Frontiers in Molecular Neuroscience,
Journal Year:
2024,
Volume and Issue:
17
Published: Oct. 11, 2024
Olfactory
loss
accompanies
at
least
139
neurological,
somatic,
and
congenital/hereditary
conditions.
This
observation
leads
to
the
question
of
whether
these
associations
are
correlations
or
they
ever
causal.
Temporal
precedence
prospective
predictive
power
suggest
that
olfactory
is
causally
implicated
in
many
medical
The
causal
relationship
between
olfaction
with
memory
dysfunction
deserves
particular
attention
because
this
sensory
system
has
only
direct
projection
centers.
Mechanisms
may
underlie
connections
conditions
include
inflammation
as
well
neuroanatomical
environmental
factors,
all
listed
here
also
associated
inflammation.
enrichment
shows
efficacy
for
both
prevention
treatment,
potentially
mediated
by
decreasing
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: Feb. 16, 2024
Abstract
More
than
200
million
COVID-19
survivors
have
lasting
symptoms
after
recovering,
but
the
duration
and
related
risk
factors
remain
uncertain.
This
study
focused
on
all
6551
patients
diagnosed
with
at
a
medical
institution
in
Hiroshima
from
March
2020
to
July
2022.
In
November
2022,
questionnaire
survey
was
conducted
regarding
post-COVID
their
duration.
The
prevalence
of
were
illustrated
using
Kaplan–Meier
method.
Risk
for
over
3
months
interfering
daily
life
assessed
via
multivariate
logistic
regression.
A
total
2421
responded:
1391
adults,
1030
children,
median
age
34
years
(IQR
9–55),
51·2%
male,
36·7%
hospitalized,
time
infection
295
days
201–538).
Upon
initial
recovery,
78·4%
adults
34·6%
children.
Three
later,
rates
47·6%
10·8%.
After
one
year,
they
31·0%
6·8%.
Regarding
interfere
life,
304
people
(12.6%)
experienced
three
months,
independent
including
age,
being
female,
diabetes
mellitus,
during
Delta
period,
current
smoking.
There
no
significant
association
between
vaccination
history
symptoms.
Age and Ageing,
Journal Year:
2025,
Volume and Issue:
54(3)
Published: March 1, 2025
Emerging
evidence
suggests
coronavirus
disease
2019
(COVID-19)
infection
may
increase
the
risk
of
developing
dementia,
although
studies
have
reported
conflicting
findings.
This
meta-analysis
aimed
to
synthesise
literature
on
association
between
COVID-19
and
new-onset
dementia.
PubMed,
Embase
Web
Science
were
searched
for
cohort
or
case-control
that
investigated
dementia
development
among
adult
survivors
compared
individuals
without
from
inception
9
November
2023.
Studies
exclusively
involved
populations
younger
than
18
years,
with
known
lacked
adequate
data
about
excluded.
Two
authors
independently
conducted
screening
eligible
studies,
extraction
bias
assessment.
The
primary
outcome
was
following
infection.
Data
pooled
using
random-effects
models,
hazard
ratios
(HRs)
95%
confidence
intervals
(CIs)
calculated.
A
total
15
retrospective
encompassing
26
408
378
participants
included.
Pooled
analysis
indicated
associated
an
increased
(HR
=
1.49,
CI:
1.33-1.68).
remained
elevated
when
non-COVID
cohorts
1.65,
1.39-1.95),
respiratory
tract
1.29,
1.12-1.49),
but
not
influenza
sepsis
cohorts.
Increased
observed
in
both
males
females,
as
well
older
65
years
1.68,
1.48-1.90),
remaining
up
24
months.
demonstrates
a
significant
which
underscores
need
cognitive
monitoring
early
intervention
address
potential
long-term
neurological
impacts.
Annals of Neurology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 22, 2024
Objective
To
investigate
neurologic
manifestations
of
post‐acute
sequelae
SARS‐CoV‐2
infection
(Neuro‐PASC)
in
post‐hospitalization
Neuro‐PASC
(PNP)
and
non‐hospitalized
(NNP)
patients
across
the
adult
lifespan.
Methods
Cross‐sectional
study
first
consecutive
200
PNP
1,100
NNP
evaluated
at
a
Neuro‐coronavirus
disease
2019
(COVID‐19)
clinic
between
May
2020
March
2023.
Patients
were
divided
into
younger
(18–44
years),
middle‐age
(45–64
older
(65+
years)
age
groups.
