Nutrients,
Год журнала:
2025,
Номер
17(3), С. 558 - 558
Опубликована: Янв. 31, 2025
Alzheimer’s
disease
(AD)
is
the
most
common
form
of
dementia
and
characterized
by
memory
impairment
that
significantly
interferes
with
daily
life.
Therapeutic
options
for
AD
substantively
modify
progression
remain
a
critical
unmet
need.
In
this
regard,
gut
microbiota
crucial
in
maintaining
human
health
regulating
metabolism
immune
responses,
increasing
evidence
suggests
probiotics,
particularly
beneficial
bacteria,
can
enhance
cognitive
functions.
Recent
studies
have
highlighted
positive
effects
Bifidobacterium
breve
MCC1274
(B.
MCC1274)
on
individuals
mild
(MCI)
schizophrenia.
Additionally,
oral
supplementation
B.
has
been
shown
to
effectively
prevent
decline
AppNL–G–F
mice.
relation
pathology,
found
reduce
amyloid-β
(Aβ)
accumulation
tau
phosphorylation
both
wild-type
(WT)
It
also
decreases
microglial
activation
increases
levels
synaptic
proteins.
review,
we
examine
AD,
exploring
potential
mechanisms
action
how
probiotic
strain
may
aid
preventing
or
treating
disease.
Furthermore,
discuss
broader
implications
improving
overall
host
provide
insights
into
future
research
directions
promising
therapy.
Oxidative Medicine and Cellular Longevity,
Год журнала:
2020,
Номер
2020, С. 1 - 17
Опубликована: Сен. 11, 2020
Alzheimer’s
disease
(AD)
is
the
most
common
form
of
dementia
characterized
by
progressive
loss
cognitive
functions
due
to
neuronal
death
mainly
in
hippocampal
and
cortical
brain.
Sulforaphene
(SF)
one
main
isothiocyanates
isolated
from
a
Chinese
herb
Raphani
Semen.
In
this
study,
we
aimed
investigate
neuroprotective
effects
SF
using
vitro
vivo
models
AD.
Streptozotocin
(STZ)
was
intracranially
injected
into
rats;
then,
(25
50
mg/kg)
given
orally
once
day
for
6
consecutive
weeks.
After
drug
treatment,
were
assessed
Morris
Water
Maze
Test
(MWMT).
MWMT,
rats
euthanized
brain
tissues
collected.
test,
BV-2
microglia
pretreated
with
(1
2
μ
M)
1
h
then
stimulated
lipopolysaccharide
(LPS)
another
23
h.
Both
molecular
histological
methods
used
unravel
action
mechanisms
elucidate
signaling
pathway.
The
MWMT
results
showed
that
treatment
significantly
improved
STZ-induced
deficits
rats.
markedly
suppressed
production
tumor
necrosis
factor-
α
(TNF-
)
interleukin-6
(IL-6)
but
increased
release
IL-10
STZ-treated
addition,
inhibited
phosphorylation
tau
protein
at
Thr205,
Ser396,
Ser404
sites,
while
enhancing
ratios
p-Akt
(Ser473)/Akt
p-GSK-3
β
(Ser9)/GSK-3
hippocampus
On
other
hand,
also
attenuated
cytotoxicity
induced
LPS
cells.
obviously
releases
nitric
oxide
(NO),
TNF-
,
IL-6
LPS-stimulated
Moreover,
mitigated
nuclear
translocation
p-NF-
κ
B
p65
ratio
Taken
together,
possessed
against
LPS-induced
neuroinflammation
cells
via
modulation
PI3K/Akt/GSK-3
pathway
inhibition
NF-
activation,
suggesting
promising
agent
worthy
further
development
AD
treatment.
The
AD
etiology
is
yet
not
properly
known.
Interactions
among
environmental
factors,
multiple
susceptibility
genes
and
aging,
contribute
to
AD.
This
study
investigates
the
factors
that
play
role
in
causing
how
changes
cellular
pathways
PUBMED
database,
MEDLINE
database
Google
Scholar
were
searched
with
no
date
restrictions
for
published
articles
involving
roles
cancers,
cell
survival,
growth,
proliferation,
development,
also
contributing
Alzheimer’s
disease.
research
explores
inverse
relationship
between
cancer,
other
behind
using
several
already
literature
find
of
Cancer
disease
have
many
aspects
such
as
P53,
estrogen,
neurotrophins
growth
cAMP,
EGFR,
Bcl-2,
apoptosis
pathways,
IGF-1,
HSV,
TDP-43,
APOE
variants,
notch
signals
presenilins,
NCAM,
TNF
alpha,
PI3K/AKT/MTOR
pathway,
telomerase,
ROS,
ACE
levels.
occurs
when
brain
neurons
weakened
survival
responses,
maintenance
mechanisms,
anti-stress
responses
Vimentin,
Carbonic
anhydrases,
HSPs,
SAPK.
