Cells,
Journal Year:
2024,
Volume and Issue:
13(16), P. 1388 - 1388
Published: Aug. 20, 2024
This
Special
Issue
of
Cells
presents
a
collection
22
published,
peer-reviewed
articles
on
the
theme
“Astrocytes
in
CNS
Disorders,”
including
9
reviews
evidence
implicating
astrocytes
etiology
specific
disorders,
and
13
original
research
papers
providing
such
[...]
Neuroscience & Biobehavioral Reviews,
Journal Year:
2024,
Volume and Issue:
162, P. 105724 - 105724
Published: May 16, 2024
Alzheimer's
disease
(AD)
is
prevalent
around
the
world,
yet
our
understanding
of
still
very
limited.
Recent
work
suggests
that
cornerstone
AD
may
include
inflammation
accompanies
it.
Failure
a
normal
pro-inflammatory
immune
response
to
resolve
lead
persistent
central
contributes
unsuccessful
clearance
amyloid-beta
plaques
as
they
form,
neuronal
death,
and
ultimately
cognitive
decline.
Individual
metabolic,
dietary
(lipid)
profiles
can
differentially
regulate
this
inflammatory
process
with
aging,
obesity,
poor
diet,
early
life
stress
other
factors
contributing
greater
risk
developing
AD.
Here,
we
integrate
evidence
for
interface
between
these
factors,
how
contribute
brain
milieu.
In
particular,
discuss
importance
appropriate
polyunsaturated
fatty
acids
(PUFA)
in
diet
metabolism
specialised
pro-resolving
mediators
(SPMs);
raising
possibility
strategies
improve
outlook.
BioMed,
Journal Year:
2025,
Volume and Issue:
5(1), P. 3 - 3
Published: Jan. 9, 2025
Background:
Alzheimer’s
disease
(AD),
the
leading
cause
of
dementia
worldwide,
poses
an
increasing
global
health
burden,
yet
its
pathogenesis
remains
poorly
understood.
Diabetes
mellitus
(DM),
characterized
by
chronic
hyperglycemia,
has
been
identified
as
a
significant
risk
factor
for
AD
development,
suggesting
potential
metabolic
and
molecular
link
between
these
diseases.
Methods:
This
study
examines
impact
sustained
high
glucose
levels
on
astrocyte-like
C6
glial
cells,
focusing
key
cellular
processes
associated
with
AD.
We
evaluated
mitochondrial
function,
oxidative
stress,
uptake,
expression
hallmark
proteins,
including
β-amyloid
hyperphosphorylated
tau.
Results:
Our
findings
demonstrate
that
exposure
triggers
hyperactivity,
increased
Tau
phosphorylation,
though
were
unaffected
within
experimental
timeframe.
Conclusions:
These
results
shed
light
early
dysfunctions
contributing
to
DM-AD
connection,
providing
valuable
insights
into
pathways
involved
identifying
therapeutic
targets
mitigate
progression
in
individuals
DM.
Alzheimer s & Dementia,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 12, 2025
Abstract
BACKGROUND
Despite
significant
astrocytic
involvement
in
Parkinson's
disease
(PD),
the
knowledge
regarding
role
of
reactive
astrogliosis
is
still
at
surface
level;
largely
due
to
lack
specific
biomarkers
track
these
processes.
Novel
astroglial
PET‐tracers
BU99008
and
Deprenyl,
hold
immense
potential
for
visualizing
PD.
However,
they
have
not
been
thoroughly
investigated
METHODS
We
employed
a
multi‐marker
approach
performed
vitro
radioligand
binding
autoradiography
studies
with
3
H‐BU99008
H‐Deprenyl
together
immunofluorescence
morphometric
analyses
frontal
cortex,
temporal
caudate
putamen
brain
regions
PD
(
n
=
4)
control
7)
cases.
RESULTS
AND
DISCUSSION
showed
distinct
behavior
displayed
diverse
array
sites
(single
or
multiple)
brains.
