Biology,
Journal Year:
2022,
Volume and Issue:
11(2), P. 316 - 316
Published: Feb. 16, 2022
In
vitro
multielectrode
array
(MEA)
systems
are
increasingly
used
as
higher-throughput
platforms
for
functional
phenotyping
studies
of
neurons
in
induced
pluripotent
stem
cell
(iPSC)
disease
models.
While
MEA
generate
large
amounts
spatiotemporal
activity
data
from
networks
iPSC-derived
neurons,
the
downstream
analysis
and
interpretation
such
high-dimensional
often
pose
a
significant
challenge
to
researchers.
this
review,
we
examine
how
technology
is
currently
deployed
iPSC
modeling
neurodevelopmental
disorders.
We
first
highlight
strengths
by
reviewing
history
its
development
original
scientific
questions
MEAs
were
intended
answer.
Methods
generating
patient
astrocytes
co-cultures
summarized.
then
discuss
challenges
associated
with
context,
present
novel
computational
methods
better
interpret
network
data.
end
suggesting
best
practices
presenting
research
publications,
propose
that
creation
public
repository
enable
collaborative
sharing
would
be
great
benefit
community.
Neuron,
Journal Year:
2022,
Volume and Issue:
110(21), P. 3484 - 3496
Published: Oct. 7, 2022
Persistent
neurological
and
neuropsychiatric
symptoms
affect
a
substantial
fraction
of
people
after
COVID-19
represent
major
component
the
post-acute
syndrome,
also
known
as
long
COVID.
Here,
we
review
what
is
understood
about
pathobiology
impact
on
CNS
discuss
possible
neurobiological
underpinnings
cognitive
affecting
survivors.
We
propose
chief
mechanisms
that
may
contribute
to
this
emerging
health
crisis.
Molecular Neurodegeneration,
Journal Year:
2022,
Volume and Issue:
17(1)
Published: March 21, 2022
Across
neurodegenerative
diseases,
common
mechanisms
may
reveal
novel
therapeutic
targets
based
on
neuronal
protection,
repair,
or
regeneration,
independent
of
etiology
site
disease
pathology.
To
address
these
and
discuss
emerging
treatments,
in
April,
2021,
Glaucoma
Research
Foundation,
BrightFocus
the
Melza
M.
Frank
Theodore
Barr
Foundation
collaborated
to
bring
together
key
opinion
leaders
experts
field
for
a
virtual
meeting
titled
"Solving
Neurodegeneration".
This
"think-tank"
style
focused
uncovering
mechanistic
roots
promising
new
catalyzed
by
goal
finding
treatments
glaucoma,
world's
leading
cause
irreversible
blindness
interest
three
hosting
foundations.
Glaucoma,
which
causes
vision
loss
through
degeneration
optic
nerve,
likely
shares
early
cellular
molecular
events
with
other
diseases
central
nervous
system.
Here
we
major
areas
overlap
between
system:
neuroinflammation,
bioenergetics
metabolism,
genetic
contributions,
neurovascular
interactions.
We
summarize
important
discussion
points
emphasis
research
that
are
most
innovative
treatment
neurodegeneration
yet
require
further
development.
The
is
highlighted
provides
unique
opportunities
collaboration
will
lead
efforts
preventing
ultimately
loss.
Acta Neuropathologica Communications,
Journal Year:
2023,
Volume and Issue:
11(1)
Published: March 13, 2023
Abstract
In
the
contexts
of
aging,
injury,
or
neuroinflammation,
activated
microglia
signaling
with
TNF-α,
IL-1α,
and
C1q
induces
a
neurotoxic
astrocytic
phenotype,
classified
as
A1,
A1-like,
neuroinflammatory
reactive
astrocytes.
contrast
to
typical
astrocytes,
which
promote
neuronal
survival,
support
synapses,
maintain
blood–brain
barrier
integrity,
these
astrocytes
downregulate
supportive
functions
begin
secrete
factors,
complement
components
like
C3,
chemokines
CXCL10,
may
facilitate
recruitment
immune
cells
across
BBB
into
CNS.
The
proportion
pro-inflammatory
increases
age
through
associated
activation,
are
particularly
abundant
in
neurodegenerative
disorders.
As
identification
astrocyte
phenotypes
progress,
their
molecular
cellular
effects
characterized
growing
array
neuropathologies.
Aging Cell,
Journal Year:
2021,
Volume and Issue:
21(1)
Published: Dec. 10, 2021
The
increase
in
senescent
cells
tissues,
including
the
brain,
is
a
general
feature
of
normal
aging
and
age-related
pathologies.
Senescent
exhibit
specific
phenotype,
which
includes
an
altered
nuclear
morphology
transcriptomic
changes.
Astrocytes
undergo
senescence
vitro
age-associated
neurodegenerative
diseases,
but
little
known
about
whether
this
process
also
occurs
physiological
aging,
as
well
its
functional
implication.
Here,
we
investigated
astrocyte
vitro,
old
mouse
brains,
post-mortem
human
brain
tissue
elderly.
We
identified
significant
loss
lamin-B1,
major
component
lamina,
hallmark
astrocytes.
showed
severe
reduction
lamin-B1
dentate
gyrus
aged
mice,
hippocampal
astrocytes,
granular
cell
layer
hippocampus
from
non-demented
was
associated
with
deformations,
represented
by
increased
incidence
invaginated
nuclei
circularity
astrocytes
hippocampus.
found
differences
levels
between
polymorphic
elderly
hippocampus,
suggesting
intra-regional-dependent
response
Moreover,
described
senescence-associated
impaired
neuritogenic
synaptogenic
capacity
Our
findings
show
that
conserved
shed
light
on
defects
lamina
structure
may
contribute
to
dysfunctions
during
aging.
Ageing Research Reviews,
Journal Year:
2021,
Volume and Issue:
68, P. 101335 - 101335
Published: April 1, 2021
Astrocyte
reactivity
is
a
hallmark
of
neuroinflammation
that
arises
with
Alzheimer's
disease
(AD)
and
nearly
every
other
neurodegenerative
condition.
While
astrocytes
certainly
contribute
to
classic
inflammatory
processes
(e.g.
cytokine
release,
waste
clearance,
tissue
repair),
newly
emerging
technologies
for
measuring
targeting
cell
specific
activities
in
the
brain
have
uncovered
essential
roles
synapse
function,
metabolism,
neurovascular
coupling,
sleep/wake
patterns.
In
this
review,
we
use
holistic
approach
incorporate,
expand
upon,
neuroinflammatory
concepts
consider
how
astrocyte
dysfunction/reactivity
modulates
multiple
pathological
clinical
hallmarks
AD.
Our
ever-evolving
understanding
signaling
neurodegeneration
not
only
revealing
new
drug
targets
treatments
dementia
but
suggesting
reimagine
AD
pathophysiological
mechanisms.
