ACS Applied Materials & Interfaces,
Journal Year:
2022,
Volume and Issue:
14(3), P. 3662 - 3674
Published: Jan. 13, 2022
Activities
of
catalase
(CAT)
and
superoxide
dismutase
(SOD)
ceria
nanoparticles
(CeO2
NPs)
provide
the
possibility
for
their
application
in
nervous
system
oxidative
stress
diseases
including
Alzheimer's
disease
(AD).
The
addition
hot
electrons
produced
by
a
plasma
photothermal
effect
can
expand
photocatalytic
activity
CeO2
to
near-infrared
region
(NIR),
significantly
improving
its
redox
performance.
Therefore,
we
coated
both
ends
gold
nanorods
(Au
NRs)
with
NPs,
photocatalysis
therapy
NIR
are
introduced
into
treatment
AD.
Meanwhile,
spatially
separate
structure
enhances
catalytic
performance
conversion
efficiency.
In
addition,
improves
permeability
blood-brain
barrier
(BBB)
overcomes
shortcomings
traditional
anti-AD
drugs.
To
further
improve
therapeutic
efficiency,
Aβ-targeted
inhibitory
peptides
were
modified
on
middle
surface
synthesize
KLVFF@Au-CeO2
(K-CAC)
nanocomposites.
We
have
verified
biocompatibility
effectiveness
at
multiple
levels
vitro
vivo,
which
profound
impact
research
clinical
transformation
nanotechnology
AD
therapy.
Proceedings of the National Academy of Sciences,
Journal Year:
2021,
Volume and Issue:
118(33)
Published: Aug. 12, 2021
Significance
The
accumulation
of
amyloid
β
(Aβ)
in
the
brain
appears
to
be
a
necessary
event
pathogenesis
Alzheimer’s
disease
(AD).
However,
processes
linked
endogenous
regulation
Aβ
production
are
still
not
completely
understood.
Here,
authors
show
that
neurons
is
tightly
regulated
by
cholesterol
synthesis
and
apoE
transport
from
astrocytes.
study
provides
molecular
context
for
understanding
why
it
correlates
with
AD.
tight
suggests
may
perform
an
important
cellular
function.
A
complete
mechanism
likely
predict
whether
selective
removal
has
potential
therapeutic
benefit.
Ageing Research Reviews,
Journal Year:
2021,
Volume and Issue:
68, P. 101343 - 101343
Published: April 16, 2021
The
absolute
reliance
of
the
mammalian
brain
on
oxygen
to
generate
ATP
renders
it
acutely
vulnerable
hypoxia,
whether
at
high
altitude
or
in
clinical
settings
anemia
pulmonary
disease.
Hypoxia
is
pivotal
pathogeneses
myriad
neurological
disorders,
including
Alzheimer's,
Parkinson's
and
other
age-related
neurodegenerative
diseases.
Conversely,
reduced
environmental
oxygen,
e.g.
sojourns
residing
altitudes,
may
impart
favorable
effects
aging
mortality.
Moreover,
controlled
hypoxia
exposure
represent
a
treatment
strategy
for
disorders.
This
review
discusses
evidence
hypoxia's
beneficial
vs.
detrimental
impacts
molecular
mechanisms
that
mediate
these
divergent
effects.
It
draws
upon
an
extensive
literature
search
hypoxia/altitude
aging,
detailed
analysis
all
identified
studies
directly
comparing
responses
young
aged
humans
rodents.
Special
attention
directed
toward
risks
benefits
elderly,
potential
therapeutic
applications
Finally,
important
questions
future
research
are
discussed.
Molecular Neurodegeneration,
Journal Year:
2020,
Volume and Issue:
15(1)
Published: Nov. 4, 2020
Abstract
Investigations
of
apolipoprotein
E
(
APOE
)
gene,
the
major
genetic
risk
modifier
for
Alzheimer’s
disease
(AD),
have
yielded
significant
insights
into
pathogenic
mechanism.
Among
three
common
coding
variants,
APOE*ε4
increases,
whereas
APOE*ε2
decreases
late-onset
AD
compared
with
APOE*ε3
.
Despite
increased
understanding
detrimental
effect
,
it
remains
unclear
how
confers
protection
against
AD.
Accumulating
evidence
suggests
that
protects
through
both
amyloid-β
(Aβ)-dependent
and
independent
mechanisms.
In
addition,
has
been
identified
as
a
longevity
suggesting
systemic
on
aging
process.
However,
is
not
entirely
benign;
carriers
exhibit
certain
cerebrovascular
diseases
neurological
disorders.
Here,
we
review
from
human
animal
studies
demonstrating
protective
propose
working
model
depicting
potential
underlying
Finally,
discuss
therapeutic
strategies
designed
to
leverage
APOE2
treat
Frontiers in Aging Neuroscience,
Journal Year:
2021,
Volume and Issue:
13
Published: June 24, 2021
While
the
central
nervous
system
compromises
2%
of
our
body
weight,
it
harbors
up
to
25%
body's
cholesterol.
Cholesterol
levels
in
brain
are
tightly
regulated
for
physiological
function,
but
mounting
evidence
indicates
that
excessive
cholesterol
accumulates
Alzheimer's
disease
(AD),
where
may
drive
AD-associated
pathological
changes.
This
seems
especially
relevant
late-onset
AD,
as
several
major
genetic
risk
factors
functionally
associated
with
metabolism.
In
this
review
we
discuss
different
systems
maintain
metabolism
healthy
brain,
and
how
dysregulation
these
processes
can
lead,
or
contribute
to,
disease.
We
will
also
AD-risk
genes
might
impact
downstream
AD
pathology.
Finally,
address
outstanding
questions
field
recent
technical
advances
CRISPR/Cas9-gene
editing
induced
pluripotent
stem
cell
(iPSC)-technology
aid
study
problems.
Journal of Clinical Medicine,
Journal Year:
2020,
Volume and Issue:
9(2), P. 495 - 495
Published: Feb. 11, 2020
The
evidence
of
a
connection
between
the
peripheral
inflammatory
processes
and
neurodegenerative
diseases
central
nervous
system
is
becoming
more
apparent.
This
review
related
literature
highlights
most
recent
clinical,
epidemiological,
in
vitro
studies
trying
to
investigate
possible
connections
periodontal
bacteria
onset
progression
Alzheimer's
disease.
was
conducted
by
searching
databases
such
as
PubMed
Scopus
using
keywords
or
combinations
Disease
AND
dementia
periodontitis
OR
periodontal.
After
eliminating
overlaps
screening
articles
not
these
issues,
we
identified
1088
records
proceeded
selection
for
an
evaluation
associative
assumptions.
hypothesis
suggested
authors
confirmed
that
bacterial
load
process
linked
disease
can
intensify
inflammation
at
level
system,
favoring
occurrence
analysis
how
directly
contribute
environment
introduction
indirect
pathogenic
proinflammatory
cytokines
locally
produced
following
colonization
defects.
