Ideggyógyászati Szemle,
Год журнала:
2024,
Номер
77(5-6), С. 151 - 159
Опубликована: Янв. 1, 2024
Background
–
Long
Covid
is
a
complex
condition
characterised
by
symptoms
that
persist
for
weeks
and
months
after
the
infection,
accompanied
cognitive
impairment
negatively
affects
daily
life.
Understanding
this
important
development
of
diagnostic
therapeutic
strategies.
Purpose
This
article
aims
to
provide
comprehensive
overview
impairment
in
long-COVID,
including
its
definition,
symptoms,
pathophysiology,
risk
factors,
assessment
tools,
imaging
abnormalities,
potential
biomarkers,
management
strategies,
long-term
outcomes,
future
directions
research.
Methods
The
search
methodology
used
review
aimed
include
wide
range
research
on
related
both
COVID-19
long-COVID.
Systematic
searches
PubMed
Google
Scholar
databases
were
conducted
using
mixture
MeSH
terms
keywords
‘cognition’,
‘cognitive
impairment’,
‘brain
fog’,
‘COVID-19’
‘long-COVID’.
was
restricted
studies
published
English
between
1
January
2019
11
February
2024,
which
presented
findings
neurological
manifestations
human
participants.
Results
Long-COVID
characterized
persistent
following
with
being
prominent
feature.
Symptoms
brain
fog,
difficulties
concentration,
memory
issues,
executive
function
deficits.
Pathophysiological
mechanisms
involve
viral
persistence,
immune
responses,
vascular
damage.
Risk
factors
age,
pre-existing
conditions,
disease
severity.
Cognitive
tools
such
as
Montreal
Assessment
(MoCA)
are
essential
diagnosis.
Imaging
studies,
MRI,
PET,
SPECT,
reveal
structural
functional
alterations.
Potential
biomarkers
C-reactive
protein,
interleukin-6,
neuron-specific
enolase.
Management
strategies
encompass
rehabilitation,
occupational
therapy,
medications,
lifestyle
modifications.
Discussion
poses
multifaceted
challenge,
significantly
impacts
patients’
lives.
A
multidisciplinary
approach,
rehabilitation
medication
when
appropriate,
effective
management.
Future
should
focus
validating
understanding
outcomes.
Conclusion
global
health
concern,
distressing
symptom.
While
pharmacological
interventions
have
potential,
they
require
careful
consideration.
Continued
crucial
improving
treatment
Frontiers in Neurology,
Год журнала:
2023,
Номер
14
Опубликована: Июль 31, 2023
COVID-19,
caused
by
the
SARS-CoV-2
virus,
is
a
respiratory
infectious
disease.
While
most
patients
recover
after
treatment,
there
growing
evidence
that
COVID-19
may
result
in
cognitive
impairment.
Recent
studies
reveal
some
individuals
experience
deficits,
such
as
diminished
memory
and
attention,
well
sleep
disturbances,
suggesting
could
have
long-term
effects
on
function.
Research
indicates
contribute
to
decline
damaging
crucial
brain
regions,
including
hippocampus
anterior
cingulate
cortex.
Additionally,
identified
active
neuroinflammation,
mitochondrial
dysfunction,
microglial
activation
patients,
implying
these
factors
be
potential
mechanisms
leading
Given
findings,
possibility
of
impairment
following
treatment
warrants
careful
consideration.
Large-scale
follow-up
are
needed
investigate
impact
function
offer
support
clinical
rehabilitation
practices.
In-depth
neuropathological
biological
can
elucidate
precise
provide
theoretical
basis
for
prevention,
intervention
research.
Considering
risks
reinfection,
it
imperative
integrate
basic
research
data
optimize
preservation
patients'
quality
life.
This
integration
will
also
valuable
insights
responding
similar
public
health
events
future.
perspective
article
synthesizes
discussing
outlining
future
directions.
