Neural Regeneration Research,
Год журнала:
2024,
Номер
20(5), С. 1258 - 1276
Опубликована: Июнь 3, 2024
The
central
nervous
system,
information
integration
center
of
the
body,
is
mainly
composed
neurons
and
glial
cells.
neuron
one
most
basic
important
structural
functional
units
with
sensory
stimulation
excitation
conduction
functions.
Astrocytes
microglia
belong
to
cell
family,
which
main
source
cytokines
represents
defense
system
system.
Nerve
cells
undergo
neurotransmission
or
gliotransmission,
regulates
neuronal
activity
via
ion
channels,
receptors,
transporters
expressed
on
nerve
membranes.
Ion
large
transmembrane
proteins,
play
crucial
roles
in
maintaining
homeostasis.
These
channels
are
also
for
control
membrane
potential
secretion
neurotransmitters.
A
variety
cellular
functions
life
activities,
including
regulation
generation
excitation,
occurrence
receptor
potential,
heart
pulsation,
smooth
muscle
peristalsis,
skeletal
contraction,
hormone
secretion,
closely
related
associated
passive
transport.
Two
types
potassium
calcium
various
neurological
disorders,
Alzheimer’s
disease,
Parkinson’s
epilepsy.
Accordingly,
drugs
that
can
affect
these
have
been
explored
deeply
provide
new
directions
treatment
disorders.
In
this
review,
we
focus
different
their
involvement
disorders
such
as
depression,
epilepsy,
autism,
rare
We
describe
several
clinical
target
could
be
used
treat
concluded
there
few
improve
pathology
diseases
by
acting
ions.
Although
a
novel
ion-channel-specific
modulators
discovered,
meaningful
therapies
largely
not
yet
realized.
lack
target-specific
drugs,
requirement
cross
blood–brain
barrier,
exact
underlying
mechanisms
all
need
further
attention.
This
review
aims
explain
urgent
problems
research
progress
comprehensive
aiming
arouse
community’s
interest
development
channel-targeting
identification
therapeutic
targets
increase
cure
rate
reduce
adverse
reactions
other
systems.
Journal of Clinical Investigation,
Год журнала:
2023,
Номер
133(12)
Опубликована: Июнь 14, 2023
Tauopathies
are
disorders
associated
with
tau
protein
dysfunction
and
insoluble
accumulation
in
the
brain
at
autopsy.
Multiple
lines
of
evidence
from
human
disease,
as
well
nonclinical
translational
models,
suggest
that
has
a
central
pathologic
role
these
disorders,
historically
thought
to
be
primarily
related
gain
toxic
function.
However,
number
tau-targeting
therapies
various
mechanisms
action
have
shown
little
promise
clinical
trials
different
tauopathies.
We
review
what
is
known
about
biology,
genetics,
therapeutic
been
tested
date.
discuss
possible
reasons
for
failures
therapies,
such
use
imperfect
models
do
not
predict
effects
drug
development;
heterogeneity
pathologies
which
may
lead
variable
responses
therapy;
ineffective
mechanisms,
targeting
wrong
species
or
epitope.
Innovative
approaches
can
help
address
some
difficulties
plagued
our
field's
development
thus
far.
Despite
limited
success
date,
we
continue
refine
understanding
tau's
pathogenic
mechanism(s)
neurodegenerative
diseases,
remain
optimistic
will
eventually
play
treatment
Cells,
Год журнала:
2024,
Номер
13(6), С. 485 - 485
Опубликована: Март 11, 2024
The
NF-κB
(nuclear
factor
K-light-chain-enhancer
of
activated
B
cells)
transcription
family
is
critical
for
modulating
the
immune
proinflammatory
response
throughout
body.
During
resting
state,
inactive
sequestered
by
IκB
in
cytoplasm.
proteasomal
degradation
activates
NF-κB,
mediating
its
translocation
into
nucleus
to
act
as
a
nuclear
upregulation
genes.
Stimuli
that
initiate
activation
are
diverse
but
canonically
attributed
cytokines
and
chemokines.
Downstream
effects
cell
type-specific
and,
majority
cases,
result
pro-inflammatory
cascades.
Acting
primary
responders
central
nervous
system,
microglia
exhibit
upon
pathological
conditions.
Under
such
circumstances,
microglial
crosstalk
with
other
types
system
can
induce
death,
further
exacerbating
disease
pathology.
In
this
review,
we
will
emphasize
role
triggering
neuroinflammation
mediated
microglia.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Май 24, 2024
Alois
Alzheimer
described
the
first
patient
with
Alzheimer’s
disease
(AD)
in
1907
and
today
AD
is
most
frequently
diagnosed
of
dementias.
a
multi-factorial
neurodegenerative
disorder
familial,
life
style
comorbidity
influences
impacting
global
population
more
than
47
million
projected
escalation
by
2050
to
exceed
130
million.
In
USA
demographic
encompasses
approximately
six
individuals,
expected
increase
surpass
13
2050,
antecedent
phase
AD,
recognized
as
mild
cognitive
impairment
(MCI),
involves
nearly
12
individuals.
