Cells,
Journal Year:
2023,
Volume and Issue:
12(20), P. 2426 - 2426
Published: Oct. 10, 2023
Alzheimer’s
disease
(AD)—the
most
common
cause
of
dementia
in
the
elderly—is
characterized
by
progressive
memory
loss
and
β-amyloid
protein
(Aβ)
accumulation
brain.
Recently,
loneliness
was
found
to
be
a
high
risk
factor
for
AD,
social
isolation
has
become
major
AD.
Oxytocin
(OXT),
main
hormone
involved
bonding,
been
implicated
interactions,
notably
building
trust
relationships.
Moreover,
or
enrichment
modulates
activation
neurons
related
OXT.
we
reported
that
OXT
reverses
learning
impairment
AD
animal
models.
Based
on
limited
number
studies
currently
available,
might
therapeutic
target
Further
are
necessary
order
better
understand
role
oxytocin
In
this
review,
described
relationships
between
OXT,
interaction.
Neurotherapeutics,
Journal Year:
2022,
Volume and Issue:
20(1), P. 195 - 206
Published: Oct. 17, 2022
Immunotherapy
against
amyloid-beta
(Aβ)
is
a
promising
option
for
the
treatment
of
Alzheimer's
disease
(AD).
Aβ
exists
as
various
species,
including
monomers,
oligomers,
protofibrils,
and
insoluble
fibrils
in
plaques.
Oligomers
protofibrils
have
been
shown
to
be
toxic,
removal
these
aggregates
might
represent
an
effective
AD.
We
characterized
binding
properties
lecanemab,
aducanumab,
gantenerumab
different
species
with
inhibition
ELISA,
immunodepletion,
surface
plasmon
resonance.
All
three
antibodies
bound
monomers
low
affinity.
However,
lecanemab
aducanumab
had
very
weak
somewhat
stronger
binding.
Lecanemab
was
distinctive
it
tenfold
compared
fibrils.
Aducanumab
preferred
over
protofibrils.
Our
results
show
profiles
that
may
explain
clinical
observed
regarding
both
efficacy
side
effects.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(22), P. 13954 - 13954
Published: Nov. 12, 2022
Alzheimer’s
disease
(AD)
is
the
most
frequent
case
of
neurodegenerative
and
becoming
a
major
public
health
problem
all
over
world.
Many
therapeutic
strategies
have
been
explored
for
several
decades;
however,
there
still
no
curative
treatment,
priority
remains
prevention.
In
this
review,
we
present
an
update
on
clinical
physiological
phase
AD
spectrum,
modifiable
non-modifiable
risk
factors
treatment
with
focus
prevention
strategies,
then
research
models
used
in
AD,
followed
by
discussion
limitations.
The
methods
can
significantly
slow
evolution
are
currently
best
strategy
possible
before
advanced
stages
disease.
Indeed,
current
drug
treatments
only
symptomatic
effects,
disease-modifying
not
yet
available.
Drug
delivery
to
central
nervous
system
complex
process
represents
challenge
developing
preventive
strategies.
Studies
underway
test
new
techniques
facilitate
bioavailability
molecules
brain.
After
deep
study
literature,
find
use
soft
nanoparticles,
particular
nanoliposomes
exosomes,
as
innovative
approach
reducing
solving
problems
brain
bioavailability.
show
promising
role
exosomes
smart
systems
able
penetrate
blood–brain
barrier
target
tissues.
Finally,
different
administration
neurological
disorders
discussed.
One
intranasal
which
should
be
preclinical
studies
diseases.
Drugs,
Journal Year:
2023,
Volume and Issue:
83(7), P. 569 - 576
Published: April 15, 2023
Two
anti-amyloid
monoclonal
antibodies
(MABs)—lecanemab
(Leqembi®)
and
aducanumab
(Aduhelm®)—have
been
approved
in
the
USA
for
treatment
of
Alzheimer's
disease
(AD).
Anti-amyloid
are
first
disease-modifying
therapies
AD
that
achieve
slowing
clinical
decline
by
intervening
basic
biological
processes
disease.
These
breakthrough
agents
can
slow
inevitable
progression
into
more
severe
cognitive
impairment.