Frontiers in Psychiatry,
Год журнала:
2023,
Номер
14
Опубликована: Июнь 21, 2023
People
who
have
been
infected
by
COVID-19
showing
persistent
symptoms
after
4
weeks
from
recovery
are
thought
to
suffer
Long-COVID
syndrome
(LC).
There
is
uncertainty
on
the
clinical
manifestations
of
LC.
We
undertook
a
systematic
review
summarize
available
evidence
about
main
psychiatric
LC.PubMed
(Medline),
Scopus,
CINHAL,
PsycINFO,
and
EMBASE
were
searched
until
May
2022.
Studies
reporting
estimation
emerging
and/or
diagnoses
among
adult
people
with
LC
included.
Pooled
prevalence
for
each
condition
was
calculated
in
absence
control
groups
compare
with.Thirty-three
reports
included
final
selection,
corresponding
282,711
participants
After
infection
recovery,
reported
following
symptoms:
depression,
anxiety,
post-traumatic
(PTS),
cognitive
sleeping
disturbances
(i.e.,
insomnia
or
hypersomnia).
The
most
common
manifestation
resulted
be
sleep
disturbances,
followed
PTS,
impairment
attention
memory
deficits).
However,
some
estimates
affected
important
outlier
effect
played
one
study.
If
study
weight
not
considered,
anxiety.LC
may
non-specific
manifestations.
More
research
needed
better
define
differentiate
it
other
post-infectious
post-hospitalization
syndromes.PROSPERO
(CRD42022299408).
The Neuroscientist,
Год журнала:
2023,
Номер
30(4), С. 421 - 439
Опубликована: Сен. 11, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2),
the
causative
agent
of
disease
2019
(COVID-19),
could
affect
brain
structure
and
function.
SARS-CoV-2
can
enter
through
different
routes,
including
olfactory,
trigeminal,
vagus
nerves,
blood
immunocytes.
may
also
from
peripheral
a
disrupted
blood-brain
barrier
(BBB).
The
neurovascular
unit
in
brain,
composed
neurons,
astrocytes,
endothelial
cells,
pericytes,
protects
parenchyma
by
regulating
entry
substances
blood.
astrocytes
highly
express
angiotensin
converting
enzyme
(ACE2),
indicating
that
BBB
be
disturbed
lead
to
derangements
tight
junction
adherens
proteins.
This
leads
increased
permeability,
leakage
components,
movement
immune
cells
into
parenchyma.
cross
microvascular
an
ACE2
receptor–associated
pathway.
exact
mechanism
dysregulation
COVID-19/neuro-COVID
is
not
clearly
known,
nor
development
long
COVID.
Various
biomarkers
indicate
severity
neurologic
complications
COVID-19
help
objectively
diagnose
those
developing
review
highlights
importance
disruption,
as
well
some
potentially
useful
COVID-19,
COVID/neuro-COVID.
The Journal of Immunology,
Год журнала:
2024,
Номер
212(4), С. 505 - 512
Опубликована: Фев. 5, 2024
As
COVID-19
continues,
an
increasing
number
of
patients
develop
long
COVID
symptoms
varying
in
severity
that
last
for
weeks,
months,
or
longer.
Symptoms
commonly
include
lingering
loss
smell
and
taste,
hearing
loss,
extreme
fatigue,
"brain
fog."
Still,
persistent
cardiovascular
respiratory
problems,
muscle
weakness,
neurologic
issues
have
also
been
documented.
A
major
problem
is
the
lack
clear
guidelines
diagnosing
COVID.
Although
some
studies
suggest
due
to
prolonged
inflammation
after
SARS-CoV-2
infection,
underlying
mechanisms
remain
unclear.
The
broad
range
COVID-19's
bodily
effects
responses
initial
viral
infection
are
poorly
understood.
This
workshop
brought
together
multidisciplinary
experts
showcase
discuss
latest
research
on
chronic
might
be
associated
with
sequelae
following
infection.
