International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(17), P. 9400 - 9400
Published: Aug. 29, 2024
In
patients
with
Alzheimer’s
disease
(AD)
and
in
animal
models,
the
increased
accumulation
of
amyloid
β
(Aβ)
retinal
blood
vessels
strongly
correlates
brain
deposits
cognitive
decline.
The
Aβ
may
result
from
impaired
transcytosis
a
dysfunctional
ocular
glymphatic
system
AD.
High-dose
fish
oil
(FO)
supplementation
has
been
shown
to
significantly
change
expression
major
facilitator
superfamily
domain-containing
protein
2a
(Mfsd2a),
key
regulator
transcytosis,
Aquaporin
4
(Aqp4),
an
essential
component
retinas
WT
mice.
We
examined
Mfsd2a
Aqp4
4-month-old
5xFAD
female
mice
supplemented
high-dose
FO
for
three
weeks.
There
was
significant
increase
compared
control
Additionally,
observed
retinas,
indicative
system,
decreased.
Simultaneously,
reduced
following
supplementation.
These
findings
suggest
that
could
serve
as
adjunct
developing
new
treatments
aimed
at
improving
regulation
or
function
AD
retina.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 29, 2024
Abstract
Background
Accumulation
of
β-amyloid
(Aβ)
in
the
brain
is
a
hallmark
Alzheimer’s
Disease
(AD).
Cerebral
deposition
Aβ
initiates
deteriorating
pathways
which
eventually
can
lead
to
AD.
However,
exact
mechanisms
are
not
known.
A
possible
pathway
could
be
that
affects
cerebral
vessels,
causing
inadequate
cerebrovascular
function.
In
present
study,
we
examined
if
accumulation
associated
with
reduced
blood
flow
response
(CBF)
neuronal
activation
by
visual
stimulation
(DCBFVis.Act)
cognitively
normal
subjects
from
Metropolit
Danish
Male
Birth
Cohort.
Methods
64
participated
study.
DCBFVis.Act
was
measured
using
arterial
spin
labelling
(ASL)
combined
blood-oxygen-level-dependent
(BOLD)
MRI.
Neuronal
obtained
flickering
checkerboard
presented
on
screen
MRI-scanner.
Brain
and
glucose
metabolism
were
assessed
PET
imaging
radiotracers
[11C]Pittsburgh
Compound-B
(PiB)
[18F]Fluorodeoxyglucose
(FDG),
respectively.
Cortical
thickness
structural
Results
correlated
negatively
(\(\beta\)
=
-32.1
[95%
confidence
interval
(CI):
-60.2
;
-4.1],
r
-0.30,
p
0.025)
PiB
standardized
uptake
value
ratio
(SUVr)
regions
activated
stimulation.
did
correlate
FDG
SUVr
1.9
[CI:
-23.8
27.6],
0.02,
0.88)
or
cortical
10.3
-8.4
29.0],
0.15,
0.27)
regions.
Resting
CBF
neither
-17.8
[CI:-71.9
36.2],
0.09,
0.51)
nor
remaining
cortex
5.2
[CI:-3.9
14.2],
0.26).
Conclusion
We
found
correlation
between
high
activation,
indicating
link
impaired
The
impairment
thinning
hypometabolism,
suggesting
affecting
vessel
function
very
early
pathology
leading
neurodegenerative
disease.