Accelerated brain age in young to early middle-aged adults after mild to moderate COVID-19 infection
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 7, 2024
Abstract
Cognitive
decline
is
a
common
adverse
effect
of
the
Coronavirus
Disease
2019
(COVID-19),
particularly
in
post-acute
disease
phase.
The
mechanisms
cognitive
impairment
after
COVID-19
(COGVID)
remain
unclear,
but
neuroimaging
studies
provide
evidence
brain
changes,
many
that
are
associated
with
aging.
Therefore,
we
calculated
Brain
Age
Gap
(BAG),
which
difference
between
age
and
chronological
age,
cohort
25
mild
to
moderate
survivors
(did
not
experience
breathlessness,
pneumonia,
or
respiratory/organ
failure)
24
non-infected
controls
(mean
=
30
+/−
8)
using
magnetic
resonance
imaging
(MRI).
BAG
was
significantly
higher
group
(F
4.22,
p
0.046)
by
2.65
years.
Additionally,
80%
demonstrated
an
accelerated
compared
13%
control
(X
2
20.0,
<
0.001).
Accelerated
correlated
lower
function
(p
0.041).
Females
99%
decreased
risk
males
(OR
0.015,
95%
CI:
0.001
0.300).
There
also
small
(1.4%)
significant
decrease
for
longer
time
since
diagnosis
0.986,
0.977
0.995).
Our
findings
novel
biomarker
COGVID
point
aging
as
potential
mechanism
this
effect.
results
offer
further
insight
regarding
gender-related
disparities
morbidity
COVID-19.
Language: Английский
Sex differences in ACE2, TMPRSS2, and HLA-DQA2 expression in gray matter: Implications for post-COVID-19 neurological symptoms
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 4, 2024
Abstract
COVID-19
has
been
associated
with
sex
differences
in
terms
of
mortality
and
morbidity.
Viral
entry
proteins
including
those
regulated
by
ACE2
TMPRSS2
may
play
a
role,
but
few
studies
have
conducted
to
date
none
examined
brain
expression.
Additionally,
HLA-DQA2
expression
emerged
as
potential
moderator
outcomes.
Using
non-invasive
imaging
transcriptomics,
we
measured
ACE2,
TMPRSS2,
mRNA
gray
matter
volumes
using
MRI
scans
obtained
from
1,045
healthy
adults
aged
21-35
years
(44%
male)
imaged
prior
the
pandemic.
(t
=
9.24,
p
<
0.001,
d
0.576),
24.66,
1.54),
3.70,
0.231)
was
significantly
higher
males
compared
females.
Bayesian
network
analysis
indicated
significant
(p
0.05)
positive
causal
paths
(B
0.282),
0.357),
HLA-DQA1
0.139)
negative
path
(males
-1,
females
1)
-0.607).
Our
results
important
implications
for
neurological
symptoms
long
COVID
complex
interactions
between
viral
immune
responses,
sex-related
disparities
symptom
reporting
diagnosis,
assessment
problems
after
COVID-19,
related
syndemics.
However,
further
research
is
needed
determine
gene
patterns
outcomes,
evaluate
additional
genes
that
influence
neurologic
status,
include
objective
assessments
Language: Английский