medRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2023,
Номер
unknown
Опубликована: Июль 23, 2023
Abstract
As
the
heterogeneity
of
symptoms
is
increasingly
recognized
among
long-COVID
patients,
it
appears
highly
relevant
to
study
potential
pathophysiological
differences
along
different
subtypes.
Preliminary
evidence
suggests
distinct
alterations
in
brain
structure
and
systemic
inflammatory
patterns
specific
groups
patients.
To
this
end,
we
analyzed
cortical
thickness
peripheral
immune
signature
between
clinical
subgroups
based
on
3T-MRI
scans
markers
n=120
participants
comprising
healthy
never-infected
controls,
COVID-19
survivors,
patients
with
without
cognitive
impairment
according
screening
Montreal
Cognitive
Assessment.
Whole-brain
comparison
4
was
conducted
by
surface-based
morphometry.
We
identified
areas
showing
a
progressive
increase
across
groups,
starting
from
individuals
who
had
never
been
infected
COVID-19,
followed
deficits
(MoCA
≥
26),
finally,
exhibiting
significant
<
26).
These
findings
highlight
continuum
associated
more
pronounced
changes
observed
experiencing
(p<0.05,
FWE-corrected).
Affected
regions
covered
prefrontal
temporal
gyri,
insula,
posterior
cingulate,
parahippocampal
gyrus,
parietal
areas.
Additionally,
discovered
immunophenotype,
elevated
levels
IL-10,
IFNγ,
sTREM2
especially
group
suffering
impairment.
demonstrate
lingering
immunological
impaired
survivors.
This
implies
complex
underlying
pathomechanism
emphasizes
necessity
investigate
whole
spectrum
post-COVID
biology
determine
targeted
treatment
strategies
targeting
sub-groups.
New England Journal of Medicine,
Год журнала:
2024,
Номер
390(9), С. 806 - 818
Опубликована: Фев. 28, 2024
BackgroundCognitive
symptoms
after
coronavirus
disease
2019
(Covid-19),
the
caused
by
severe
acute
respiratory
syndrome
2
(SARS-CoV-2),
are
well-recognized.
Whether
objectively
measurable
cognitive
deficits
exist
and
how
long
they
persist
unclear.MethodsWe
invited
800,000
adults
in
a
study
England
to
complete
an
online
assessment
of
function.
We
estimated
global
score
across
eight
tasks.
hypothesized
that
participants
with
persistent
(lasting
≥12
weeks)
infection
onset
would
have
impairments
executive
functioning
memory
be
observed
such
participants,
especially
those
who
reported
recent
poor
or
difficulty
thinking
concentrating
("brain
fog").ResultsOf
141,583
started
assessment,
112,964
completed
it.
In
multiple
regression
analysis,
had
recovered
from
Covid-19
whom
resolved
less
than
4
weeks
at
least
12
similar
small
cognition
as
compared
no–Covid-19
group,
not
been
infected
SARS-CoV-2
unconfirmed
(−0.23
SD
[95%
confidence
interval
{CI},
−0.33
−0.13]
−0.24
CI,
−0.36
−0.12],
respectively);
larger
group
were
seen
unresolved
(−0.42
SD;
95%
−0.53
−0.31).
Larger
during
periods
which
original
virus
B.1.1.7
variant
was
predominant
later
variants
(e.g.,
−0.17
for
vs.
B.1.1.529
variant;
−0.20
−0.13)
hospitalized
intensive
care
unit
admission,
−0.35
−0.49
−0.20).
Results
analyses
propensity-score–matching
analyses.
comparison
memory,
reasoning,
function
tasks
associated
largest
(−0.33
SD);
these
correlated
weakly
symptoms,
including
brain
fog.
No
adverse
events
reported.ConclusionsParticipants
measured
shorter-duration
although
short-duration
still
recovery.
Longer-term
persistence
any
clinical
implications
remain
uncertain.
(Funded
National
Institute
Health
Care
Research
others.)
COVID-19
(SARS-CoV-2)
has
been
associated
with
neurological
sequelae
even
in
those
patients
mild
respiratory
symptoms.
Patients
experiencing
cognitive
symptoms
such
as
"brain
fog"
and
other
neurologic
for
8
or
more
weeks
define
"long
haulers".
There
is
limited
information
regarding
damage
to
grey
matter
(GM)
structures
occurring
Advanced
imaging
techniques
can
quantify
brain
volume
depletions
related
infection
which
important
conventional
Brain
MRI
often
fails
identify
disease
correlates.
3-dimensional
voxel-based
morphometry
(3D
VBM)
analyzes,
segments
quantifies
key
volumes
allowing
comparisons
between
haulers"
normative
data
drawn
from
healthy
controls,
values
based
on
percentages
of
intracranial
volume.This
a
retrospective
single
center
study
analyzed
24
consecutive
infected
long
term
Each
patient
underwent
3D
VBM
at
median
time
85
days
following
laboratory
confirmation.
