Understanding
the
phenomena
underlying
non-selective
susceptibility
to
ischemia
of
py-ramidal
neurons
in
CA3
area
hippocampus
is
important
from
point
view
elu-cidating
mechanisms
memory
loss
and
development
post-ischemic
dementia.
We
used
an
ischemic
model
Alzheimer's
disease
study
changes
amyloid
protein
precursor
gene
expression,
its
cleavage
enzymes
tau
af-ter
a
10-minute
brain
with
12,
18,
24-month
survival.
Quantitative
reverse
tran-scriptase
PCR
assay
showed
that
expression
all
genes
contribute
pro-duction
was
dysregulated
within
2
years
after
ischemia.
The
above
control
values
at
times
study.
α-secretase
also
exceeded
throughout
In
contrast,
β-secretase
reaching
maximum
increase
12
months
ischemia,
below
18
again
24
Presenilin
1
significantly
elevated
follow-up
period,
peak
both
occurring
This
suggests
studied
are
involved
non-amyloidogenic
processing
precursor.
Also,
observation
present
is-chemia.
Data
indicate
episode
long-term
survival
causes
damage
death
pyramidal
manner
dependent
on
modified
protein.
Thus
defining
new
mechanism
neuronal
addition
modification
is-chemia
useful
identifying
disease.
Journal of Alzheimer s Disease Reports,
Год журнала:
2024,
Номер
8(1), С. 1381 - 1393
Опубликована: Март 1, 2024
Background
In
the
sporadic
model
of
Alzheimer's
disease
(AD),
induced
by
intracerebroventricular
streptozotocin
(STZ)
administration,
cognitive
impairment
is
accompanied
specific
astrocytic
changes
in
hippocampus
prior
to
amyloid
deposition.
Objective
Hypothesizing
that
synthesis
GABA,
via
MAO-B,
contributes
ammonia
elevation,
thereby
compromising
antioxidant
defense
and
ATP
synthesis,
possibly
contributing
damage,
we
determined
hippocampal
levels
glutamine
synthetase
(GS),
monoamine
oxidase
B
(MAO-B)
other
enzymes
related
GABA
metabolism.
Methods
Immunoblotting
RT-PCR
assays
were
carried
out
samples
Wistar
rats,
at
4
16
weeks
post-STZ,
STZ-induced
AD
model,
corresponding
pre-amyloid
phases,
respectively.
Results
We
observed
a
reduction
GS
activity
increased
MAO-B
content,
both
weeks,
reinforcing
idea
astroglial
dysfunction
precedes
phase.
These
alterations
an
increase
content
ornithine
decarboxylase
1
(ODC1),
which
catalyzes
putrescine
(substrate
for
MAO-B),
gene
expression
arginine-glycine
amidinotransferase
(AGAT),
enzyme
involved
creatine,
generation
agonists.
only
seen
phase
model.
Conclusions
Our
findings
contribute
explain
greater
damage
occurs
energy
metabolism
this
stage,
addition
GABAergic
loss.
The
reinforce
importance
STZ
further
our
understanding
phases.
Journal of Alzheimer s Disease,
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 16, 2024
Changes
in
the
Alzheimer's
disease-related
apolipoprotein
genes
expression,
occurring
parallel
with
brain
ischemia-induced
neurodegeneration
hippocampal
CA3
area,
may
be
crucial
for
development
of
memory
loss
and
dementia.
Understanding
the
phenomena
underlying
non-selective
susceptibility
to
ischemia
of
py-ramidal
neurons
in
CA3
area
hippocampus
is
important
from
point
view
elu-cidating
mechanisms
memory
loss
and
development
post-ischemic
dementia.
We
used
an
ischemic
model
Alzheimer's
disease
study
changes
amyloid
protein
precursor
gene
expression,
its
cleavage
enzymes
tau
af-ter
a
10-minute
brain
with
12,
18,
24-month
survival.
Quantitative
reverse
tran-scriptase
PCR
assay
showed
that
expression
all
genes
contribute
pro-duction
was
dysregulated
within
2
years
after
ischemia.
The
above
control
values
at
times
study.
α-secretase
also
exceeded
throughout
In
contrast,
β-secretase
reaching
maximum
increase
12
months
ischemia,
below
18
again
24
Presenilin
1
significantly
elevated
follow-up
period,
peak
both
occurring
This
suggests
studied
are
involved
non-amyloidogenic
processing
precursor.
Also,
observation
present
is-chemia.
Data
indicate
episode
long-term
survival
causes
damage
death
pyramidal
manner
dependent
on
modified
protein.
Thus
defining
new
mechanism
neuronal
addition
modification
is-chemia
useful
identifying
disease.
