Antibodies,
Год журнала:
2023,
Номер
12(4), С. 81 - 81
Опубликована: Дек. 8, 2023
Neurodegenerative
diseases
(NDDs)
affect
millions
of
people
worldwide.
They
develop
due
to
the
pathological
accumulation
and
aggregation
various
misfolded
proteins,
axonal
synaptic
loss
dysfunction,
inflammation,
cytoskeletal
abnormalities,
defects
in
DNA
RNA,
neuronal
death.
This
leads
activation
immune
responses
release
antibodies
against
them.
Recently,
it
has
become
clear
that
autoantibodies
(Aabs)
can
contribute
demyelination,
loss,
brain
cognitive
dysfunction.
significantly
changed
understanding
participation
humoral
autoimmunity
neurodegenerative
disorders.
It
is
crucial
understand
how
neuroinflammation
involved
neurodegeneration,
aid
improving
diagnostic
therapeutic
value
Aabs
future.
review
aims
provide
data
on
system's
role
NDDs,
pathogenic
some
specific
molecules
associated
with
most
common
their
potential
as
biomarkers
for
monitoring
diagnosing
NDDs.
suggested
autoimmune
aspects
NDDs
will
facilitate
early
diagnosis
help
elucidate
previously
unknown
pathobiology
these
diseases.
Abstract
The
progressive
accumulation
of
α-synuclein
(α-Syn)
aggregates
is
believed
to
contribute
Parkinson’s
disease
(PD)
pathogenesis.
Nevertheless,
the
earliest
pre-degenerative
molecular,
functional,
neuroinflammatory
and
metabolic
changes
associated
with
α-Syn-pathology
deposition
still
need
be
disclosed
staged.
Here,
we
investigated
these
events
in
a
transgenic
mouse
model
early
prodromal
PD
expressing
C-terminally
truncated
human
(1-120
amino
acids)
α-Syn
under
guidance
rat
tyrosine
hydroxylase
(TH)
promoter
by
using
two-photon
confocal
microscopy,
functional
behavioural
studies,
longitudinal
Magnetic
Resonance
Imaging
(MRI)
Positron
Emission
Tomography
plus
Computed
(PET-CT)
followed
conventional
or
radiomic
analysis.
We
found
that
before
onset
frank
dopaminergic
striatal
fibres
deafferentation,
mice
exhibited
significant
alterations
synapse
homeostasis
connectivity,
accompanied
other
widespread
brain
changes.
In
particular,
observed
early,
transient
increase
Vesicular
Monoamine
Transporter
2
(VMAT2)
dopamine
transporter
(DAT),
turnover,
depolarization-dependent
release
loss
DAT
inhibition-related
facilitation.
These
occurred
absence
deficits
were
signs
stiffness
without
motility
impairment.
PET-CT
confirmed
but
binding
dorsal
striatum,
raise
neuroinflammation
marker
[18F]-VC701
as
corroborated
Ionized
calcium-binding
adaptor
molecule
1
(Iba1)
immunolabeling.
MRI
studies
evidenced
atrophy
volume
reduction
different
areas
mice.
Radiomic-based
analysis
[18F]-FDG-PET-CT
revealed
increasing
texture
supportive
throughout
brain.
Finally,
also
pathology
diffusion
non-catecholaminergic
neurons
motor
cortex.
Our
findings
indicate
drives
unexpected
molecular
connectivity
at
synapses
parallel
spreading,
neuroinflammation,
leading
explicit
nigrostriatal
deafferentation
Nanomaterials,
Год журнала:
2025,
Номер
15(10), С. 704 - 704
Опубликована: Май 8, 2025
Intrinsically
disordered
proteins
(IDPs),
such
as
tau,
beta-amyloid
(Aβ),
and
alpha-synuclein
(αSyn),
are
prone
to
misfolding,
resulting
in
pathological
aggregation
propagation
that
drive
neurodegenerative
diseases,
including
Alzheimer’s
disease
(AD),
frontotemporal
dementia
(FTD),
Parkinson’s
(PD).
Misfolded
IDPs
aggregate
into
oligomers
fibrils,
exacerbating
progression
by
disrupting
cellular
functions
the
central
nervous
system,
triggering
neuroinflammation
neurodegeneration.
Furthermore,
aggregated
exhibit
prion-like
behavior,
acting
seeds
released
extracellular
space,
taken
up
neighboring
cells,
have
a
propagating
pathology
across
different
regions
of
brain.
Conventional
inhibitors,
small
molecules,
peptides,
antibodies,
face
challenges
stability
blood–brain
barrier
penetration,
limiting
their
efficacy.
In
recent
years,
nanotechnology-based
strategies,
multifunctional
nanoplatforms
or
nanoparticles,
emerged
promising
tools
address
these
challenges.
These
leverage
tailored
designs
prevent
remodel
reduce
associated
neurotoxicity.
This
review
discusses
advances
designed
target
Aβ,
αSyn
aggregation,
with
focus
on
roles
reducing
We
examine
critical
aspects
nanoplatform
design,
choice
material
backbone
targeting
moieties,
which
influence
interactions
IDPs.
also
highlight
key
mechanisms
interaction
between
inhibit
redirect
cascade
towards
nontoxic,
off-pathway
species,
disrupt
fibrillar
structures
soluble
forms.
further
outline
future
directions
for
enhancing
IDP
clearance,
achieving
spatiotemporal
control,
improving
cell-specific
targeting.
nanomedicine
strategies
offer
compelling
paths
forward
developing
more
effective
targeted
therapies
diseases.
Antibodies,
Год журнала:
2023,
Номер
12(4), С. 81 - 81
Опубликована: Дек. 8, 2023
Neurodegenerative
diseases
(NDDs)
affect
millions
of
people
worldwide.
They
develop
due
to
the
pathological
accumulation
and
aggregation
various
misfolded
proteins,
axonal
synaptic
loss
dysfunction,
inflammation,
cytoskeletal
abnormalities,
defects
in
DNA
RNA,
neuronal
death.
This
leads
activation
immune
responses
release
antibodies
against
them.
Recently,
it
has
become
clear
that
autoantibodies
(Aabs)
can
contribute
demyelination,
loss,
brain
cognitive
dysfunction.
significantly
changed
understanding
participation
humoral
autoimmunity
neurodegenerative
disorders.
It
is
crucial
understand
how
neuroinflammation
involved
neurodegeneration,
aid
improving
diagnostic
therapeutic
value
Aabs
future.
review
aims
provide
data
on
system's
role
NDDs,
pathogenic
some
specific
molecules
associated
with
most
common
their
potential
as
biomarkers
for
monitoring
diagnosing
NDDs.
suggested
autoimmune
aspects
NDDs
will
facilitate
early
diagnosis
help
elucidate
previously
unknown
pathobiology
these
diseases.