Results
Younger
individuals
accounted
for
142
(71%)
995
1100
(90.5%)
patients.
Significant
age‐related
differences
frequencies
comorbidities
abnormal
findings
demonstrated
higher
prevalence
Conversely,
10
months
from
COVID‐19
onset,
we
found
significant
symptoms
indicating
lower
prevalence,
therefore,
symptom
burden,
individuals.
Moreover,
there
subjective
impression
fatigue
(median
[interquartile
range
(IQR)]
patient‐reported
outcomes
measurement
information
system
[PROMIS]
score:
64
[57–69],
63
[57–68],
60.5
[50.8–68.3];
p
=
0.04)
sleep
disturbance
[IQR]
PROMIS
57
[51–63],
56
[53–63],
54
[46.8–58];
0.002)
group,
commensurate
with
impairment
quality
life
(QoL)
among
Finally,
objective
executive
function
National
Institutes
Health
[NIH]
toolbox
48
[35–63],
49
[38–63],
54.5
[45–66.3];
0.01),
working
memory
NIH
47
[40–53],
50
[44–57],
[43–58];
0.0002)
patients,
worst
performance
coming
group.
Interpretation
are
disproportionally
affected
by
regardless
acute
severity.
Although
people
more
frequently
have
comorbidities,
suffer
burden
cognitive
dysfunction
contributing
to
decreased
QoL.
principally
affects
adults
their
prime,
profound
public
health
socioeconomic
impacts
warranting
dedicated
resources
prevention,
diagnosis
interventions.
ANN
NEUROL
2024
Frontiers in Human Neuroscience,
Journal Year:
2023,
Volume and Issue:
17
Published: Nov. 9, 2023
This
study
aimed
to
apply
Sankey
plots
and
exponential
bar
for
visualizing
the
trajectory
of
post-COVID
brain
fog,
memory
loss,
concentration
loss
in
a
cohort
previously
hospitalized
COVID-19
survivors.A
sample
1,266
patients
due
during
first
wave
pandemic
were
assessed
at
8.4
(T1),
13.2
(T2),
18.3
(T3)
months
after
hospital
discharge.
They
asked
about
presence
following
self-reported
cognitive
symptoms:
fog
(defined
as
self-perception
sluggish
or
fuzzy
thinking),
unusual
forgetfulness),
not
being
able
maintain
attention).
We
symptoms
that
individuals
had
experienced
previously,
they
attributed
them
acute
infection.
Clinical
hospitalization
data
collected
from
medical
records.The
revealed
prevalence
was
8.37%
(n
=
106)
T1,
4.7%
60)
T2,
5.1%
65)
T3,
whereas
14.9%
189)
11.4%
145)
12.12%
154)
T3.
Finally,
decreased
6.86%
87)
4.78%
2.63%
33)
The
recovery
curves
show
decreasing
trend,
indicating
these
recovered
years
regression
models
did
reveal
any
record
associated
with
long
term.The
use
shows
fluctuating
evolution
In
addition,
decrease
No
risk
factors
identified
this
cohort.
BMC Geriatrics,
Journal Year:
2024,
Volume and Issue:
24(1)
Published: Dec. 14, 2024
Abstract
Background
The
relationship
between
COVID-19
infection
and
a
possible
increased
likelihood
of
older
adults
developing
new-onset
dementia
(NOD)
remains
elusive.
Methods
A
thorough
search
was
performed
across
several
databases
including
MEDLINE/PubMed,
PsycINFO,
Scopus,
medRxiv,
PQDT
Global
for
studies
published
in
English
from
January
2020
to
December
2023.
Only
original
investigations
exploring
the
link
NOD
were
selected
inclusion.
We
assessed
risk
NOD,
using
Risk
Ratio
(RR)
measurement.
Control
groups
categorized
as:
(i)
non-COVID
cohort
with
other
respiratory
infections
[control
group
(C1)];
(ii)
otherwise
unspecified
health
status
(C2)].
Follow-up
periods
divided
into
intervals
3,
6,
12,
24
months
post-COVID.
Results
11
(involving
939,824
post-COVID-19
survivors
6,765,117
controls)
included
review.
Across
median
observation
period
12
post-COVID,
overall
incidence
about
1.82%
COVID-infected
group,
compared
0.35%
non-COVID-infected
group.
pooled
meta-analysis
showed
significantly
among
adult
non-COVID-19
controls
(RR
=
1.58,
95%
CI
1.21–2.08).
