Biomolecules and Biomedicine,
Год журнала:
2023,
Номер
24(2), С. 219 - 229
Опубликована: Ноя. 28, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection
initially
results
in
distress
symptoms
but
can
also
lead
to
central
nervous
system
(CNS)
and
neurological
manifestations,
significantly
impacting
disease
2019
(COVID-19)
patients
with
neurodegenerative
diseases.
Additionally,
strict
lockdown
measures
introduced
curtail
the
spread
of
COVID-19
have
raised
concerns
over
wellbeing
dementia
and/or
Alzheimer’s
disease.
The
aim
this
review
was
discuss
overlapping
molecular
pathologies
potential
bidirectional
relationship
between
dementia,
as
well
impact
lockdown/restriction
on
neuropsychiatric
(NPS)
dementia.
Furthermore,
we
aimed
assess
NPS
caregivers,
exploring
its
effects
quality
extent
care
they
provide
patients.We
utilized
PubMed
Google
Scholar
databases
search
for
articles
COVID-19,
disease,
lockdown,
caregivers.
Our
highlights
that
face
an
increased
risk
complications.
these
are
likely
experience
greater
cognitive
decline.
It
appears
issues
primarily
caused
by
SARS-CoV-2
appear
be
further
exacerbated
restrictive/lockdown
measures.
Moreover,
during
pandemic
negatively
impacted
both
NPSs
caregivers
their
perception
patients.
Thus,
additional
safeguard
measures,
along
pharmacological
non-pharmacological
approaches,
needed
protect
light
possible
future
pandemics.
Frontiers in Aging Neuroscience,
Год журнала:
2024,
Номер
15
Опубликована: Янв. 8, 2024
Currently,
there
exists
a
limited
comprehension
regarding
the
correlation
between
COVID-19
and
Alzheimer’s
disease
(AD).
To
elucidate
interrelationship
its
impact
on
outcomes,
comprehensive
investigation
was
carried
out
utilising
time-unrestricted
searches
of
reputable
databases
such
as
Scopus,
PubMed,
Web
Science,
Google
Scholar.
Our
objective
to
evaluate
various
medical
conditions
severe
COVID-19-related
events.
We
focused
identifying
analysing
articles
that
discussed
clinical
characteristics
patients,
particularly
those
pertaining
events
ICU
admission,
mechanical
ventilation,
pneumonia,
mortality
acute
respiratory
distress
syndrome
(ARDS)
serious
lung
condition
causes
low
blood
oxygen.
Through
careful
data
analysis
information
gathering,
we
tried
figure
how
likely
it
people
with
conditions,
like
AD,
would
have
research
investigated
potential
mechanisms
link
AD
COVID-19.
The
ability
virus
directly
invade
central
nervous
system
role
ACE-2
receptors
were
investigated.
Furthermore,
OAS1
gene
served
genetic
In
context
COVID-19,
our
findings
suggest
individuals
may
be
more
susceptible
experiencing
outcomes.
Consequently,
is
crucial
provide
personalised
care
management
for
this
demographic.
Further
required
attain
intricate
well
ramifications
patient
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(7), С. 3830 - 3830
Опубликована: Март 29, 2024
Long
COVID
(LongC)
is
associated
with
a
myriad
of
symptoms
including
cognitive
impairment.
We
reported
at
the
beginning
COVID-19
pandemic
that
neuronal-enriched
or
L1CAM+
extracellular
vesicles
(nEVs)
from
people
LongC
contained
proteins
Alzheimer’s
disease
(AD).
Since
time,
subset
prior
infection
continue
to
report
neurological
problems
more
than
three
months
after
infection.
Blood
markers
better
characterize
are
elusive.
To
further
identify
neuronal
LongC,
we
maximized
number
nEVs
isolated
plasma
by
developing
hybrid
EV
Microfluidic
Affinity
Purification
(EV-MAP)
technique.
and
complaints,
AD,
HIV
mild
Using
OLINK
platform
assesses
384
proteins,
identified
11
significant
increased
in
2
decreased
(BST1,
GGT1).