The
results
trials
MABs
support
amyloid
hypothesis
as
a
target
drug
development.
success
reflects
relentless
application
neuroscience
knowledge
to
solving
major
challenges
facing
humankind.
these
transformative
will
foster
development
MABs,
other
types
therapies,
treatments
targets
biology,
new
approaches
an
array
neurodegenerative
disorders.
Monoclonal
have
side
effects
and,
during
period
initiation,
patients
must
be
closely
monitored
occurrence
amyloid-related
imaging
abnormalities
(ARIA)
infusion
reactions.
A
successful
step
therapy
defines
desirable
features
next
phase
therapeutic
including
less
frequent
ARIA,
convenient
administration,
greater
efficacy.
Unprecedented
make
demands
on
care
partners,
clinicians,
payers,
health
systems.
Collaboration
among
stakeholders
is
essential
take
advantage
benefits
offered
them
widely
available.
usher
era
define
landscape
what
possible
Molecular Brain,
Journal Year:
2024,
Volume and Issue:
17(1)
Published: July 17, 2024
Abstract
Alzheimer’s
disease
(AD)
is
a
degenerative
neurological
condition
that
gradually
impairs
cognitive
abilities,
disrupts
memory
retention,
and
impedes
daily
functioning
by
impacting
the
cells
of
brain.
A
key
characteristic
AD
accumulation
amyloid-beta
(Aβ)
plaques,
which
play
pivotal
roles
in
progression.
These
plaques
initiate
cascade
events
including
neuroinflammation,
synaptic
dysfunction,
tau
pathology,
oxidative
stress,
impaired
protein
clearance,
mitochondrial
disrupted
calcium
homeostasis.
Aβ
also
closely
associated
with
other
hallmark
features
AD,
underscoring
its
significance.
generated
through
cleavage
amyloid
precursor
(APP)
plays
dual
role
depending
on
processing
pathway.
The
non-amyloidogenic
pathway
reduces
production
has
neuroprotective
anti-inflammatory
effects,
whereas
amyloidogenic
leads
to
peptides,
Aβ40
Aβ42,
contribute
neurodegeneration
toxic
effects
AD.
Understanding
multifaceted
Aβ,
particularly
crucial
for
developing
effective
therapeutic
strategies
target
metabolism,
aggregation,
clearance
aim
mitigating
detrimental
consequences
disease.
This
review
aims
explore
mechanisms
functions
under
normal
abnormal
conditions,
examining
both
beneficial
effects.
Diagnostics,
Journal Year:
2021,
Volume and Issue:
11(8), P. 1473 - 1473
Published: Aug. 14, 2021
Decades
of
experimental
and
clinical
research
have
contributed
to
unraveling
many
mechanisms
in
the
pathogenesis
Alzheimer's
disease
(AD),
but
puzzle
is
still
incomplete.
Although
we
can
suppose
that
there
no
complete
set
pieces,
recent
growth
open
data-sharing
initiatives
collecting
lifestyle,
clinical,
biological
data
from
AD
patients
has
provided
a
potentially
unlimited
amount
information
about
disease,
far
exceeding
human
ability
make
sense
it.
Moreover,
integrating
Big
Data
multi-omics
studies
provides
potential
explore
pathophysiological
entire
continuum
AD.
In
this
context,
Artificial
Intelligence
(AI)
offers
wide
variety
methods
analyze
large
complex
order
improve
knowledge
field.
review,
focus
on
findings
future
challenges
for
AI
research.
particular,
discuss
use
Computer-Aided
Diagnosis
tools
diagnosis
support
practices
prediction
individual
risk
conversion
as
well
patient
stratification
finally
develop
effective
personalized
therapies.
Biomolecules,
Journal Year:
2022,
Volume and Issue:
12(11), P. 1676 - 1676
Published: Nov. 11, 2022
Damage
or
loss
of
brain
cells
and
impaired
neurochemistry,
neurogenesis,
synaptic
nonsynaptic
plasticity
the
lead
to
dementia
in
neurodegenerative
diseases,
such
as
Alzheimer's
disease
(AD).
Injury
synapses
neurons
accumulation
extracellular
amyloid
plaques
intracellular
neurofibrillary
tangles
are
considered
main
morphological
neuropathological
features
AD.
Age,
genetic
epigenetic
factors,
environmental
stressors,
lifestyle
contribute
risk
AD
onset
progression.