All
had
relatively
not
requiring
oxygen
supplementation,
hospitalization,
assisted
ventilation.
was
obtained
whole
forebrain
parenchyma,
cortical
(CGM),
hippocampus,
thalamus.The
results
demonstrate
statistically
significant
depletion
CGM
patients.
Reduced
likely
influences
their
may
impair
post
patient's
quality
life
productivity.This
contributes
understanding
effects
neurocognitive
function,
potential
producing
serious
personal
economic
consequences,
ongoing
challenges
public
health
systems.
Frontiers in Microbiology,
Год журнала:
2023,
Номер
14
Опубликована: Ноя. 23, 2023
The
reduced
pathogenicity
of
the
omicron
BA.1
sub-lineage
compared
to
earlier
variants
is
well
described,
although
whether
such
attenuation
retained
for
later
like
BA.5
and
XBB
remains
controversial.
We
show
that
isolates
were
significantly
more
pathogenic
in
K18-hACE2
mice
than
a
isolate,
showing
increased
neurotropic
potential,
resulting
fulminant
brain
infection
mortality,
similar
seen
original
ancestral
isolates.
also
infected
human
cortical
organoids
greater
extent
In
brains
mice,
neurons
main
target
infection,
neuronal
progenitor
cells
immature
infected.
results
herein
suggest
evolving
may
have
increasing
potential.
Scientific Reports,
Год журнала:
2024,
Номер
14(1)
Опубликована: Фев. 29, 2024
Abstract
Post-COVID-19
syndrome
is
a
serious
complication
following
SARS-CoV-2
infection,
characterized
primarily
by
fatigue
and
cognitive
complaints.
Although
first
metabolic
structural
imaging
alterations
in
have
been
identified,
their
functional
consequences
remain
unknown.
Thus,
we
explored
the
impact
of
on
connectome
brain
providing
deeper
understanding
pathophysiological
mechanisms.
In
cross-sectional
observational
study,
resting-state
magnetic
resonance
data
66
patients
with
after
mild
infection
(mean
age
42.3
years,
57
female)
healthy
controls
42.1
38
mean
time
seven
months
acute
COVID-19
were
analysed
using
graph
theoretical
approach.
Network
features
quantified
measures
including
distance,
nodal
degree,
betweenness
Katz
centrality,
compared
between
both
groups.
Graph
correlated
clinical
quantifying
fatigue,
function,
affective
symptoms
sleep
disturbances.
Alterations
mainly
found
brainstem,
olfactory
cortex,
cingulate
thalamus
cerebellum
average
infection.
Additionally,
strong
correlations
severity,
functioning
daytime
sleepiness
from
scales
observed.
Our
study
confirms
relevance
changes
as
mediating
factors
for
persistent
improves
our
understanding.
Brain Behavior and Immunity,
Год журнала:
2023,
Номер
116, С. 175 - 184
Опубликована: Ноя. 28, 2023
As
the
heterogeneity
of
symptoms
is
increasingly
recognized
among
long-COVID
patients,
it
appears
highly
relevant
to
study
potential
pathophysiological
differences
along
different
subtypes.
Preliminary
evidence
suggests
distinct
alterations
in
brain
structure
and
systemic
inflammatory
patterns
specific
groups
patients.
To
this
end,
we
analyzed
cortical
thickness
peripheral
immune
signature
between
clinical
subgroups
based
on
3
T-MRI
scans
markers
n
=
120
participants
comprising
healthy
never-infected
controls
(n
30),
COVID-19
survivors
29),
patients
with
26)
without
35)
cognitive
impairment
according
screening
Montreal
Cognitive
Assessment.
Whole-brain
comparison
4
was
conducted
by
surface-based
morphometry.
We
identified
areas
showing
a
progressive
increase
across
groups,
starting
from
individuals
who
had
never
been
infected
COVID-19,
followed
survivors,
deficits
(MoCA
≥
26),
finally,
exhibiting
significant
<
26).
These
findings
highlight
continuum
associated
more
pronounced
changes
observed
experiencing
(p
0.05,
FWE-corrected).
Affected
regions
covered
prefrontal
temporal
gyri,
insula,
posterior
cingulate,
parahippocampal
gyrus,
parietal
areas.
Additionally,
discovered
immunophenotype,
elevated
levels
IL-10,
IFNγ,
sTREM2
especially
group
suffering
impairment.
demonstrate
lingering
immunological
impaired
survivors.
This
implies
complex
underlying
pathomechanism
emphasizes
necessity
investigate
whole
spectrum
post-COVID
biology
determine
targeted
treatment
strategies
targeting
sub-groups.
NeuroImage Clinical,
Год журнала:
2024,
Номер
43, С. 103631 - 103631
Опубликована: Янв. 1, 2024
The
COVID-19
pandemic
has
affected
millions
worldwide,
causing
mortality
and
multi-organ
morbidity.
Neurological
complications
have
been
recognized.
This
study
aimed
to
assess
brain
structural,
microstructural,
connectivity
alterations
in
patients
with
COVID-19-related
olfactory
or
cognitive
impairment
using
post-acute
(time
from
onset:
264[208-313]
days)
multi-directional
diffusion-weighted
MRI
(DW-MRI).