In
these
are
upregulated
maintained.
Evolutionarily
conserved
mechanisms
FOXO
impaired
Countermeasures
or
compensatory
by
affected
Tau,
Beta
Amyloid,
S100,
last
attempts
which
may
be
protective
certain
time,
can
speed
up
microenvironment
via
C-ABL
activation,
GSK3,
neuro-inflammation.
relationship;
any
cancer
sustain
downregulated
neuro-degeneration.
When
aged
genetically
susceptible
age
related
gene
expression
changes,
altered
regulation
death
they
Amyloid
Plaques,
NFTs,
this
provides
neuroprotection
time
ultimately
become
pathological
developing
new
potential
diagnostic
tests,
interventions
treatments.
Journal of Neuroinflammation,
Год журнала:
2016,
Номер
13(1)
Опубликована: Апрель 27, 2016
Transient
receptor
potential
ankyrin
1
(TRPA1)
channel
plays
an
important
role
in
pain
and
inflammation.
However,
little
is
known
about
the
significance
of
TRPA1
pathophysiology
Alzheimer's
disease
(AD).Wild-type
(WT),
TRPA1(-/-),
amyloid
precursor
protein
(APP)/presenilin
(PS1)
transgenic
(APP/PS1
Tg)
mice,
mouse
model
AD,
APP/PS1
Tg/TRPA1(-/-)
mice
were
used
to
examine
pathogenesis
AD.
Western
blot
was
for
expression;
immunohistochemistry
histological
examination.
The
behaviors
evaluated
by
locomotion,
nesting
building,
Y-maze
Morris
water
maze
tests;
levels
interleukin
(IL)-1β,
IL-4,
IL-6
IL-10
activities
phosphatase
2B
(PP2B),
NF-κB
nuclear
factor
activated
T
cells
(NFAT)
measured
conventional
assay
kits;
Fluo-8
NW
calcium
(Ca(2+))
kit
measurement
intracellular
Ca(2+)
level
primary
astrocytes
HEK293
cells.The
expression
channels
higher
brains,
mainly
hippocampus,
from
Tg
than
WT
mice.
Ablation
TRPA1-channel
function
alleviated
behavioral
dysfunction,
Aβ
plaque
deposition
pro-inflammatory
cytokine
production
but
increased
astrogliosis
brain
lesions.
influx
elicited
both
TRPA1-transfected
treated
with
fibrilized
Aβ1-42;
these
abrogated
pharmacological
inhibition
activity,
disruption
or
removal
extracellular
Ca(2+).
Inhibition
activity
exacerbated
Aβ1-42-induced
inhibited
Aβ1-42-increased
PP2B
activation,
cytokines
transcriptional
factors
NFAT
Pharmacological
diminished
cytokines,
activation
astrocytes.TRPA1
-
signaling
may
play
a
crucial
regulating
astrocyte-derived
inflammation
Molecular & Cellular Proteomics,
Год журнала:
2021,
Номер
20, С. 100081 - 100081
Опубликована: Янв. 1, 2021
As
the
body
fluid
that
directly
interchanges
with
extracellular
of
central
nervous
system
(CNS),
cerebrospinal
(CSF)
serves
as
a
rich
source
for
CNS-related
disease
biomarker
discovery.
Extensive
proteome
profiling
has
been
conducted
CSF,
but
studies
aimed
at
unraveling
site-specific
CSF
N-glycoproteome
are
lacking.
Initial
efforts
into
N-glycoproteomics
study
in
yield
limited
coverage,
hindering
further
experimental
design
glycosylation-based
discovery
CSF.
In
present
study,
we
have
developed
an
N-glycoproteomic
approach
combines
enhanced
N-glycopeptide
sequential
enrichment
by
hydrophilic
interaction
chromatography
(HILIC)
and
boronic
acid
electron
transfer
higher-energy
collision
dissociation
(EThcD)
large-scale
intact
analysis.
The
application
to
analyses
human
samples
enabled
identifications
total
2893
N-glycopeptides
from
511
N-glycosites
285
N-glycoproteins.
To
our
knowledge,
this
is
largest
dataset
reported
date.
Such
provides
molecular
basis
better
understanding
structure-function
relationships
glycoproteins
their
roles
physiological
pathological
processes.
accumulating
evidence
suggests
defects
glycosylation
involved
Alzheimer's
(AD)
pathogenesis,
comparative
in-depth
analysis
was
healthy
control
AD
patients,
which
yielded
comparable
coverage
distinct
expression
pattern
different
categories
glycoforms,
such
decreased
fucosylation
samples.
Altered
patterns
were
detected
number
N-glycoproteins
including
alpha-1-antichymotrypsin,
ephrin-A3
carnosinase
CN1
etc.,
serve
potentially
interesting
targets
may
eventually
lead
elucidation
role
progression.