These
factors
associated
with
structural
functional
changes
brain,
leading
cognitive
decline.
Biomarkers
reflect
cause
specific
function,
especially
pathways
neurotransmission,
neuroinflammation,
bioenergetics,
apoptosis,
oxidative
nitrosative
stress.
Even
initial
stages,
is
Aβ
neurotoxicity,
mitochondrial
dysfunction,
tau
neurotoxicity.
The
integrative
amyloid-tau-mitochondrial
hypothesis
assumes
that
primary
neurotoxicity
oligomers
oligomers,
their
mutual
synergy.
For
development
new
efficient
drugs,
targeting
elimination
potentiation
effects,
unwanted
protein
interactions
biomarkers
(mainly
dysfunction)
early
stage
seems
promising.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(5), P. 2727 - 2727
Published: Feb. 27, 2024
New
data
suggest
that
the
aggregation
of
misfolded
native
proteins
initiates
and
drives
pathogenic
cascade
leads
to
Alzheimer's
disease
(AD)
other
age-related
neurodegenerative
disorders.
We
propose
a
unifying
single
toxin
theory
brain
neurodegeneration
identifies
new
targets
approaches
development
disease-modifying
treatments.
An
extensive
body
genetic
evidence
suggests
soluble
aggregates
beta-amyloid
(Aβ)
as
primary
neurotoxin
in
pathogenesis
AD.
insights
from
fluid
biomarkers,
imaging,
clinical
studies
provide
further
for
decisive
impact
toxic
Aβ
species
initiation
progression
Understanding
distinct
roles
insoluble
amyloid
on
AD
has
been
key
missing
piece
puzzle.
Data
trials
with
anti-amyloid
agents
recent
advances
diagnosis
demonstrate
driving
insult
biologically
defined
is
neurotoxicity
aggregates,
called
oligomers
protofibrils,
rather
than
relatively
inert
mature
fibrils
plaques.
Amyloid
appear
be
factor
causing
synaptic
impairment,
neuronal
stress,
spreading
tau
pathology,
eventual
cell
death
lead
syndrome
dementia.
All
biochemical
effects
changes
are
observed
response
or
downstream
effect
this
initial
by
oligomers.
Other
disorders
follow
similar
pattern
pathogenesis,
which
normal
important
biological
functions
become
trapped
aging
due
impaired
clearance
then
misfold
aggregate
into
neurotoxic
exhibit
prion-like
behavior.
These
spread
through
cause
disease-specific
neurodegeneration.
Targeting
inhibition
step
blocking
misfolding
healthy
potential
slow
arrest
progression,
if
treatment
administered
early
course
disorders,
it
may
delay
prevent
onset
symptoms.
The Journal of Prevention of Alzheimer s Disease,
Journal Year:
2025,
Volume and Issue:
12(1), P. 100022 - 100022
Published: Jan. 1, 2025
The
advancement
of
disease-modifying
treatments
(DMTs)
for
Alzheimer's
disease
(AD),
along
with
the
approval
three
amyloid-targeting
therapies
in
US
and
several
other
countries,
represents
a
significant
development
treatment
landscape,
offering
new
hope
addressing
this
once
untreatable
chronic
progressive
disease.
However,
challenges
persist
that
could
impede
successful
integration
class
drugs
into
clinical
practice.
These
include
determining
patient
eligibility,
appropriate
use
diagnostic
tools
genetic
testing
care
pathways,
effective
detection
monitoring
side
effects,
improving
healthcare
system's
readiness
by
engaging
both
primary
dementia
specialists.
Additionally,
there
are
logistical
concerns
related
to
infrastructure,
as
well
cost-effectiveness
reimbursement
issues.
This
article
brings
together
insights
from
diverse
group
international
researchers
experts
outlines
potential
opportunities,
urging
all
stakeholders
prepare
introduction
DMTs.
We
emphasize
need
develop
criteria,
including
characteristics,
specifically
European
system,
ensure
administered
most
suitable
patients.
It
is
crucial
improve
skills
knowledge
physicians
accurately
interpret
biomarker
results,
share
decision-making
patients,
recognize
treatment-related
monitor
long-term
treatment.
advocate
investment
registries
unbiased
follow-up
studies
better
understand
effectiveness,
evaluate
optimize
Utilizing
starting
point
combination
should
also
be
priority.
