Hypertension,
Journal Year:
2024,
Volume and Issue:
81(5), P. 991 - 1007
Published: March 1, 2024
Elevated
blood
pressure
is
a
well-established
risk
factor
for
age-related
cognitive
decline.
Long
linked
to
impairment
on
vascular
bases,
increasing
evidence
suggests
potential
association
of
hypertension
with
the
neurodegenerative
pathology
underlying
Alzheimer
disease.
Hypertension
well
known
disrupt
structural
and
functional
integrity
cerebral
vasculature.
However,
mechanisms
by
which
these
alterations
lead
brain
damage,
enhance
pathology,
promote
remain
be
established.
Furthermore,
critical
questions
concerning
whether
lowering
antihypertensive
medications
prevents
have
not
been
answered.
Recent
developments
in
neurovascular
biology,
imaging,
epidemiology,
as
new
clinical
trials,
provided
insights
into
issues.
In
particular,
basic
findings
link
between
dysfunction
pathobiology
neurodegeneration
shed
light
overlap
pathology.
this
review,
we
will
examine
progress
made
relationship
and,
after
evaluation
evidence,
attempt
identify
remaining
knowledge
gaps
future
research
directions
that
may
advance
our
understanding
one
leading
health
challenges
time.
Theranostics,
Journal Year:
2023,
Volume and Issue:
13(10), P. 3434 - 3450
Published: Jan. 1, 2023
Background:
Alzheimer's
disease
(AD),
one
of
the
most
common
forms
dementia,
is
a
widely
studied
neurodegenerative
characterized
by
Aβ
accumulation
and
tau
hyperphosphorylation.
Currently,
there
no
effective
cure
available
for
AD.The
astrocyte
AQP4
polarized
distribution-mediated
glymphatic
system
essential
abnormal
clearance
potential
therapeutic
target
AD.However,
role
exercise
on
distribution
association
between
phenotype
polarization
are
poorly
understood.Methods:
Using
streptozotocin
(STZ)-induced
sporadic
AD
rat
model,
we
investigated
effects
high-intensity
interval
training
pathologies.The
Branes
maze
task
was
conducted
to
measure
spatial
learning
memory.Immunofluorescence
staining
NeuN
with
TUNEL,
Fluoro-Jade
C,
relative
neuronal
damage
markers
applied
apoptosis,
neurodegeneration,
damage.Sholl
analysis
carried
out
analyze
morphology
microglia.Line-scan
analysis,
3D
rendering,
orthogonal
view
were
colocalization.Western
blot
enzyme-linked
immunosorbent
assay
(ELISA)
examine
Aβ,
respectively.An
APP/PS1
transgenic
mice
model
used
confirm
key
findings.Results:
High-intensity
(HIIT)
alleviates
cognitive
dysfunction
in
STZ-induced
AD-like
models
provides
neuroprotection
against
damage,
loss.Additionally,
HIIT
improved
drainage
from
cortex
hippocampus
via
kidney.Further
mechanistic
studies
support
that
beneficial
might
be
due,
part,
glial
cells
neurotoxic
towards
neuroprotective
phenotype.Furthermore,
an
intriguing
finding
our
study
strongly
correlated
phenotype.We
found
A2
exhibited
more
evident
than
A1
phenotype.
Conclusion:Our
findings
indicate
ameliorates
disease-like
pathology
regulating
phenotype-associated
polarization.These
changes
promote
p-tau
brain
tissue
through
kidney.
Annals of Neurology,
Journal Year:
2023,
Volume and Issue:
94(3), P. 442 - 456
Published: May 27, 2023
Glymphatic
function
has
not
yet
been
explored
in
behavioral
variant
frontotemporal
dementia
(bvFTD).
The
spatial
correlation
between
regional
glymphatic
and
bvFTD
remains
unknown.
Alzheimer s & Dementia,
Journal Year:
2024,
Volume and Issue:
20(5), P. 3251 - 3269
Published: March 19, 2024
Abstract
INTRODUCTION
Although
glymphatic
function
is
involved
in
Alzheimer's
disease
(AD),
its
potential
for
predicting
the
pathological
and
clinical
progression
of
AD
sequential
association
with
core
biomarkers
poorly
understood.
METHODS
Whole‐brain
activity
was
measured
by
diffusion
tensor
image
analysis
along
perivascular
space
(DTI‐ALPS)
participants
dementia
(
n
=
47),
mild
cognitive
impairment
(MCI;
137),
normal
controls
235)
from
Disease
Neuroimaging
Initiative.
RESULTS
ALPS
index
significantly
lower
than
MCI
or
controls.
Lower
associated
faster
changes
amyloid
positron
emission
tomography
(PET)
burden
signature
region
interest
volume,
higher
risk
amyloid‐positive
transition
progression,
rates
amyloid‐
neurodegeneration‐related
decline.
Furthermore,
associations
decline
were
fully
mediated
PET
brain
atrophy.
DISCUSSION
Glymphatic
failure
may
precede
pathology,
predicts
deposition,
neurodegeneration,
AD.
Highlights
The
(ALPS)
reduced
patients
(AD)
dementia,
prodromal
AD,
preclinical
predicted
accelerated
beta
(Aβ)
Aβ‐positive
transition.
decrease
occurs
before
cerebrospinal
fluid
Aβ42
reaches
positive
threshold.
atrophy,
Aβ
atrophy
link
Hypertension,
Journal Year:
2024,
Volume and Issue:
81(5), P. 991 - 1007
Published: March 1, 2024
Elevated
blood
pressure
is
a
well-established
risk
factor
for
age-related
cognitive
decline.
Long
linked
to
impairment
on
vascular
bases,
increasing
evidence
suggests
potential
association
of
hypertension
with
the
neurodegenerative
pathology
underlying
Alzheimer
disease.
Hypertension
well
known
disrupt
structural
and
functional
integrity
cerebral
vasculature.
However,
mechanisms
by
which
these
alterations
lead
brain
damage,
enhance
pathology,
promote
remain
be
established.
Furthermore,
critical
questions
concerning
whether
lowering
antihypertensive
medications
prevents
have
not
been
answered.
Recent
developments
in
neurovascular
biology,
imaging,
epidemiology,
as
new
clinical
trials,
provided
insights
into
issues.
In
particular,
basic
findings
link
between
dysfunction
pathobiology
neurodegeneration
shed
light
overlap
pathology.
this
review,
we
will
examine
progress
made
relationship
and,
after
evaluation
evidence,
attempt
identify
remaining
knowledge
gaps
future
research
directions
that
may
advance
our
understanding
one
leading
health
challenges
time.