Diagnostics,
Год журнала:
2023,
Номер
13(10), С. 1716 - 1716
Опубликована: Май 12, 2023
Cohort
studies
that
quantify
volumetric
brain
data
among
individuals
with
different
levels
of
COVID-19
severity
are
presently
limited.
It
is
still
uncertain
whether
there
exists
a
potential
correlation
between
disease
and
the
effects
on
integrity.
Our
objective
was
to
assess
impact
measured
volume
in
patients
asymptomatic/mild
severe
after
recovery
from
infection,
compared
healthy
controls,
using
artificial
intelligence
(AI)-based
MRI
volumetry.
A
total
155
participants
were
prospectively
enrolled
this
IRB-approved
analysis
three
cohorts
mild
course
(n
=
51,
MILD),
hospitalised
48,
SEV),
controls
56,
CTL)
all
undergoing
standardised
protocol
brain.
Automated
AI-based
determination
various
volumes
mL
calculation
normalised
percentiles
performed
mdbrain
software,
3D
T1-weighted
magnetisation-prepared
rapid
gradient
echo
(MPRAGE)
sequence.
The
automatically
analysed
for
differences
groups.
estimated
influence
demographic/clinical
variables
determined
multivariate
analysis.
There
statistically
significant
regions
groups,
even
exclusion
intensive
care,
reductions
patients,
which
increased
(SEV
>
MILD
mainly
affected
supratentorial
grey
matter,
frontal
parietal
lobes,
right
thalamus.
Severe
addition
established
demographic
parameters
such
as
age
sex,
predictor
loss
upon
In
conclusion,
neocortical
degeneration
detected
who
had
recovered
SARS-CoV-2
infection
worsening
greater
initial
affecting
fronto-parietal
thalamus,
regardless
ICU
treatment.
This
suggests
direct
link
subsequent
atrophy,
may
have
major
implications
clinical
management
future
cognitive
rehabilitation
strategies.
American Journal of Neuroradiology,
Год журнала:
2024,
Номер
45(5), С. 647 - 654
Опубликована: Апрель 4, 2024
BACKGROUND
AND
PURPOSE:
There
is
a
paucity
of
data
on
long-term
neuroimaging
findings
from
individuals
who
have
developed
the
post-coronavirus
2019
(COVID-19)
condition.
Only
2
studies
investigated
correlations
between
cognitive
assessment
results
and
structural
MR
imaging
in
this
population.
This
study
aimed
to
elucidate
outcomes
participants
with
post-COVID-19
condition
correlate
these
MATERIALS
METHODS:
A
cohort
53
underwent
3T
brain
T1
FLAIR
sequences
obtained
median
1.8
years
after
Severe
Acute
Respiratory
Syndrome
coronavirus
(SARS-CoV-2)
infection.
comprehensive
neuropsychological
battery
was
used
assess
several
domains
same
individuals.
Correlations
whole-brain
voxel-based
morphometry
were
performed.
Different
ROIs
FreeSurfer
perform
other
features.
RESULTS:
According
Frascati
criteria,
more
than
one-half
had
deficits
attentional
(55%,
n
=
29)
executive
(59%,
31)
domains,
while
40%
(n
21)
impairment
memory
domain.
1
participant
(1.89%)
showed
problems
visuospatial
visuoconstructive
domains.
We
observed
that
reduced
cortical
thickness
left
parahippocampal
region
(t(48)
2.28,
P
=
.03)
right
caudal-middle-frontal
2.20,
positively
correlated
CONCLUSIONS:
Our
suggest
associated
alterations
structure
brain.
These
macrostructural
changes
may
provide
insight
into
nature
symptoms.
Reviews in Medical Virology,
Год журнала:
2024,
Номер
34(6)
Опубликована: Ноя. 1, 2024
Abstract
The
emergence
of
severe
acute
respiratory
syndrome
coronavirus
2
(SARS‐CoV‐2)
in
December
2019
triggered
a
swift
global
spread,
leading
to
devastating
pandemic.
Alarmingly,
approximately
one
four
individuals
diagnosed
with
disease
(COVID‐19)
experience
varying
degrees
cognitive
impairment,
raising
concerns
about
potential
increase
neurological
sequelae
cases.
Neuroinflammation
seems
be
the
key
pathophysiological
hallmark
linking
mild
COVID‐19
fatigue,
and
patients,
highlighting
interaction
between
nervous
immune
systems
following
SARS‐CoV‐2
infection.
Several
hypotheses
have
been
proposed
explain
how
virus
disrupts
physiological
pathways
trigger
inflammation
within
CNS,
potentially
neuronal
damage.
These
include
neuroinvasion,
systemic
inflammation,
disruption
lung
gut‐brain
axes,
reactivation
latent
viruses.
This
review
explores
origins
neuroinflammation
underlying
neuroimmune
cross‐talk,
important
unanswered
questions
field.
Addressing
these
fundamental
issues
could
enhance
our
understanding
virus's
impact
on
CNS
inform
strategies
mitigate
its
detrimental
effects.