Phytotherapy Research,
Год журнала:
2024,
Номер
38(3), С. 1589 - 1609
Опубликована: Янв. 29, 2024
Abstract
The
severe
acute
respiratory
syndrome
coronavirus
2
(SARS‐CoV‐2)
causes
COVID‐19
disease.
Through
its
viral
spike
(S)
protein,
the
virus
enters
and
infects
epithelial
cells
by
utilizing
angiotensin‐converting
enzyme
as
a
host
cell's
receptor
protein.
pandemic
had
profound
impact
on
global
public
health
economies.
Although
various
effective
vaccinations
medications
are
now
available
to
prevent
treat
COVID‐19,
natural
compounds
derived
from
medicinal
plants,
particularly
flavonoids,
demonstrated
therapeutic
potential
Flavonoids
exhibit
dual
antiviral
mechanisms:
direct
interference
with
invasion
inhibition
of
replication.
Specifically,
they
target
key
molecules,
proteases,
involved
in
infection.
These
showcase
significant
immunomodulatory
anti‐inflammatory
properties,
effectively
inhibiting
inflammatory
cytokines.
Additionally,
emerging
evidence
supports
flavonoids
mitigate
progression
individuals
obesity
positively
influencing
lipid
metabolism.
This
review
aims
elucidate
molecular
structure
SARS‐CoV‐2
underlying
mechanism
action
virus.
study
evaluates
anti‐SARS‐CoV‐2
properties
exhibited
flavonoid
compounds,
specific
interest
their
mechanisms
action,
applications
for
prevention
treatment
COVID‐19.
Nevertheless,
portion
existing
knowledge
is
based
theoretical
frameworks
findings
vitro
investigations.
Further
research
required
better
assess
effectiveness
combating
SARS‐CoV‐2,
particular
emphasis
vivo
clinical
Journal of Personalized Medicine,
Год журнала:
2024,
Номер
14(2), С. 170 - 170
Опубликована: Янв. 31, 2024
Postural
orthostatic
tachycardia
syndrome
(POTS)
is
a
common
accompaniment
of
variety
chronic,
inflammatory
diseases,
including
long
COVID,
as
are
small,
insoluble,
'fibrinaloid'
microclots.
We
here
develop
the
argument,
with
accompanying
evidence,
that
fibrinaloid
microclots,
through
their
ability
to
block
flow
blood
microcapillaries
and
thus
cause
tissue
hypoxia,
not
simply
correlated
but
in
fact,
by
preceding
it,
may
be
chief
intermediary
POTS,
which
body's
exaggerated
'physiological'
response
hypoxia.
Similar
reasoning
accounts
for
symptoms
bundled
under
term
'fatigue'.
Amyloids
known
membrane
disruptors,
when
targets
nerve
membranes,
this
can
explain
neurotoxicity
hence
autonomic
nervous
system
dysfunction
contributes
POTS.
Taken
together
view,
we
indicate
microclots
serve
link
POTS
fatigue
COVID
manner
at
once
both
mechanistic
explanatory.
This
has
clear
implications
treatment
such
diseases.
Biology,
Год журнала:
2023,
Номер
12(8), С. 1106 - 1106
Опубликована: Авг. 9, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
is
a
single-stranded
RNA
virus
and
member
of
the
corona
family,
primarily
affecting
upper
system
lungs.
Like
many
other
viruses,
SARS-CoV-2
can
spread
to
organ
systems.
Apart
from
causing
diarrhea,
another
very
common
but
debilitating
complication
caused
by
neurological
symptoms
cognitive
difficulties,
which
occur
in
up
two
thirds
hospitalized
COVID-19
patients
range
shortness
concentration
overall
declined
speed
executive
or
memory
function
impairment.
Neuro-cognitive
dysfunction
“brain
fog”
are
frequently
present
cases,
last
several
months
after
infection,
leading
disruption
daily
life.