Similar
risks
observed
subgroup
analyses
restricted
an
observational
1.56,
1.21–2.01),
as
well
five
that
employed
propensity
score
matching
sufficiently
effectively
control
multiple
confounding
covariates
1.46,
1.10–1.94).
C1
shared
comparably
(overall
RR
1.13,
0.92–1.38).
Discussion
Under
normal
circumstances,
we
believe
is
likely
be
factor
over
time.
While
due
appears
similar
associated
infections,
it
warrants
necessitates
investigation
longer
observations.
Investigative Ophthalmology & Visual Science,
Journal Year:
2024,
Volume and Issue:
65(5), P. 16 - 16
Published: May 8, 2024
Research
on
Alzheimer's
disease
(AD)
and
precursor
states
demonstrates
a
thinner
retinal
nerve
fiber
layer
(NFL)
compared
to
age-similar
controls.
Because
AD
age-related
macular
degeneration
(AMD)
both
impact
older
adults
share
risk
factors,
we
asked
if
thicknesses,
including
NFL,
are
associated
with
cognition
in
AMD.
Exploration of neuroscience,
Journal Year:
2025,
Volume and Issue:
4
Published: March 24, 2025
The
SAR-CoV-2
virus
has
evolved
to
co-exist
with
human
hosts,
albeit
at
a
substantial
energetic
cost
resulting
in
post-infection
neurological
manifestations
[Neuro-post-acute
sequelae
of
SARS-CoV-2
infection
(PASC)]
that
significantly
impact
public
health
and
economic
productivity
on
global
scale.
One
the
main
molecular
mechanisms
responsible
for
development
Neuro-PASC,
individuals
all
ages,
is
formation
inadequate
proteolysis/clearance
phase-separated
amyloid
crystalline
aggregates—a
hallmark
feature
aging-related
neurodegenerative
disorders.
Amyloidogenesis
during
viral
persistence
natural,
inevitable,
protective
defense
response
exacerbated
by
SARS-CoV-2.
Acting
as
chemical
catalyst,
accelerates
hydrophobic
collapse
heterogeneous
nucleation
amorphous
amyloids
into
stable
β-sheet
aggregates.
clearance
aggregates
most
effective
slow
wave
sleep,
when
high
levels
adenosine
triphosphate
(ATP)—a
biphasic
modulator
biomolecular
condensates—and
melatonin
are
available
solubilize
removal.
dysregulation
mitochondrial
dynamics
SARS-CoV-2,
particular
fusion
fission
homeostasis,
impairs
proper
distinct
subpopulations
can
remedy
challenges
created
diversion
substrates
away
from
oxidative
phosphorylation
towards
glycolysis
support
replication
maintenance.
subsequent
reduction
ATP
inhibition
synthesis
sleep
results
incomplete
brain
aggregates,
leading
commonly
associated
age-related
Exogenous
not
only
prevents
dysfunction
but
also
elevates
production,
effectively
augmenting
solubilizing
effect
moiety
ensure
timely,
optimal
disaggregation
pathogenic
prevention
attenuation
Neuro-PASC.
Current Opinion in Infectious Diseases,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 1, 2025
Purpose
of
review
Since
its
emergence
in
2020,
the
COVID-19
pandemic
has
created
a
global
surge
survivors
experiencing
neurologic
effects
from
SARS-CoV-2
infection.
This
aims
to
provide
an
updated
synthesis
acute
and
chronic
neurological
manifestations
COVID-19,
outline
current
therapeutic
strategies
for
these
conditions.
Recent
findings
Epidemiological
studies
have
shown
that
patients
with
symptoms
during
infection
tend
poorer
hospital
functional
outcomes.
While
risk
adverse
including
cognitive
dysfunction,
headache,
autonomic
fatigue
are
thought
be
greatest
following
original
strain
alpha
variant,
they
remain
prevalent
after
subsequent
less
virulent
strains
as
well.
Some
recent
work
also
found
link
between
structural
brain
changes.
However,
ongoing
trials
show
promising
results
pharmacologic
nonpharmacologic
treatments
targeting
postacute
sequelae
COVID-19.
Summary
Lingering
still
pose
considerable
individual,
healthcare
system,
socioeconomic
repercussions.
Both
preventive
multimodal
treatment
approaches
necessary
address
Further
research
is
required
assess
lasting
impacts
on
nervous
particularly
potential
contribution
development
neurodegenerative
diseases.