International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(16), P. 12648 - 12648
Published: Aug. 10, 2023
Long
COVID,
also
called
post-acute
sequelae
of
SARS-CoV-2,
is
characterized
by
a
multitude
lingering
symptoms,
including
impaired
cognition,
that
can
last
for
many
months.
This
symptom,
often
"brain
fog",
affects
the
life
quality
numerous
individuals,
increasing
medical
complications
as
well
healthcare
expenditures.
The
etiopathogenesis
SARS-CoV-2-induced
cognitive
deficit
unclear,
but
most
likely
cause
chronic
inflammation
maintained
viral
remnant
thriving
in
select
body
reservoirs.
These
sanctuaries
are
comprised
fused,
senescent
cells,
microglia
and
astrocytes,
pathogen
convert
into
neurotoxic
phenotypes.
Moreover,
enteric
nervous
system
contains
neurons
glia,
virus
lingers
gastrointestinal
tract
well,
accounting
intestinal
symptoms
long
COVID.
Fusogens
proteins
overcome
repulsive
forces
between
cell
membranes,
allowing
to
coalesce
with
host
cells
enter
cytoplasm.
In
intracellular
compartment,
hijacks
actin
cytoskeleton,
fusing
each
other
engendering
pathological
syncytia.
Cell-cell
fusion
enables
infect
healthy
neighboring
cells.
We
surmise
syncytia
formation
drives
impairment
facilitating
"seeding"
hyperphosphorylated
Tau,
documented
COVID-19.
our
previous
work,
we
hypothesized
SARS-CoV-2
induces
premature
endothelial
senescence,
permeability
blood-brain
barrier.
migration
microbes
and/or
their
components
circulation,
eventually
reaching
brain
where
they
may
induce
dysfunction.
For
example,
translocated
lipopolysaccharides
or
microbial
DNA
Tau
hyperphosphorylation,
memory
problems.
this
perspective
article,
examine
pathogenetic
mechanisms
potential
biomarkers
cell-free
DNA,
interleukin
22,
phosphorylated
beneficial
effect
transcutaneous
vagal
nerve
stimulation.
Antioxidants,
Journal Year:
2022,
Volume and Issue:
11(5), P. 954 - 954
Published: May 12, 2022
Understanding
the
sequelae
of
COVID-19
is
utmost
importance.
Neuroinflammation
and
disturbed
redox
homeostasis
are
suggested
as
prevailing
underlying
mechanisms
in
neurological
propagation
long-COVID.
We
aimed
to
investigate
whether
variations
antioxidant
genetic
profile
might
be
associated
with
Neurological
examination
(SOD2,
GPXs
GSTs)
determination,
well
as,
genotype
analysis
Nrf2
ACE2,
were
conducted
on
167
patients.
Polymorphisms
determined
by
appropriate
PCR
methods.
Only
polymorphisms
GSTP1AB
GSTO1
independently
long-COVID
manifestations.
Indeed,
individuals
carrying
GSTP1
Val
or
Asp
allele
exhibited
lower
odds
myalgia
development,
both
combination.
Furthermore,
combined
presence
Ile
Ala
alleles
cumulative
risk
regarding
carriers
GPX1
LeuLeu/GPX3
CC
genotype.
Moreover,
GSTM1-null/GPX1LeuLeu
more
prone
developing
"brain
fog",
while
this
probability
further
enlarged
if
A
was
also
present.
The
fact
that
certain
variants
enzymes,
combination,
affect
manifestations,
emphasizes
involvement
susceptibility
when
SARS-CoV-2
infection
initiated
host
cells,
months
after.
Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(2), P. 377 - 377
Published: Jan. 27, 2023
With
a
growing
number
of
patients
entering
the
recovery
phase
following
infection
with
SARS-CoV-2,
understanding
long-term
neurological
consequences
disease
is
important
to
their
care.
The
complications
post-acute
sequelae
SARS-CoV-2
(NC-PASC)
represent
myriad
symptoms
including
headaches,
brain
fog,
numbness/tingling,
and
other
that
many
people
report
long
after
acute
has
resolved.
Emerging
reports
are
being
published
concerning
COVID-19
its
chronic
effects,
yet
limited
knowledge
mechanisms
challenged
therapeutic
efforts.
To
address
these
issues,
we
review
broadly
literature
spanning
2020-2022
proposed
underlying
NC-PASC,
outline
associated
COVID-19,
discuss
potential
clinical
interventions.
Journal of Clinical Medicine,
Journal Year:
2023,
Volume and Issue:
12(13), P. 4253 - 4253
Published: June 25, 2023
The
role
of
mitochondria
in
post
coronavirus
disease
2019
(post-COVID-19)
complications
is
unclear,
especially
the
long-term
pulmonary
complications.
