International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(16), P. 12912 - 12912
Published: Aug. 18, 2023
Multiple
sclerosis
(MS)
is
a
complex
autoimmune
disease
of
the
central
nervous
system
(CNS),
characterized
by
demyelination
and
neurodegeneration.
Oligodendrocytes
play
vital
role
in
maintaining
integrity
myelin,
protective
sheath
around
nerve
fibres
essential
for
efficient
signal
transmission.
However,
MS,
oligodendrocytes
become
dysfunctional,
leading
to
myelin
damage
axonal
degeneration.
Emerging
evidence
suggests
that
metabolic
changes,
including
mitochondrial
dysfunction
alterations
glucose
lipid
metabolism,
contribute
significantly
pathogenesis
MS.
Mitochondrial
observed
both
immune
cells
within
CNS
MS
patients.
Impaired
function
leads
energy
deficits,
affecting
crucial
processes
such
as
impulse
transmission
transport,
ultimately
contributing
Moreover,
linked
generation
reactive
oxygen
species
(ROS),
exacerbating
inflammation.
Altered
metabolism
affects
supply
required
oligodendrocyte
synthesis.
Dysregulated
results
changes
composition
its
stability
integrity.
Importantly,
low
levels
polyunsaturated
fatty
acids
are
associated
with
upregulated
enhanced
catabolism.
Understanding
intricate
relationship
between
these
mechanisms
developing
targeted
therapies
preserve
promote
neurological
recovery
individuals
Addressing
aspects
may
offer
new
insights
into
potential
therapeutic
strategies
halt
progression
improve
quality
life
Aging and Disease,
Journal Year:
2023,
Volume and Issue:
unknown, P. 0 - 0
Published: Jan. 1, 2023
Alzheimer’s
disease,
one
of
the
most
common
forms
dementia,
is
characterized
by
a
slow
progression
cognitive
impairment
and
neuronal
loss.
Currently,
approved
treatments
for
AD
are
hindered
various
side
effects
limited
efficacy.
Despite
considerable
research,
practical
have
not
been
developed.
Increasing
evidence
shows
that
glial
cells,
especially
microglia
astrocytes,
essential
in
initiation
AD.
During
progression,
activated
resident
increases
ability
resting
astrocytes
to
transform
into
reactive
promoting
neurodegeneration.
Extensive
clinical
molecular
studies
show
involvement
astrocyte-mediated
neuroinflammation
pathology,
indicating
may
be
potential
therapeutic
targets
This
review
will
summarize
significant
recent
advances
pathogenesis
three
parts.
First,
we
typical
pathological
changes
discuss
terms
function
phenotypic
changes.
Second,
describe
astrocytes’
physiological
role
These
roles
include
inflammatory
response,
“eat
me”
“don’t
eat
signals,
Aβ
seeding,
propagation,
clearance,
synapse
loss,
synaptic
pruning,
remyelination,
demyelination.
Last,
pharmacological
non-pharmacological
therapies
targeting
We
conclude
development
Therefore,
understanding
new
critical
future
trials.
Moreover,
pharmacological,
with
specific
investigating
damage
repair,
promising
research
direction
regarding
treatment
prevention.
ACS Chemical Neuroscience,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 25, 2025
Glioblastoma
multiforme
(GBM)
is
a
highly
aggressive
brain
cancer
with
median
survival
of
15
months.
Despite
advancements
in
conventional
treatment
approaches
such
as
surgery
and
chemotherapy,
the
prognosis
remains
poor.
This
study
investigates
use
rapid
evaporative
ionization
mass
spectrometry
(REIMS)
for
real-time
overall
time
classification
GBM
samples
uses
matrix-assisted
laser
desorption
imaging
(MALDI-MSI)
to
compare
lipidomic
differences
within
tumors.
A
total
45
biopsies
were
analyzed
develop
prediction
model
IDH-wild
type
GBM.
REIMS
patterns
from
28
patients
classified
97.7%
correct
rate,
identifying
key
discriminators
between
short-term
(0–12
months)
prolonged
(>12
survivors.
Cross-validation
additional
showed
that
correctly
66.7
69.4%
accuracy,
respectively.
MALDI-MSI
was
performed
confirm
derived
data.
Results
indicated
42
33
discriminating
features
survival,
Proteomic
profiling
by
isolating
tumor
regions
via
laser-capture
microdissection
(LMD)
liquid
chromatography-tandem
(LC-MS/MS).
Subsequently,
1387
proteins
identified,
which
79
significantly
altered.
In
conclusion,
this
shows
rapidly
predicts
glioblastoma
times
based
on
profiles
during
electrosurgical
dissection.
confirmed
these
specific
region
sections.
LMD-guided
LC-MS/MS-based
proteomics
revealed
altered
pathways
survival.
research,
including
comprehensive
predictive
GBM,
could
guide
resection
surgeries
accurate
tissue
identification
well
provide
insights
into
mechanisms,
possibly
related
therapy
response.
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(5)
Published: May 21, 2024
Abstract
Seipin
is
one
key
mediator
of
lipid
metabolism
that
highly
expressed
in
adipose
tissues
as
well
the
brain.
Lack
gene,
Bscl2
,
leads
to
not
only
severe
metabolic
disorders
but
also
cognitive
impairments
and
motor
disabilities.
Myelin,
composed
mainly
lipids,
facilitates
nerve
transmission
important
for
coordination
learning.
Whether
deficiency-leaded
defects
learning
underlined
by
dysregulation
its
consequent
myelin
abnormalities
remains
be
elucidated.