Fourteen
were
AD
forty
impairment
elevated
one
(IVD).
One
common
protein
(BST1)
was
HIV.
Six
(MIF,
ENO1,
MESD,
NUDT5,
TNFSF14
FYB1)
expressed
both
no
AD.
This
study
begins
differences
similarities
response
versus
Molecular Neurodegeneration,
Год журнала:
2024,
Номер
19(1)
Опубликована: Апрель 19, 2024
Abstract
The
unprecedented
pandemic
of
COVID-19
swept
millions
lives
in
a
short
period,
yet
its
menace
continues
among
survivors
the
form
post-COVID
syndrome.
An
exponentially
growing
number
suffer
from
cognitive
impairment,
with
compelling
evidence
trajectory
accelerated
aging
and
neurodegeneration.
novel
enigmatic
nature
this
yet-to-unfold
pathology
demands
extensive
research
seeking
answers
for
both
molecular
underpinnings
potential
therapeutic
targets.
Ferroptosis,
an
iron-dependent
cell
death,
is
strongly
proposed
underlying
mechanism
post-COVID-19
neurodegeneration
discourse.
incites
neuroinflammation,
iron
dysregulation,
reactive
oxygen
species
(ROS)
accumulation,
antioxidant
system
repression,
renin-angiotensin
(RAS)
disruption,
clock
gene
alteration.
These
events
pave
way
ferroptosis,
which
shows
signature
COVID-19,
premature
aging,
neurodegenerative
disorders.
In
search
treatment,
melatonin
shines
as
promising
ferroptosis
inhibitor
repeatedly
reported
safety
tolerability.
According
to
various
studies,
has
proven
efficacy
attenuating
severity
certain
manifestations,
validating
reputation
anti-viral
compound.
Melatonin
well-documented
anti-aging
properties
combating
neurodegenerative-related
pathologies.
can
block
leading
since
it
efficient
anti-inflammatory,
chelator,
antioxidant,
angiotensin
II
antagonist,
regulator.
Therefore,
we
propose
culprit
behind
melatonin,
well-fitting
inhibitor,
treatment.
Clinical Microbiology Reviews,
Год журнала:
2024,
Номер
37(4)
Опубликована: Сен. 18, 2024
SUMMARYSARS-CoV-2
can
not
only
cause
respiratory
symptoms
but
also
lead
to
neurological
complications.
Research
has
shown
that
more
than
30%
of
SARS-CoV-2
patients
present
neurologic
during
COVID-19
(A.
Pezzini
and
A.
Padovani,
Nat
Rev
Neurol
16:636-644,
2020,
https://doi.org/10.1038/s41582-020-0398-3).
Increasing
evidence
suggests
invade
both
the
central
nervous
system
(CNS)
(M.S.
Xydakis,
M.W.
Albers,
E.H.
Holbrook,
et
al.
Lancet
20:
753-761,
2021
https://doi.org/10.1016/S1474-4422(21)00182-4
)
peripheral
(PNS)
(M.N.
Soares,
M.
Eggelbusch,
E.
Naddaf,
J
Cachexia
Sarcopenia
Muscle
13:11-22,
2022,
https://doi.org/10.1002/jcsm.12896),
resulting
in
a
variety
disorders.
This
review
summarized
CNS
complications
caused
by
infection,
including
encephalopathy,
neurodegenerative
diseases,
delirium.
Additionally,
some
PNS
disorders
such
as
skeletal
muscle
damage
inflammation,
anosmia,
smell
or
taste
impairment,
myasthenia
gravis,
Guillain-Barré
syndrome,
ICU-acquired
weakness,
post-acute
sequelae
were
described.
Furthermore,
mechanisms
underlying
SARS-CoV-2-induced
discussed,
entering
brain
through
retrograde
neuronal
hematogenous
routes,
disrupting
normal
function
cytokine
storms,
inducing
cerebral
ischemia
hypoxia,
thus
leading
Moreover,
an
overview
long-COVID-19
is
provided,
along
with
recommendations
for
care
therapeutic
approaches
experiencing
Journal of Alzheimer s Disease,
Год журнала:
2023,
Номер
95(4), С. 1301 - 1337
Опубликована: Сен. 12, 2023
Malignant
brain
aging
corresponds
to
accelerated
age-related
declines
in
functions
eventually
derailing
the
self-sustaining
forces
that
govern
independent
vitality.
establishes
path
toward
dementing
neurodegeneration,
including
Alzheimer's
disease
(AD).