Importantly,
captured
pronounced
regions,
corroborated
by
marked
changes
markers,
morphology,
cellular
Highlights
Astroglial
tracers
Deprenyl
range
different
levels
affinity
proportions
(%)
healthy
(CN)
(PD)
highly
(permanent)
high‐affinity
(HA)
site
nanomolar
range,
which
might
be
consistent
across
pathologies.
highlighted
tracer
behavior,
indicating
that
targeting
subpopulations
states
astrocytes
CN
prominent
advanced/end
stages
PD,
substantiated
increase
intercellular
adhesion
molecule
1
(ICAM‐1)–positive
morphology
Journal of Neurochemistry,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 17, 2024
Abstract
Glial
fibrillary
acidic
protein
(GFAP)
is
a
well‐established
biomarker
of
reactive
astrogliosis
in
the
central
nervous
system
because
its
elevated
levels
following
brain
injury
and
various
neurological
disorders.
The
advent
ultra‐sensitive
methods
for
measuring
low‐abundant
proteins
has
significantly
enhanced
our
understanding
GFAP
serum
or
plasma
patients
with
diverse
diseases.
Clinical
studies
have
demonstrated
that
holds
promise
both
as
diagnostic
prognostic
biomarker,
including
but
not
limited
to
individuals
Alzheimer's
disease.
exhibits
forms
structures,
herein
referred
proteoform
complexity,
encompassing
conformational
dynamics,
isoforms
post‐translational
modifications
(PTMs).
In
this
review,
we
explore
how
complexity
influences
detection,
which
may
affect
differential
performance
different
biological
fluids
can
provide
valuable
insights
into
underlying
processes.
Additionally,
proteoforms
are
often
disease‐specific,
review
provides
suggestions
highlights
areas
focus
on
development
new
assays
GFAP,
isoforms,
PTMs,
discharge
mechanisms,
breakdown
products,
higher‐order
species
interacting
partners.
By
addressing
knowledge
gaps
highlighted
aim
support
clinical
translation
interpretation
CSF
blood
reliable,
reproducible
specific
tests.
To
enhance
disease
pathology
comprehension
optimise
thorough
detected
biofluids
essential.
image
Cellular and Molecular Neurobiology,
Journal Year:
2024,
Volume and Issue:
44(1)
Published: Oct. 23, 2024
The
neurotoxicant
trimethyltin
(TMT)
triggers
cognitive
impairment
and
hippocampal
neurodegeneration.
TMT
is
a
useful
research
tool
for
the
study
of
Alzheimer's
disease
(AD)
pathogenesis
treatment.
Although
antidiabetic
agent
metformin
has
shown
promising
neuroprotective
effects,
however,
its
precise
modes
action
in
neurodegenerative
disorders
need
to
be
further
elucidated.
In
this
study,
we
investigated
whether
can
mitigate
cognition
To
induce
an
AD-like
phenotype,
was
injected
i.p.
(8
mg/kg)
administered
daily
p.o.
3
weeks
at
200
mg/kg.
Our
results
showed
that
administration
group
mitigated
learning
memory
Barnes
maze,
novel
object
recognition
(NOR)
task,
Y
attenuated
oxidative,
inflammatory,
cell
death/pyroptotic
factors,
also
reversed
neurodegeneration-related
proteins
such
as
presenilin
1
p-Tau.
Hippocampal
level
AMP-activated
protein
kinase
(AMPK)
key
regulator
energy
homeostasis
improved
following
Additionally,
reduced
acetylcholinesterase
(AChE)
activity,
glial
fibrillary
acidic
(GFAP)-positive
reactivity,
prevented
loss
CA1
pyramidal
neurons.
This
TMT-induced
neurodegeneration
may
pave
way
develop
new
therapeutics
combat
against
deficits
under
neurotoxic
conditions.
Journal of Alzheimer s Disease,
Journal Year:
2024,
Volume and Issue:
100(3), P. 1017 - 1037
Published: July 12, 2024
Alzheimer's
disease
(AD)
is
the
most
common
neurodegenerative
disease.
Unfortunately,
efficient
and
affordable
treatments
are
still
lacking
for
this
disorder,
it
therefore
urgent
to
identify
new
pharmacological
targets.
Astrocytes
playing
a
crucial
role
in
tuning
of
synaptic
transmission
several
studies
have
pointed
out
severe
astrocyte
reactivity
AD.
Reactive
astrocytes
show
altered
physiology
function,
suggesting
they
could
early
pathophysiology