Cumulative
evidence
suggests
that
affects
vasculature
extra-pulmonary
systems
directly
indirectly,
impairment
endothelial
even
multi-organ
damage.
The
post
long-lasting
neurocognitive
impairments
have
not
been
studied
fully
their
underlying
mechanism
remains
elusive.
In
this
review,
we
summarize
current
understanding
effects
on
vascular
how
leads
patients.
Annals of Allergy Asthma & Immunology,
Год журнала:
2023,
Номер
132(4), С. 440 - 454
Опубликована: Ноя. 10, 2023
Mast
cells
(MC)
are
ubiquitous
in
the
body,
and
they
critical
for
not
only
allergic
diseases
but
also
immunity
inflammation,
including
having
potential
involvement
pathophysiology
of
dysautonomias
neuroinflammatory
disorders.
MC
located
perivascularly
close
to
nerve
endings
sites
such
as
carotid
bodies,
heart,
hypothalamus,
pineal
gland,
adrenal
gland
that
would
allow
them
regulate
be
affected
by
autonomic
nervous
system
(ANS).
stimulated
allergens
many
other
triggers
some
from
ANS
can
affect
release
neurosensitizing,
proinflammatory,
vasoactive
mediators.
Hence,
may
able
homeostatic
functions
seem
dysfunctional
conditions,
postural
orthostatic
tachycardia
syndrome,
autism
spectrum
disorder,
myalgic
encephalomyelitis/chronic
fatigue
Long-COVID
syndrome.
The
evidence
indicates
there
is
a
possible
association
between
these
conditions
associated
with
activation.
There
no
effective
treatment
any
form
than
minimizing
symptoms.
Given
ways
could
activated
numerous
mediators
released,
it
important
develop
inhibit
stimulation
ANS-relevant
Frontiers in Cellular Neuroscience,
Год журнала:
2024,
Номер
18
Опубликована: Окт. 25, 2024
Neurovascular
unit
(NVU)
inflammation
via
activation
of
glial
cells
and
neuronal
damage
plays
a
critical
role
in
neurodegenerative
diseases.
Though
the
exact
mechanism
disease
pathogenesis
is
not
understood,
certain
biomarkers
provide
valuable
insight
into
pathogenesis,
severity,
progression
therapeutic
efficacy.
These
markers
can
be
used
to
assess
pathophysiological
status
brain
including
neurons,
astrocytes,
microglia,
oligodendrocytes,
specialized
microvascular
endothelial
cells,
pericytes,
NVU,
blood-brain
barrier
(BBB)
disruption.
Damage
or
derangements
tight
junction
(TJ),
adherens
(AdJ),
gap
(GJ)
components
BBB
lead
increased
permeability
neuroinflammation
various
disorders
disorders.
Thus,
neuroinflammatory
evaluated
blood,
cerebrospinal
fluid
(CSF),
tissues
determine
neurological
progression,
responsiveness.
Chronic
common
age-related
Alzheimer's
(AD),
Parkinson's
(PD),
dementia.
Neurotrauma/traumatic
injury
(TBI)
also
leads
acute
chronic
responses.
The
expression
some
may
altered
many
years
even
decades
before
onset
In
this
review,
we
discuss
neuroinflammation,
neurodegeneration
associated
with
disorders,
especially
those
neurovascular
pathologies.
CSF,
tissues.
Neurofilament
light
(NfL),
ubiquitin
C-terminal
hydrolase-L1
(UCHL1),
fibrillary
acidic
protein
(GFAP),
Ionized
calcium-binding
adaptor
molecule
1
(Iba-1),
transmembrane
119
(TMEM119),
aquaporin,
endothelin-1,
platelet-derived
growth
factor
receptor
beta
(PDGFRβ)
are
important
markers.
Recent
BBB-on-a-chip
modeling
offers
promising
potential
for
providing
an
in-depth
understanding
neurotherapeutics.
Integration
these
clinical
practice
could
potentially
enhance
early
diagnosis,
monitor
improve
outcomes.