The
full
spectrum
of
AD
includes
progressive
dysfunction
neurons,
oligodendrocytes,
astrocytes,
microglia,
and
microvascular
systems,
is
mechanistically
driven
by
insulin
insulin-like
growth
factor
(IGF)
deficiencies
resistances
with
accompanying
deficits
energy
balance,
increased
cellular
stress,
inflammation,
impaired
perfusion,
mimicking
core
features
diabetes
mellitus.
underlying
pathophysiological
derangements
result
mitochondrial
dysfunction,
abnormal
protein
aggregation,
oxidative
endoplasmic
reticulum
aberrant
autophagy,
post-translational
modification
proteins,
all
which
are
signature
both
dysregulated
insulin/IGF-1-mechanistic
target
rapamycin
(mTOR)
signaling.
This
article
connects
dots
from
benign
malignant
neurodegeneration
reviewing
salient
pathologies
associated
initially
adaptive
later
dysfunctional
mTOR
signaling
brain.
Effective
therapeutic
preventive
measures
must
be
two-pronged
designed
1)
address
complex
shifting
impairments
through
re-purpose
effective
anti-diabetes
therapeutics
brain,
2)
minimize
impact
extrinsic
mediators
transitions,
e.g.,
inflammatory
states,
obesity,
systemic
resistance
diseases,
repeated
bouts
general
anesthesia,
minimizing
exposures
or
implementing
neuroprotective
measures.
Journal of Alzheimer s Disease,
Год журнала:
2024,
Номер
100(4), С. 1099 - 1119
Опубликована: Июль 12, 2024
Alzheimer's
disease
(AD)
accounts
for
most
dementia
cases,
but
we
lack
a
complete
understanding
of
the
mechanisms
responsible
core
pathology
associated
with
(e.g.,
amyloid
plaque
and
neurofibrillary
tangles).
Inflammation
has
been
identified
as
key
contributor
AD
pathology,
recent
evidence
pointing
towards
Reelin
dysregulation
being
inflammation.
Here
describe
signaling
outline
existing
research
involving
in
Research
is
described
pertaining
to
inflammatory
immunological
functions
before
propose
mechanism
through
which
inflammation
renders
susceptible
resulting
induction
exacerbation
pathology.
Based
on
this
hypothesis,
it
predicted
that
disorders
both
(including
peripheral
neuroinflammation)
upregulated
expression
downregulation)
have
elevated
risk
developing
AD.
We
conclude
description
various
Frontiers in Psychiatry,
Год журнала:
2024,
Номер
15
Опубликована: Март 25, 2024
Current
views
on
immunity
support
the
idea
that
extends
beyond
defense
functions
and
is
tightly
intertwined
with
several
other
fields
of
biology
such
as
virology,
microbiology,
physiology
ecology.
It
also
critical
for
our
understanding
autoimmunity
cancer,
two
topics
great
biological
relevance
public
health
considerations
disease
prevention
treatment.
Central
to
this
review,
immune
system
known
interact
intimately
nervous
has
been
recently
hypothesized
be
involved
not
only
in
autonomic
limbic
bio-behaviors
but
cognitive
function.
Herein
we
review
structural
architecture
brain
network
response.
Furthermore,
elaborate
upon
implications
inflammatory
processes
affecting
brain-immune
interactions
reported
pathological
conditions
due
SARS-Cov-2
virus
infection,
namely
acute
post-acute
COVID-19.
Moreover,
discuss
how
current
neuroimaging
techniques
combined
ad
hoc
clinical
autopsies
histopathological
analyses
could
critically
affect
validity
translation
studies
human
using
neuroimaging.
