Frontiers in Cellular Neuroscience,
Journal Year:
2020,
Volume and Issue:
14
Published: Nov. 11, 2020
SARS-CoV-2,
which
causes
the
Coronavirus
Disease
2019
(COVID-19)
pandemic,
has
a
strong
brain
neurotropism
via
binding
to
receptor
angiotensin-converting
enzyme
2
expressed
by
neurones
and
glial
cells,
including
astrocytes
microglia.
Systemic
infection
accompanies
severe
cases
of
COVID-19
also
triggers
substantial
increase
in
circulating
levels
chemokines
interleukins
that
compromise
blood-brain
barrier,
enter
parenchyma
affect
its
defensive
systems,
Brain
areas
devoid
barrier
such
as
circumventricular
organs
are
particularly
vulnerable
inflammatory
mediators.
The
performance
microglia,
well
immune
cells
required
for
health,
is
considered
critical
defining
neurological
damage
outcome
COVID-19.
In
this
review,
we
discuss
implication
neuroinflammation,
adaptive
innate
immunity,
autoimmunity,
astrocytic
microglial
homeostatic
functions
psychiatric
aspects
consequences
SARS-CoV-2
during
ageing,
presence
systemic
comorbidities,
exposed
pregnant
mother
foetus
will
be
specifically
covered.
Physiological Reviews,
Journal Year:
2017,
Volume and Issue:
98(1), P. 239 - 389
Published: Dec. 24, 2017
Astrocytes
are
neural
cells
of
ectodermal,
neuroepithelial
origin
that
provide
for
homeostasis
and
defense
the
central
nervous
system
(CNS).
highly
heterogeneous
in
morphological
appearance;
they
express
a
multitude
receptors,
channels,
membrane
transporters.
This
complement
underlies
their
remarkable
adaptive
plasticity
defines
functional
maintenance
CNS
development
aging.
tightly
integrated
into
networks
act
within
context
tissue;
astrocytes
control
at
all
levels
organization
from
molecular
to
whole
organ.
FEBS Journal,
Journal Year:
2015,
Volume and Issue:
282(21), P. 4067 - 4079
Published: Aug. 16, 2015
With
the
endothelium
as
its
central
unit,
blood-brain
barrier
(BBB)
is
a
complex
multicellular
structure
separating
nervous
system
(CNS)
from
systemic
circulation.
Disruption
of
BBB
has
now
been
implicated
in
multitude
acute
and
chronic
CNS
disorders
indicating
potentially
devastating
effects
breakdown
on
brain
function.
However,
healthy
not
an
impermeable
wall,
but
rather
communication
'centre',
responding
to
passing
signals
between
blood.
New
studies
are
identifying
BBB-specific
transport
pathways
that
tightly
regulate
entry
exit
molecules
brain.
They
revealing
highly
plastic
which
dynamic
changes
components
like
paracellular
tight
junction
complexes
can
contribute
maintenance.
Here,
we
provide
succinct
overview
current
state-of-play
research
summarize
novel
findings
into
regulation
homeostatic
Journal of Cerebral Blood Flow & Metabolism,
Journal Year:
2016,
Volume and Issue:
37(1), P. 4 - 24
Published: Nov. 12, 2016
The
age-associated
decline
of
the
neurological
and
cognitive
functions
becomes
more
serious
challenge
for
developed
countries
with
increasing
number
aged
populations.
morphological
biochemical
changes
in
aging
brain
are
subjects
many
extended
research
projects
worldwide
a
long
time.
However,
crucial
role
blood-brain
barrier
(BBB)
impairment
disruption
pathological
processes
neurodegenerative
disorders
received
special
attention
just
few
years.
This
article
gives
an
overview
on
major
elements
its
supporting
mechanisms
also
their
alterations
during
development,
physiological
process
(Alzheimer's
disease,
multiple
sclerosis,
Parkinson's
pharmacoresistant
epilepsy).
Besides
cellular
(endothelial
cells,
astrocytes,
pericytes,
microglia,
neuronal
elements)
BBB
neurovascular
unit,
at
molecular
level
(tight
junction
proteins,
adheres
membrane
transporters,
basal
lamina,
extracellular
matrix)
summarized.
recognition
new
players
initiators
neurodegeneration
may
offer
avenues
novel
therapeutic
approaches
treatment
numerous
chronic
currently
without
effective
medication.
Frontiers in Aging Neuroscience,
Journal Year:
2019,
Volume and Issue:
11
Published: March 19, 2019
Astrocytes,
one
of
the
largest
glial
cell
population
in
Central
Nervous
System,
play
key
function
several
events
brain
development
and
function,
such
as
synapse
formation
control
neurotransmitters
release
uptake,
production
trophic
factors
neuronal
survival.
Initially
described
a
homogenous
population,
evidences
have
pointed
that
astrocytes
are
highly
heterogeneous,
both
morphologically
functionally,
within
same
region,
across
different
regions.
Recent
findings
suggest
heterogeneity
expression
profile
proteins
involved
astrocyte
may
predict
selective
vulnerability
regions
to
specific
diseases,
well
age-related
cognitive
decline.
However,
molecular
mechanisms
underlying
these
changes,
either
aging
disease
scarce.
Neuroinflammation,
hallmark
neurodegenerative
diseases
aging,
is
reported
dubious
impact
on
activation,
cells
pro-
anti-inflammatory
cytokines
chemokines,
anti-oxidants,
free
radicals,
neurotrophic
factors.
Despite
emerging
evidence
supporting
reactive
duality
their
phenotype,
neurotoxic
or
neuroprotective
properties,
depending
age
stimuli,
cellular
interplays
regional
still
matter
discussion.
In
this
review,
we
will
summarize
recent
phenotypes,
likely
for
during
neural
diseases.
We
focus
molecules
triggered
by
Finally,
discuss
new
how
modulation
phenotype
could
synaptic
deficits
dysfunction
present
pathological
states.
Biomedical Journal,
Journal Year:
2018,
Volume and Issue:
41(1), P. 21 - 33
Published: Feb. 1, 2018
Alzheimer's
Disease
(AD)
is
a
chronic
neurodegenerative
disorder
and
the
most
common
type
of
dementia
(60–80%
cases).
In
2016,
nearly
44
million
people
were
affected
by
AD
or
related
dementia.
characterized
progressive
neuronal
damages
leading
to
subtle
latter
obvious
decline
in
cognitive
functions
including
symptoms
such
as
memory
loss
confusion,
which
ultimately
require
full-time
medical
care.
Its
neuropathology
defined
extracellular
accumulation
amyloid-β
(Aβ)
peptide
into
amyloid
plaques,
intraneuronal
neurofibrillary
tangles
(NFT)
consisting
aggregated
hyper-
abnormal
phosphorylation
tau
protein.
The
latter,
identified
also
Tau
pathology,
observed
broad
spectrum
neurological
diseases
commonly
referred
"Tauopathies".
Besides
these
lesions,
sustained
neuroinflammatory
processes
occur,
involving
notably
micro-
astro-glial
activation,
contribute
disease
progression.
Recent
findings
from
genome
wide
association
studies
further
support
an
instrumental
role
neuroinflammation.
While
interconnections
existing
between
this
innate
immune
response
pathogenesis
are
widely
described
complex,
elaborated
evolving,
only
few
focused
on
pathology.
An
adaptive
takes
place
conjointly
during
course,
indicated
presence
vascular
parenchymal
T-cell
patients'
brain.
underlying
mechanisms
infiltration
its
consequences
with
regards
pathology
remain
understudied
so
far.
present
review,
we
highlight
interplays
innate/adaptive
responses.