Frontiers in Neuroscience,
Год журнала:
2022,
Номер
16
Опубликована: Сен. 1, 2022
Currently,
there
is
no
disease-modifying
treatment
available
for
Alzheimer's
and
Parkinson's
disease
(AD
PD)
that
includes
the
highly
controversial
approval
of
Aβ-targeting
antibody
aducanumab
AD.
Hence,
still
an
unmet
need
a
neuroprotective
drug
in
both
AD
PD.
Type
2
diabetes
risk
factor
Glucagon-like
peptide
1
(GLP-1)
hormone
growth
has
shown
effects
preclinical
studies,
success
GLP-1
mimetics
phase
II
clinical
trials
PD
raised
new
hope.
are
currently
on
market
as
treatments
type
diabetes.
analogs
safe,
well
tolerated,
resistant
to
desensitization
characterized
clinic.
Herein,
we
review
existing
evidence
illustrate
pathways
induced
following
GLP-1R
activation
neurons,
microglia
astrocytes.
The
latter
include
synaptic
protection,
improvements
cognition,
learning
motor
function,
amyloid
pathology-ameliorating
properties
(Aβ,
Tau,
α-synuclein),
suppression
Ca
Redox Biology,
Год журнала:
2017,
Номер
14, С. 450 - 464
Опубликована: Окт. 19, 2017
Oxidative
stress
is
known
to
play
an
important
role
in
the
pathogenesis
of
a
number
diseases.
In
particular,
it
linked
etiology
Alzheimer's
disease
(AD),
age-related
neurodegenerative
and
most
common
cause
dementia
elderly.
Histopathological
hallmarks
AD
are
intracellular
neurofibrillary
tangles
extracellular
formation
senile
plaques
composed
amyloid-beta
peptide
(Aβ)
aggregated
form
along
with
metal-ions
such
as
copper,
iron
or
zinc.
Redox
active
metal
ions,
for
example
can
catalyze
production
Reactive
Oxygen
Species
(ROS)
when
bound
amyloid-β
(Aβ).
The
ROS
thus
produced,
particular
hydroxyl
radical
which
reactive
one,
may
contribute
oxidative
damage
on
both
Aβ
itself
surrounding
molecule
(proteins,
lipids,
…).
This
review
highlights
existing
link
between
AD,
consequences
towards
molecules
terms
damage.
addition,
implication
ions
their
interaction
redox
properties
leading
discussed,
vitro
vivo
oxidation
peptide,
at
molecular
level.
Cold Spring Harbor Perspectives in Medicine,
Год журнала:
2012,
Номер
2(3), С. a006312 - a006312
Опубликована: Янв. 10, 2012
Apolipoprotein
E
(APOE)
genotype
is
the
major
genetic
risk
factor
for
Alzheimer
disease
(AD);
ε4
allele
increases
and
ε2
protective.
In
central
nervous
system
(CNS),
apoE
produced
by
glial
cells,
present
in
high-density-like
lipoproteins,
interacts
with
several
receptors
that
are
members
of
low-density
lipoprotein
receptor
(LDLR)
family,
a
protein
binds
to
amyloid-β
(Aβ)
peptide.
There
variety
mechanisms
which
isoform
may
influence
AD.
substantial
evidence
differential
effects
on
AD
influenced
ability
affect
Aβ
aggregation
clearance
brain.
Other
also
likely
play
role
CNS
function
as
well
AD,
including
synaptic
plasticity,
cell
signaling,
lipid
transport
metabolism,
neuroinflammation.
ApoE
receptors,
LDLRs,
Apoer2,
very
(VLDLRs),
receptor-related
1
(LRP1)
appear
both
metabolism
toxicity.
Therapeutic
strategies
based
include
influencing
apoE/Aβ
interactions,
structure,
lipidation,
LDLR
family
member
function,
signaling.
Understanding
normal
disease-related
biology
connecting
apoE,
provide
novel
insights
into
pathogenesis
treatment.
Cold Spring Harbor Perspectives in Medicine,
Год журнала:
2012,
Номер
2(6), С. a006262 - a006262
Опубликована: Фев. 21, 2012
Colin
L.
Masters1
and
Dennis
J.
Selkoe2
The
Mental
Health
Research
Institute,
University
of
Melbourne,
Parkville
3010,
Australia
Center
for
Neurologic
Diseases,
Harvard
Medical
School
Brigham
Women's
Hospital,
Boston,
Massachusetts
02115
Correspondence:
c.masters{at}unimelb.edu.au
Journal of Cerebral Blood Flow & Metabolism,
Год журнала:
2013,
Номер
33(10), С. 1500 - 1513
Опубликована: Авг. 7, 2013
The
blood–brain
barrier
(BBB)
plays
critical
roles
in
the
maintenance
of
central
nervous
system
(CNS)
homeostasis.
Dysfunction
BBB
occurs
a
number
CNS
diseases,
including
Alzheimer's
disease
(AD).
A
prevailing
hypothesis
AD
field
is
amyloid
cascade
that
states
amyloid-β
(Aβ)
deposition
initiates
molecular
events
cause
neurodegeneration,
leading
to
onset
and
progression.
In
this
review,
participation
other
mechanisms
neurodegeneration
will
be
discussed.
We
specifically
focus
on
three
aspects
dysfunction:
disruption,
perturbation
transporters,
secretion
neurotoxic
substances
by
BBB.
also
discuss
interaction
with
components
neurovascular
unit
relation
potential
contribution
risk
factors
dysfunction.
From
results
discussed
herein,
we
conclude
dysfunction
contributes
through
could
initiated
presence
or
absence
Aβ
pathology.