Advances
are
expected
translate
into
novel
therapeutic
avenues
a
vast
array
domains
including
autoimmune
diseases
or
viral
infections
Long
Molecular Neurodegeneration,
Год журнала:
2025,
Номер
20(1)
Опубликована: Янв. 29, 2025
Abstract
Alzheimer’s
disease
(AD)
is
a
debilitating
neurodegenerative
that
marked
by
profound
neurovascular
dysfunction
and
significant
cell-specific
alterations
in
the
brain
vasculature.
Recent
advances
high
throughput
single-cell
transcriptomics
technology
have
enabled
study
of
human
vasculature
at
an
unprecedented
depth.
Additionally,
understudied
niche
cerebrovascular
cells,
such
as
endothelial
mural
their
subtypes
been
scrutinized
for
understanding
cellular
transcriptional
heterogeneity
AD.
Here,
we
provide
overview
rich
signatures
derived
from
recent
single-nucleus
transcriptomic
studies
vascular
cells
implications
targeted
therapy
We
conducted
in-depth
literature
search
using
Medline
Covidence
to
identify
pertinent
AD
utilized
technologies
post-mortem
tissue
focusing
on
differences
cell
types
cognitively
normal
older
adults.
also
discuss
impaired
crosstalk
between
neuroglial
units,
well
astrocytes
contextualize
findings
distinct
smooth
muscle
fibroblasts,
pericytes
highlight
pathways
potential
therapeutic
interventions
concerted
multi-omic
effort
with
spatial
technology,
neuroimaging,
neuropathology.
Overall,
detailed
account
crucial
unit.
Graphical
Endothelial
mediate
dysregulated
cell-cell
interactions
The
unit
(NVU)
composed
various
types,
including
(pericytes,
cells),
fibroblast
neurons,
microglia,
astrocytes.
Dysregulated
involve
multiple
pathways,
notably
immune
responses,
angiogenesis
common
both
cells.
involving
neuroinflammation
amyloid
clearance
are
prominent
while
exhibit
related
growth
factors,
cytoskeletal
remodeling
synaptic
function.
In
addition,
within
NVU
gliovascular
(GVU)
altered
AD,
communication
evident,
increased
pericytes,
decreased
astrocytes,
neurons.
Figure
created
BioRender.com.
Abbreviations:
Alzheimer's
disease;
NVU,
Neurovascular
unit;
CNS,
Central
Nervous
System.
NeuroSci,
Год журнала:
2025,
Номер
6(1), С. 16 - 16
Опубликована: Фев. 14, 2025
Background:
Alzheimer's
disease
(AD)
is
the
fifth
leading
cause
of
death
for
Americans
older
than
65.
Though
fluctuations
have
been
noticed
over
past
two
decades,
mortality
patients
increased
considerably
during
COVID-19
pandemic.
This
study
aims
to
explore
temporal
trends
in
AD-associated
(ADAM)
and
disparities
these
trends,
we
aim
discern
changes
Methods:
The
CDC
WONDER
Multiple
Cause-of-Death
Public
Use
Records
from
1999
2022
were
used
extract
population
data
on
deaths
related
AD
stratify
them
based
age,
biological
sex,
race,
ethnicity,
place
death,
census
region,
state.
ICD-10
codes
G30.0,
G30.1,
G30.8,
G30.9
identify
AD-related
mortality.
Statistical
analysis
was
performed
using
Joinpoint
Regression
Program
version
5.0.2.
Results:
We
confirmed
an
increase
rate
all
races,
sexes,
places
age
groups
above
65,
states/census
regions.
Interestingly,
age-adjusted
(AAMR)
consistently
higher
females
compared
males.
Non-Hispanic
whites
had
highest
by
race
ethnicity.
At
intersection
White
AAMR
with
AD.
Lastly,
noted
at
hospice
facilities
as
other
death.
Conclusions:
Our
findings
demonstrate
that
number
due
exacerbated
recent
pandemic
disproportionately
affected.
relating
ADAM
uncovered
this
may
assist
healthcare
administrators
policymakers
their
decisions.
Additionally,
might
help
initiate
larger
studies
focusing
novel
risk/prognostic
factors