leading
cause
of
death
and
disability
that
places
great
physical,
social,
financial
burden
on
individuals
the
health
system.
In
this
review,
we
summarize
new
research
into
metabolic
changes
described
in
clinical
TBI
trials,
some
which
have
already
shown
promise
for
informing
classification
staging.
We
focus
our
discussion
derangements
glucose
metabolism,
cell
respiration/mitochondrial
function
to
ketone
lipid
metabolism/oxidation
emphasize
potentially
novel
biomarkers
outcome
prediction
intervention
offer
insights
possible
underlying
mechanisms
from
preclinical
pathology.
Finally,
discuss
nutrition
supplementation
studies
aim
harness
gut/microbiome-brain
connection
manipulate
systemic/cellular
metabolism
improve
post-TBI
recovery.
Taken
together,
narrative
review
summarizes
published
TBI-associated
highlighting
potential
metabolite
use,
cellular
processes
linking
these
markers
pathology
as
well
limitations
future
considerations
“omics”
work.
Trends in Endocrinology and Metabolism,
Год журнала:
2022,
Номер
33(7), С. 451 - 462
Опубликована: Май 7, 2022
Cognitive
dysfunction
is
a
common
adverse
consequence
of
traumatic
brain
injury
(TBI).
After
injury,
the
and
other
organs
trigger
series
complex
metabolic
changes,
including
reduced
glucose
metabolism,
enhanced
lipid
peroxidation,
disordered
neurotransmitter
secretion,
imbalanced
trace
element
synthesis.
In
recent
years,
several
research
clinical
studies
have
demonstrated
that
metabolism
directly
or
indirectly
affects
cognitive
after
TBI,
but
mechanisms
remain
unclear.
Drugs
improve
symptoms
caused
by
TBI
are
under
investigation
treatments
target
processes
expected
to
function
in
future.
This
review
explores
impact
disorders
on
provides
new
strategies
for
treatment
disorders.
Nutrients,
Год журнала:
2022,
Номер
14(14), С. 2940 - 2940
Опубликована: Июль 18, 2022
Carbohydrates
are
important
macronutrients
in
human
and
rodent
diet
patterns
that
play
a
key
role
crucial
metabolic
pathways
provide
the
necessary
energy
for
proper
body
functioning.
Sugar
homeostasis
intake
require
complex
hormonal
nervous
control
to
balance.
Added
sugar
processed
food
results
metabolic,
cardiovascular,
disorders.
Epidemiological
reports
have
shown
enhanced
consumption
of
sweet
products
children
adults,
especially
reproductive
age
pregnant
women,
which
can
lead
susceptibility
offspring's
health
diseases
early
life
or
adulthood
proneness
mental
In
this
review,
we
discuss
impacts
high-sugar
(HSD)
during
perinatal
and/or
postnatal
periods
on
neural
behavioural
disturbances
as
well
development
substance
use
disorder
(SUD).
Since
several
emotional
recognized
predictors
SUD,
also
present
how
HSD
enhances
impulsive
behaviour,
stress,
anxiety
depression.
Apart
from
influence
these
mood
disturbances,
added
render
addiction.
Both
addictive
substances
change
sensitivity
brain
rewarding
neurotransmission
signalling.
The
collected
studies
could
be
assessing
intake,
via
maternal
dietary
patterns,
clinical
perspective
SUD
prevention
pre-existing
Methodology:
This
narrative
review
focuses
roles
foods
glucose
fructose
(SUD)
drugs
abuse.
literature
was
reviewed
by
two
authors
independently
according
topic
review.
We
searched
PubMed
Scopus
databases
Multidisciplinary
Digital
Publishing
Institute
open
access
scientific
journals
using
following
keyword
search
strategy
depending
theme
chapter:
"high-sugar
diet"
OR
"high-carbohydrate
"sugar"
"glucose"
"fructose"
"added
sugar"
AND
keywords.
excluded
inaccessible
pay-walled
articles,
abstracts,
conference
papers,
editorials,
letters,
commentary,
short
notes.
Reviews,
experimental
studies,
epidemiological
data,
published
since
1990s,
were
chapter
structure.
After
search,
all
duplicates
thrown
out
full
texts
read,
findings
rescreened.
selection
process,
appropriate
papers
included
Antioxidants,
Год журнала:
2022,
Номер
11(1), С. 170 - 170
Опубликована: Янв. 17, 2022
Oxidative
stress
and
neuroinflammation
are
common
bases
for
disease
onset
progression
in
many
neurodegenerative
diseases.
In
Parkinson
disease,
which
is
characterized
by
the
degeneration
of
dopaminergic
neurons
resulting
dopamine
depletion,
pathogenesis
differs
between
hereditary
solitary
forms
often
unclear.
addition
to
pathogenicity
alpha-synuclein
as
a
pathological
marker,
involvement
itself
its
interactions
with
glial
cells
(astrocyte
or
microglia)
have
attracted
attention.
Pacemaking
activity,
hallmark
neurons,
essential
homeostatic
maintenance
adequate
concentrations
synaptic
cleft,
but
it
imposes
burden
on
mitochondrial
oxidative
glucose
metabolism,
leading
reactive
oxygen
species
production.
Astrocytes
provide
endogenous
neuroprotection
brain
producing
releasing
antioxidants
response
stress.
Additionally,
protective
function
astrocytes
can
be
modified
microglia.
Some
types
microglia
themselves
thought
exacerbate
pro-inflammatory
factors
(M1
microglia).
