Human Molecular Genetics,
Год журнала:
2021,
Номер
30(10), С. 847 - 864
Опубликована: Фев. 16, 2021
The
purpose
of
this
study
is
to
the
neuroprotective
role
selective
serotonin
reuptake
inhibitor
(SSRI),
citalopram,
against
Alzheimer's
disease
(AD).
Multiple
SSRIs,
including
are
reported
treat
patients
with
depression,
anxiety
and
AD.
However,
their
protective
cellular
mechanisms
have
not
been
studied
completely.
In
current
study,
we
investigated
citalopram
impaired
mitochondrial
dynamics,
defective
biogenesis,
mitophagy
synaptic
dysfunction
in
immortalized
mouse
primary
hippocampal
cells
(HT22)
expressing
mutant
APP
(SWI/IND)
mutations.
Using
quantitative
RT-PCR,
immunoblotting,
biochemical
methods
transmission
electron
microscopy
methods,
assessed
full-length
APP/C-terminal
fragments
Aβ
levels
mRNA
protein
genes
mAPP-HT22
treated
citalopram.
Increased
fission
genes,
decreased
fusion
autophagy,
were
found
relative
WT-HT22
cells.
compared
revealed
reduced
increased
fusion,
genes.
Our
data
agree
levels.
Transmission
significantly
numbers
length
cells;
these
reversed
citalopram-treated
Cell
survival
rates
citalopram-untreated
mAPP-HT22.
Further,
mAPP
C-terminal
werealso
These
findings
suggest
that
reduces
toxicities
may
a
Aβ-induced
injuries
Biomedicines,
Год журнала:
2021,
Номер
9(5), С. 524 - 524
Опубликована: Май 7, 2021
Alzheimer's
disease
(AD)
is
a
neurodegenerative
associated
with
human
aging.
Ten
percent
of
individuals
over
65
years
have
AD
and
its
prevalence
continues
to
rise
increasing
age.
There
are
currently
no
effective
modifying
treatments
for
AD,
resulting
in
increasingly
large
socioeconomic
personal
costs.
Increasing
age
an
increase
low-grade
chronic
inflammation
(inflammaging)
that
may
contribute
the
process
AD.
Although
exact
mechanisms
remain
unclear,
aberrant
elevation
reactive
oxygen
nitrogen
species
(RONS)
levels
from
several
endogenous
exogenous
processes
brain
not
only
affect
cell
signaling,
but
also
trigger
cellular
senescence,
inflammation,
pyroptosis.
Moreover,
compromised
immune
privilege
allows
infiltration
peripheral
cells
infectious
agents
play
role.
Additionally,
meta-inflammation
as
well
gut
microbiota
dysbiosis
drive
neuroinflammatory
process.
Considering
inflammatory/immune
pathways
dysregulated
parallel
cognitive
dysfunction
elucidating
relationship
between
central
nervous
system
facilitate
development
safe
therapy
We
discuss
some
current
ideas
on
inflammaging
appear
summarize
details
few
immunomodulatory
strategies
being
developed
selectively
target
detrimental
aspects
neuroinflammation
without
affecting
defense
against
pathogens
tissue
damage.
Biomolecules,
Год журнала:
2022,
Номер
12(3), С. 371 - 371
Опубликована: Фев. 25, 2022
Alzheimer’s
and
Parkinson’s
diseases
are
the
two
most
common
forms
of
neurodegenerative
diseases.
The
exact
etiology
these
disorders
is
not
well
known;
however,
environmental,
molecular,
genetic
influences
play
a
major
role
in
pathogenesis
Using
disease
(AD)
as
archetype,
pathological
findings
include
aggregation
Amyloid
Beta
(Aβ)
peptides,
mitochondrial
dysfunction,
synaptic
degradation
caused
by
inflammation,
elevated
reactive
oxygen
species
(ROS),
cerebrovascular
dysregulation.
This
review
highlights
neuroinflammatory
neuroprotective
epigallocatechin-3-gallate
(EGCG):
medicinal
component
green
tea,
known
nutraceutical
that
has
shown
promise
modulating
AD
progression
due
to
its
antioxidant,
anti-inflammatory,
anti-aging
abilities.
report
also
re-examines
current
literature
provides
innovative
approaches
for
EGCG
be
used
preventive
measure
alleviate
other
disorders.
Annual Review of Biochemistry,
Год журнала:
2023,
Номер
92(1), С. 299 - 332
Опубликована: Март 31, 2023
According
to
the
endosymbiotic
theory,
most
of
DNA
original
bacterial
endosymbiont
has
been
lost
or
transferred
nucleus,
leaving
a
much
smaller
(∼16
kb
in
mammals),
circular
molecule
that
is
present-day
mitochondrial
(mtDNA).
The
ability
mtDNA
escape
mitochondria
and
integrate
into
nuclear
genome
was
discovered
budding
yeast,
along
with
genes
regulate
this
process.
Mitochondria
have
emerged
as
key
regulators
innate
immunity,
it
now
recognized
released
cytoplasm,
outside
cell,
circulation
activates
multiple
immune
signaling
pathways.
Here,
we
first
review
mechanisms
through
which
including
several
inducible
pores
defective
mitophagy
autophagy.
Next,
cover
how
different
forms
activate
specific
nucleic
acid
sensors
inflammasomes.
Finally,
discuss
intracellular
extracellular
release,
circulating
cell-free
promotes
systemic
inflammation,
are
implicated
human
diseases,
viral
infections,
senescence
aging.