This
study
aims
to
investigate
association
between
post-COVID-19
and
mitochondrial
regulatory
proteins
context
oxidative
stress.Patients
who
had
recovered
from
COVID-19
were
enrolled.
According
evidence
persistent
interstitial
lung
lesions
on
computed
tomography
(CT),
patients
divided
into
a
group
(P(+))
control
without
(P(-)).
We
randomly
selected
80
for
investigation
(40
subjects
each
group).
Biomarkers
levels
determined
by
enzyme-linked
immunosorbent
assay
(ELISA).The
serum
concentrations
significantly
higher
P(+)
group,
including
PTEN-induced
kinase
1
(PINK1):
1.62
[1.02-2.29]
ng/mL
vs.
1.34
[0.94-1.74]
(p
=
0.046);
Dynamin-1-like
protein
(DNM1L):
1.6
[0.9-2.4]
IQR
0.9
[0.5-1.6]
0.004);
Mitofusin-2
(MFN2):
0.3
[0.2-0.5]
0.2
[0.1-0.3]
0.001).
Patients
also
chemokine
ligand
18
(PARC,
CCL18),
IL-6,
tumour
necrosis
factor-alpha
(TNF-α)
cytokines
than
P(-)
group.
concentration
interferon
alpha
(IFN-α)
was
decreased
Furthermore,
we
observed
statistically
significant
correlations
advanced
glycation
end
product
(sRAGE)
TNF-α
(Pearson's
factor
R
0.637;
p
<
0.001)
DNM1L
IFN-α
0.501;
0.002)
patients.Elevated
biomarkers
with
indicate
their
possible
pathobiology
sequelae.
Oxidative
stress
associated
immune
response
inflammation
after
COVID-19.
could
be
promising
biomarker
predicting
may
potential
target
therapeutic
intervention
Cellular and Molecular Neurobiology,
Journal Year:
2022,
Volume and Issue:
43(5), P. 1685 - 1695
Published: Sept. 14, 2022
SARS-CoV-2
pandemic
has
caused
a
collapse
of
the
world
health
systems.
Now,
vaccines
and
more
effective
therapies
have
reversed
this
crisis
but
scenario
is
further
aggravated
by
appearance
new
pathology,
occurring
as
infection
consequence:
long-COVID-19.
This
term
commonly
used
to
describe
signs
symptoms
that
continue
or
develop
after
acute
COVID-19
up
several
months.
In
review,
consequences
disease
on
mental
neurological
implications
due
long-COVID
are
described.
Furthermore,
appropriate
nutritional
approach
some
recommendations
relieve
pathology
presented.
Data
collected
indicated
in
next
future
will
affect
an
increasing
number
individuals
interdisciplinary
action
needed
counteract
it.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(16), P. 12648 - 12648
Published: Aug. 10, 2023
Long
COVID,
also
called
post-acute
sequelae
of
SARS-CoV-2,
is
characterized
by
a
multitude
lingering
symptoms,
including
impaired
cognition,
that
can
last
for
many
months.
This
symptom,
often
"brain
fog",
affects
the
life
quality
numerous
individuals,
increasing
medical
complications
as
well
healthcare
expenditures.
The
etiopathogenesis
SARS-CoV-2-induced
cognitive
deficit
unclear,
but
most
likely
cause
chronic
inflammation
maintained
viral
remnant
thriving
in
select
body
reservoirs.
These
sanctuaries
are
comprised
fused,
senescent
cells,
microglia
and
astrocytes,
pathogen
convert
into
neurotoxic
phenotypes.
Moreover,
enteric
nervous
system
contains
neurons
glia,
virus
lingers
gastrointestinal
tract
well,
accounting
intestinal
symptoms
long
COVID.
Fusogens
proteins
overcome
repulsive
forces
between
cell
membranes,
allowing
to
coalesce
with
host
cells
enter
cytoplasm.
In
intracellular
compartment,
hijacks
actin
cytoskeleton,
fusing
each
other
engendering
pathological
syncytia.
Cell-cell
fusion
enables
infect
healthy
neighboring
cells.
We
surmise
syncytia
formation
drives
impairment
facilitating
"seeding"
hyperphosphorylated
Tau,
documented
COVID-19.
our
previous
work,
we
hypothesized
SARS-CoV-2
induces
premature
endothelial
senescence,
permeability
blood-brain
barrier.
migration
microbes
and/or
their
components
circulation,
eventually
reaching
brain
where
they
may
induce
dysfunction.
For
example,
translocated
lipopolysaccharides
or
microbial
DNA
Tau
hyperphosphorylation,
memory
problems.
this
perspective
article,
examine
pathogenetic
mechanisms
potential
biomarkers
cell-free
DNA,
interleukin
22,
phosphorylated
beneficial
effect
transcutaneous
vagal
nerve
stimulation.