In
present
study,
we
verified
expression
oligodendrocytes
(OLs)
their
precursors,
oligodendrocyte
precursor
cells
(OPCs),
demonstrated
deficiency
compromised
OPC
differentiation,
which
led
decreased
OL
numbers,
protein,
myelinated
fiber
proportion
thickness
myelin.
Deficiency
resulted
impaired
spatial
cognition
mice.
Mechanistically,
suppressed
sphingolipid
metabolism-related
genes
OPCs
caused
morphological
droplets
(LDs),
markedly
impeded
differentiation.
Importantly,
rosiglitazone,
agonist
PPAR-gamma,
substantially
restored
phenotypes
resulting
from
deficiency,
such
aberrant
LDs,
reduced
sphingolipids,
obstructed
neurobehavioral
defects.
Collectively,
study
elucidated
how
deficiency-induced
deficits
via
impairing
myelination,
may
pave
way
developing
novel
intervention
strategy
treating
metabolism-involved
neurological
disorders.
Frontiers in Genetics,
Journal Year:
2024,
Volume and Issue:
15
Published: Feb. 15, 2024
Classic
galactosemia
(CG,
OMIM
#230400,
ORPHA:
79,239)
is
a
hereditary
disorder
of
galactose
metabolism
that,
despite
treatment
with
restriction,
affects
brain
function
in
85%
the
patients.
Problems
cognitive
function,
neuropsychological/social
emotional
difficulties,
neurological
symptoms,
and
abnormalities
neuroimaging
electrophysiological
assessments
are
frequently
reported
this
group
patients,
an
enormous
individual
variability.
In
review,
we
describe
role
impaired
on
dysfunction
based
state
art
knowledge.
Several
proposed
disease
mechanisms
discussed,
as
well
time
damage
potential
options.
Furthermore,
combine
data
from
longitudinal,
cross-sectional
retrospective
studies
observations
specialist
teams
treating
to
depict
course
over
time.
Based
current
insights,
majority
patients
do
not
exhibit
decline.
A
subset
often
early
onset
cerebral
cerebellar
volume
loss,
can
nevertheless
experience
worsening.
While
large
number
CG
suffer
anxiety
depression,
increased
complaints
about
memory
depression
at
older
age
likely
multifactorial
origin.
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: Feb. 21, 2024
Abstract
The
COVID-19
pandemic
caused
by
the
SARS-CoV-2
virus
has
greatly
affected
global
health.
Emerging
evidence
suggests
a
complex
interplay
between
Alzheimer’s
disease
(AD),
diabetes
(DM),
and
COVID-19.
Given
COVID-19’s
involvement
in
increased
risk
of
other
diseases,
there
is
an
urgent
need
to
identify
novel
targets
drugs
combat
these
interconnected
health
challenges.
Lysophosphatidic
acid
receptors
(LPARs),
belonging
G
protein-coupled
receptor
family,
have
been
implicated
various
pathological
conditions,
including
inflammation.
In
this
regard,
study
aimed
investigate
LPARs
(specifically
LPAR1,
3,
6)
tri-directional
relationship
AD,
DM,
through
network
analysis,
as
well
explore
therapeutic
potential
selected
anti-AD,
anti-DM
LPAR,
SPIKE
antagonists.
We
used
Coremine
Medical
database
genes
related
Furthermore,
STRING
analysis
was
interacting
partners
LPAR3,
LPAR6.
Additionally,
literature
search
revealed
78
on
market
or
clinical
studies
that
were
for
treating
either
AD
DM.
carried
out
docking
against
we
modeled
LPAR6
with
spike
protein
performed
LPAR-Spike
complex.
177
common
Protein–protein
demonstrated
LPAR
(1,3
&
efficiently
binds
viral
protein,
suggesting
them
infection.
anti-AD
LPARs,
LPARs-SPIKE
promising
candidates,
lupron,
neflamapimod,
nilotinib,
stating
importance
drug
repurposing
discovery
process.
These
exhibited
ability
bind
inhibit
activity
interfere
LPAR-SPIKE
interaction.
Through
combined
targeted-based
intervention
approach,
identified
several
could
be
repurposed
due
their
expected
interference
LPAR(1,
complexes.
addition,
it
can
also
hypothesized
co-administration
during
infection
may
not
only
help
mitigate
impact
but
potentially
contribute
prevention
management
post-COVID
complications
Communications Biology,
Journal Year:
2024,
Volume and Issue:
7(1)
Published: May 10, 2024
Abstract
Classical
metabolomic
and
new
metabolic
network
methods
were
used
to
study
the
developmental
features
of
autism
spectrum
disorder
(ASD)
in
newborns
(
n
=
205)
5-year-old
children
53).
Eighty
percent
impact
ASD
was
caused
by
14
shared
biochemical
pathways
that
led
decreased
anti-inflammatory
antioxidant
defenses,
increased
physiologic
stress
molecules
like
lactate,
glycerol,
cholesterol,
ceramides.
CIRCOS
plots
a
parameter,
$$\dot{{{\boldsymbol{V}}}}\!$$
V°
net
,
revealed
differences
both
kind
degree
connectivity.
Of
50
450
polar
lipid
metabolites
examined,
regulation
purine
most
changed.
Purine
hub
analysis
17-fold
reversal
typically
developing
children.
This
did
not
occur
ASD.
These
results
previously
unknown
phenotypes,
identified
states
correlation
network,
underscored
role
mitochondrial
functional
changes,
metabolism,
purinergic
signaling
disorder.
