Neurobiology of Disease,
Journal Year:
2024,
Volume and Issue:
196, P. 106505 - 106505
Published: April 19, 2024
Alzheimer's
and
Parkinson's
diseases
are
two
of
the
most
frequent
neurological
diseases.
The
clinical
features
AD
memory
decline
cognitive
dysfunction,
while
PD
mainly
manifests
as
motor
dysfunction
such
limb
tremors,
muscle
rigidity
abnormalities,
slow
gait.
Abnormalities
in
cholesterol,
sphingolipid,
glycerophospholipid
metabolism
have
been
demonstrated
to
directly
exacerbate
progression
by
stimulating
Aβ
deposition
tau
protein
tangles.
Indirectly,
abnormal
lipids
can
increase
burden
on
brain
vasculature,
induce
insulin
resistance,
affect
structure
neuronal
cell
membranes.
Abnormal
lipid
leads
through
inducing
accumulation
α-syn,
mitochondria
endoplasmic
reticulum,
ferroptosis.
Great
progress
has
made
targeting
abnormalities
for
treatment
recent
years,
like
metformin,
insulin,
peroxisome
proliferator-activated
receptors
(PPARs)
agonists,
monoclonal
antibodies
apolipoprotein
E
(ApoE).
This
review
comprehensively
summarizes
involvement
dysregulated
pathogenesis
PD,
application
Lipid
Monitoring,
emerging
regulatory
drug
targets.
A
better
understanding
lipidological
bases
may
pave
way
developing
effective
prevention
methods
neurodegenerative
disorders.
Lipids in Health and Disease,
Journal Year:
2025,
Volume and Issue:
24(1)
Published: Feb. 8, 2025
The
liver‒brain
axis
is
critical
in
neurodegenerative
diseases
(NDs),
with
lipid
metabolism
influencing
neuroinflammation
and
microglial
function.
A
systematic
investigation
of
the
genetic
relationship
between
abnormalities
ND,
namely,
Alzheimer's
disease
(AD),
Parkinson's
(PD),
multiple
sclerosis
(MS),
amyotrophic
lateral
(ALS),
lacking.
To
assess
potential
causal
links
ND
six
parameters,
two-sample
Mendelian
randomization
(MR)
was
used.
Large-scale
European
ancestry
GWAS
data
for
parameters
(AD,
ALS,
PD,
MS)
were
Genetic
variants
demonstrating
significant
correlations
(P
<
5
×
10-8)
identified
employed
as
instrumental
variables
(IVs)
after
proper
validation.
research
incorporated
UK
Biobank
genomic
to
examine
associations
parameters.
analysis
included
primary
MR,
sensitivity
analyses,
multivariable
which
considered
mediators.
MR
via
inverse-variance
weighted
method
revealed
effects
cholesterol
(CHOL,
OR
=
1.10,
95%
CI:
1.03-1.18,
P
4.23
10⁻3)
low-density
lipoprotein
(LDLC,
1.03-1.17,
3.28
on
risk
validated
across
methods.
Potential
observed
ApoB
ALS
inversely
correlated
AD,
whereas
no
found
PD
or
MS.
CHOL
LDLC
demonstrated
heterogeneity
pleiotropy,
supporting
their
reliability.
Higher
levels
associated
increased
risk,
suggesting
a
link,
hypothesis
ND.
Current
evidence
does
not
support
role
MS
etiology,
other
NDs
may
be
more
complex
warrants
further
investigation.
ACS Nano,
Journal Year:
2024,
Volume and Issue:
18(34), P. 23014 - 23031
Published: Aug. 15, 2024
Although
conventional
intervention
to
microglia
can
mitigate
neuroinflammation
in
the
short
term,
immune
disorders
by
peripheral
inflammatory
cells
infiltrate
continuously,
resulting
an
overactivated
microenvironment
of
Parkinson's
disease
(PD).
Here,
we
design
engineered
extracellular
vesicle-based
nanoformulations
(EVNs)
address
multiple
factors
for
management
PD.
Specifically,
EVN
is
developed
coating
CCR2-enriched
mesenchymal
stem
cell-derived
vesicles
(MSC
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(10), P. 1204 - 1204
Published: Sept. 25, 2024
Astrocytes
are
one
of
the
key
glial
types
central
nervous
system
(CNS),
accounting
for
over
20%
total
cells
in
brain.
Extensive
evidence
has
established
their
indispensable
functions
maintenance
CNS
homeostasis,
as
well
broad
involvement
neurological
conditions.
In
particular,
astrocytes
can
participate
various
neuroinflammatory
processes,
e.g.,
releasing
a
repertoire
cytokines
and
chemokines
or
specific
neurotrophic
factors,
which
result
both
beneficial
detrimental
effects.
It
become
increasingly
clear
that
such
astrocyte-mediated
neuroinflammation,
together
with
its
complex
crosstalk
other
immune
cells,
designates
neuronal
survival
functional
integrity
neurocircuits,
thus
critically
contributing
to
disease
onset
progression.
this
review,
we
focus
on
current
knowledge
responses
astrocytes,
summarizing
common
features
Moreover,
highlight
several
vital
questions
future
research
promise
novel
insights
into
diagnostic
therapeutic
strategies
against
those
debilitating
diseases.
Biomolecules,
Journal Year:
2025,
Volume and Issue:
15(2), P. 250 - 250
Published: Feb. 8, 2025
Many
studies
now
emphasize
the
intricate
relationship
between
lipid
metabolism
and
osteoarthritis
(OA),
a
leading
cause
of
disability.
This
narrative
review
examines
alterations
in
levels
phospholipids
(PLs)
sphingolipids
(SLs)
synovial
fluid
(SF),
plasma,
serum,
articular
tissues;
discusses
their
role
joint
lubrication,
inflammation,
cartilage
degradation;
describes
potential
as
diagnostic
markers
therapeutic
targets.
Key
findings
include
stage-dependent
elevated
specific
PLs
SLs
SF,
blood,
tissue
OA
patients,
implicating
them
possible
biomarkers
disease
severity
progression.
Studies
suggest
that
beyond
involvement
these
lipids
individual
species,
such
lysophosphatidylcholine
(LPC)
16:0,
lysophosphatidic
acid
(LPA),
ceramide-1-phosphate
(C1P),
sphingosine-1-phosphate
(S1P),
contribute
to
pain,
degradation
joints
through
various
signaling
pathways.
Cross-species
comparisons
dogs
mice
experience
similar
lipidomic
changes
during
humans,
rendering
valuable
models
for
studying
lipid-related
mechanisms.
SF
appear
originate
primarily
from
blood
capillaries
diffusion.
In
addition,
are
produced
locally
by
fibroblast-like
synoviocytes
(FLSs)
influenced
cytokines
growth
factors
regulate
biosynthesis
lubrication.
Emerging
research
has
identified
genes
UGCG
ESYT1
regulators
OA.
Further,
we
examine
suitability
targeting
PL
SL
pathways
treat
OA,
emphasizing
need
further
translate
into
clinical
applications.