Although
these
inflammatory
may
further
trigger
conversion
astrocytes,
induce
astrocytic
neuroprotective
effects
(A2
astrocytes)
simultaneously.
Interestingly,
both
express
receptors,
upregulated
presence
neuroinflammation.
The
anti-inflammatory
receptor
stimulation
also
attracting
attention
because
functions
greatly
affected
depletion
therapeutic
replacement
disease.
this
review
article,
we
will
focus
antioxidative
their
synergism
dopamine.
Signal Transduction and Targeted Therapy,
Год журнала:
2023,
Номер
8(1)
Опубликована: Авг. 23, 2023
Abstract
As
key
organelles
involved
in
cellular
metabolism,
mitochondria
frequently
undergo
adaptive
changes
morphology,
components
and
functions
response
to
various
environmental
stresses
demands.
Previous
studies
of
research
have
gradually
evolved,
from
focusing
on
morphological
change
analysis
systematic
multiomics,
thereby
revealing
the
mitochondrial
variation
between
cells
or
within
population
a
single
cell.
The
phenomenon
features
is
defined
as
heterogeneity.
Moreover,
heterogeneity
has
been
reported
influence
variety
physiological
processes,
including
tissue
homeostasis,
repair,
immunoregulation,
tumor
progression.
Here,
we
comprehensively
review
different
tissues
under
pathological
states,
involving
variant
DNA,
RNA,
protein
lipid
components.
Then,
mechanisms
that
contribute
are
also
summarized,
such
mutation
genome
import
proteins
result
DNA
Additionally,
multiple
perspectives
investigated
better
comprehend
mysteries
cells.
Finally,
summarize
prospective
heterogeneity-targeting
therapies
terms
alleviating
oxidative
damage,
reducing
carbon
stress
enhancing
biogenesis
relieve
conditions.
possibility
recent
technological
advances
targeted
gene
editing
discussed.
Alzheimer s Research & Therapy,
Год журнала:
2024,
Номер
16(1)
Опубликована: Янв. 9, 2024
Abstract
Background
Alzheimer’s
dementia
(AD)
pathogenesis
involves
complex
mechanisms,
including
microRNA
(miRNA)
dysregulation.
Integrative
network
and
machine
learning
analysis
of
miRNA
can
provide
insights
into
AD
pathology
prognostic/diagnostic
biomarkers.
Methods
We
performed
co-expression
to
identify
modules
associated
with
AD,
its
neuropathology
markers,
cognition
using
brain
tissue
profiles
from
the
Religious
Orders
Study
Rush
Memory
Aging
Project
(ROS/MAP)
(
N
=
702)
as
a
discovery
dataset.
association
hub
miRNAs
cognition.
After
selecting
target
genes
miRNAs,
we
their
then
pathway-based
enrichment
analysis.
For
replication,
consensus
ROS/MAP
dataset
an
independent
16)
Gene
Expression
Omnibus
(GEO).
Furthermore,
approach
assess
performance
for
classification.
Results
Network
identified
glucose
metabolism
pathway-enriched
module
(M3)
significantly
Five
(miR-129-5p,
miR-433,
miR-1260,
miR-200a,
miR-221)
M3
had
significant
associations
clinical
and/or
pathologic
traits,
miR129-5p
by
far
strongest
across
all
phenotypes.
Gene-set
corresponding
enriched
biological
pathways
ErbB,
AMPK,
MAPK,
mTOR
signaling
pathways.
Consensus
two
AD-associated
(miR-129-5p
miR-221).
Machine
showed
that
classification
(area
under
curve
(AUC)
0.807)
age,
sex,
APOE
ε4
carrier
status
was
improved
6.3%
inclusion
five
miRNAs.
Conclusions
signatures,
especially
miR-129-5p,
cognition,
enhancing
our
understanding
leading
better
potential
diagnostic/prognostic
Abstract
The
microenvironment
mediated
by
the
microglia
(MG)
M1/M2
phenotypic
switch
plays
a
decisive
role
in
neuronal
fate
and
cognitive
function
of
Alzheimer's
disease
(AD).
However,
impact
metabolic
reprogramming
on
microglial
polarization
its
underlying
mechanism
remains
elusive.
This
study
reveals
that
cordycepin
improved
memory
APP/PS1
mice,
as
well
attenuated
damage
triggering
MG‐M2
characterized
increased
OXPHOS
glycolysis,
rather
than
directly
protecting
neurons.
Simultaneously,
partially
alleviates
mitochondrial
induced
inhibitors
further
promoting
transformation
increasing
survival.
Through
confirmation
distribution
mitochondria
via
isolation
followed
HPLC‐MS/MS
techniques,
HKII
PDK2
are
identified
potential
targets
cordycepin.
By
investigating
effects
inhibitors,
through
which
targeted
to
elevate
ECAR
levels
glycolysis
pathway
while
targeting
enhance
OCR
PDH‐mediated
pathway,
thereby
inducing
polarization,
survival
exerting
an
anti‐AD
is
elucidated.
The journal of nutrition health & aging,
Год журнала:
2024,
Номер
28(8), С. 100306 - 100306
Опубликована: Июнь 28, 2024
Ketogenic
diets
(KD)
have
shown
remarkable
effects
in
many
disease
areas.
It
has
been
demonstrated
numerous
animal
experiments
that
KD
is
effective
the
treatment
of
Alzheimer's
(AD).
But
clinical
effect
treating
AD
uncertain.