The
economic
outlay
for
management
AD-related
decline
estimated
at
355
billion
USD.
addition,
intensifying
prevalence
cases
countries
modest
intermediate
income
further
enhances
urgency
therapeutically
cost-effective
treatments
improving
quality
patients
their
families.
This
narrative
review
evaluates
pathophysiological
basis
an
initial
focus
on
therapeutic
efficacy
limitations
existing
drugs
that
provide
symptomatic
relief:
acetylcholinesterase
inhibitors
(AChEI)
donepezil,
galantamine,
rivastigmine,
N-methyl-D-aspartate
receptor
(NMDA)
allosteric
modulator,
memantine.
hypothesis
amyloid-β
(Aβ)
tau
are
appropriate
targets
have
potential
halt
progress
critically
analyzed
particular
clinical
trial
data
anti-Aβ
monoclonal
antibodies
(MABs),
namely,
aducanumab,
lecanemab
donanemab.
challenges
dogma
targeting
Aβ
will
benefit
majority
subjects
MABs
unlikely
be
“magic
bullet”.
A
comparison
benefits
disadvantages
different
classes
forms
determining
new
directions
research
alternative
drug
undergoing
pre-clinical
assessments.
we
discuss
stress
importance
treatment
co-morbidities,
including
hypertension,
diabetes,
obesity
depression
known
risk
developing
AD.
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Янв. 10, 2025
Microbiome
abnormalities
(dysbiosis)
significantly
contribute
to
the
progression
of
Alzheimer's
disease
(AD).
However,
therapeutic
efficacy
microbiome
modulators
in
protecting
against
these
ailments
remains
poorly
studied.
Herein,
we
tested
a
cocktail
unique
probiotics,
including
5
Lactobacillus
and
Enterococcus
strains
isolated
from
infant
gut
with
proven
modulating
capabilities.
We
aimed
determine
probiotics
cocktail's
ameliorating
AD
pathology
humanized
mouse
model
APP/PS1
strains.
Remarkably,
feeding
mice
1
×
1011
CFU
per
day
drinking
water
for
16
weeks
reduced
cognitive
decline
(measured
by
Morris
Water
Maze
test)
markers,
such
as
Aβ
aggregation,
microglia
activation,
neuroinflammation,
preserved
blood-brain
barrier
(BBB)
tight
junctions.
The
beneficial
effects
were
linked
inflammatory
microbiome,
leading
decreased
permeability
inflammation
both
systemic
circulation
brain.
Although
male
female
showed
overall
improvements
cognition
biological
females
did
not
exhibit
specific
markers
related
permeability,
suggesting
that
underlying
mechanisms
may
differ
depending
on
sex.
In
conclusion,
our
results
suggest
this
could
serve
prophylactic
agent
reduce
pathology.
This
is
achieved
beneficially
improving
intestinal
junction
proteins,
reducing
BBB,
decreasing
gut,
blood
circulation,
brain,
ultimately
mitigating
decline.
Ageing Research Reviews,
Год журнала:
2024,
Номер
101, С. 102481 - 102481
Опубликована: Сен. 3, 2024
Alzheimer's
disease
(AD)
is
the
most
common
cause
of
dementia
and
accounts
for
60-70
%
all
cases.
It
affects
millions
people
worldwide.
AD
poses
a
substantial
economic
burden
on
societies
healthcare
systems.
progressive
neurodegenerative
disorder
characterized
by
cognitive
decline,
memory
loss,
impaired
daily
functioning.
As
prevalence
continues
to
increase,
understanding
its
pathogenesis,
improving
diagnostic
methods,
developing
effective
therapeutics
have
become
paramount.
This
comprehensive
review
delves
into
intricate
mechanisms
underlying
AD,
explores
current
state
techniques,
examines
emerging
therapeutic
strategies.
By
revealing
complexities
this
aims
contribute
growing
body
knowledge
surrounding
devastating
disease.
Cells,
Год журнала:
2025,
Номер
14(3), С. 168 - 168
Опубликована: Янв. 22, 2025
The
recent
approval
of
lecanemab
highlights
that
the
amyloid
beta
(Aβ)
protein
is
an
important
pathological
target
in
Alzheimer’s
disease
(AD)
and
further
emphasizes
significance
neuroinflammatory
pathways
regulating
Aβ
accumulation.
Indeed,
accumulation
triggers
microglia
activation,
which
are
key
mediators
neuroinflammation.
inflammatory
responses
this
process
can
lead
to
neuronal
damage
functional
decline.
Microglia
secrete
proinflammatory
cytokines
accelerate
death
release
anti-inflammatory
growth
factors
contributing
recovery
protection.
Thus,
play
a
dual
role
neurodegeneration
neuroprotection,
complicating
their
function
AD.
Therefore,
elucidating
complex
interactions
between
protein,
microglia,
neuroinflammation
essential
for
developing
new
strategies
treating
This
review
investigates
receptors
involved
activating
aims
enhance
understanding
how
these
processes
impact
AD,
as
well
they
be
regulated.
also
analyzed
studies
reported
existing
literature
ongoing
clinical
trials.
Overall,
will
contribute
regulatory
mechanisms
therapies
slow
progression
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.
