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.
Journal of Neuroscience Research,
Год журнала:
2024,
Номер
102(2)
Опубликована: Фев. 1, 2024
Abstract
Synapses
serve
as
the
points
of
communication
between
neurons,
consisting
primarily
three
components:
presynaptic
membrane,
synaptic
cleft,
and
postsynaptic
membrane.
They
transmit
signals
through
release
reception
neurotransmitters.
Synaptic
plasticity,
ability
synapses
to
undergo
structural
functional
changes,
is
influenced
by
proteins
such
growth‐associated
proteins,
vesicle
density
neurotrophic
growth
factors.
Furthermore,
maintaining
plasticity
consumes
more
than
half
brain's
energy,
with
a
significant
portion
this
energy
originating
from
ATP
generated
mitochondrial
metabolism.
Consequently,
quantity,
distribution,
transport,
function
mitochondria
impact
stability
brain
metabolism,
thereby
participating
in
regulation
fundamental
processes
including
neuronal
differentiation,
neurite
outgrowth,
synapse
formation,
neurotransmitter
release.
This
article
provides
comprehensive
overview
associated
common
factors
two,
well
relationship
metabolism
plasticity.
Journal of the Neurological Sciences,
Год журнала:
2023,
Номер
451, С. 120730 - 120730
Опубликована: Июль 11, 2023
Parkinson's
disease
(PD),
the
most
common
neurological
motor
system
disorder,
which
characterised
by
irreversible
loss
of
dopaminergic
neurones
in
substantia
nigra
pars
compacta,
and
leads
to
deficiency
dopamine
striatum.
Deposited
Lewy
bodies
(LBs)
diseased
nerve
terminals
are
pathological
hallmark
PD,
alpha-synuclein
(α-Syn)
is
prominent
protein
LBs.
The
tight
association
between
α-Syn
molecular
pathology
PD
has
generatly
increaed
interest
using
species
as
biomarkers
diagnose
early
PD.
not
confined
central
nervous
system,
it
also
present
peripheral
tissues,
such
human
skin.
assessment
skin
potential
be
a
diagnostic
method
that
only
excellent
sensitivity,
specificity,
reproducibility,
but
convenient
acceptable
patients.
In
this
review,
we
(i)
integrate
biochemical,
aggregation
structural
features
α-Syn;
(ii)
map
distribution
brain,
biological
fluids,
tissues;
(iii)
critical
comparative
analysis
previous
studies
have
measured
Finally,
provide
an
outlook
on
future
biopsy
approach
for
highlight
its
implications
clinical
trials,
decision-making,
treatment
strategies
well
development
new
therapies.
Protein
regions
which
are
intrinsically
disordered,
exist
as
an
ensemble
of
rapidly
interconverting
structures.
Cooling
proteins
to
cryogenic
temperatures
for
dynamic
nuclear
polarization
(DNP)
magic
angle
spinning
(MAS)
NMR
studies
suspends
most
the
motions,
resulting
in
peaks
that
broad
but
not
featureless.
To
demonstrate
detailed
conformational
restraints
can
be
retrieved
from
peak
shapes
frozen
alone,
we
developed
and
used
a
simulation
framework
assign
features
conformers
ensemble.
We
validated
our
simulations
by
comparing
them
spectra
α-synuclein
acquired
under
different
experimental
conditions.
Our
assignments
discrete
dihedral
populations
suggest
structural
constraints
attainable
The
ability
infer
has
important
implications
DNP
MAS
with
disorder
living
cells
because
chemical
shifts
accessible
measured
parameter.
Current Issues in Molecular Biology,
Год журнала:
2025,
Номер
47(4), С. 259 - 259
Опубликована: Апрель 8, 2025
Chronic
pain,
defined
by
persistent
pain
beyond
normal
healing
time,
is
a
pervasive
and
debilitating
condition
affecting
up
to
30–50%
of
adults
globally.
In
parallel,
neurodegenerative
diseases
(NDs)
such
as
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
amyotrophic
lateral
sclerosis
(ALS)
are
characterized
progressive
neuronal
loss
cognitive
or
motor
decline,
often
underpinned
pathological
protein
misfolding
aggregation.
Emerging
evidence
suggests
potential
mechanistic
link
between
chronic
NDs,
with
contributing
neuroinflammatory
states
homeostasis
disturbances
that
mirror
processes
in
neurodegeneration.
This
review
explores
the
hypothesis
aggregation
serve
bridge
We
systematically
examine
molecular
pathways
misfolding,
proteostasis
dysfunction
shared
neuroimmune
mechanisms,
highlighting
prion-like
propagation
misfolded
proteins,
neuroinflammation,
oxidative
stress
common
denominators.
further
discuss
from
experimental
models
clinical
studies
linking
accelerated
pathology—including
tau
accumulation,
amyloid
dysregulation,
microglial
activation—and
consider
how
these
insights
open
avenues
for
novel
therapeutics.
Targeting
aggregation,
enhancing
chaperone
function,
modulating
unfolded
response
(UPR),
attenuating
glial
activation
explored
strategies
mitigate
possibly
slow
Understanding
this
intersection
not
only
elucidates
pain’s
role
decline
but
also
interventions
addressing
inflammation
could
yield
dual
benefits
management
modification.
Molecular Medicine,
Год журнала:
2025,
Номер
31(1)
Опубликована: Апрель 26, 2025
Abstract
The
irreversible
degeneration
of
dopamine
neurons
induced
by
α-synuclein
(α-syn)
aggregation
in
the
substantia
nigra
is
central
pathological
feature
Parkinson's
disease
(PD).
Neuroimaging
and
autopsy
studies
consistently
confirm
significant
iron
accumulation
brain
PD
patients,
suggesting
a
critical
role
for
progression.
Current
research
has
established
that
overload
induces
ferroptosis
dopaminergic
neurons,
evidence
indicates
impact
on
pathology
extends
beyond
ferroptosis.
Iron
also
plays
regulatory
modulating
α-syn,
affecting
its
aggregation,
spatial
conformation,
post-translational
modifications,
mRNA
stability.
Iron-induced
α-syn
can
contribute
to
neurodegeneration
through
additional
mechanisms,
potentially
creating
feedback
loop
which
further
enhances
accumulation,
thus
perpetuating
vicious
cycle
neurotoxicity.
Given
α-syn’s
intrinsically
disordered
structure,
targeting
metabolism
presents
promising
therapeutic
strategy
PD.
Therefore,
development
chelators,
alone
or
combination
with
other
drugs,
may
offer
beneficial
approach
alleviating
symptoms
slowing
Nature Communications,
Год журнала:
2025,
Номер
16(1)
Опубликована: Май 1, 2025
Neurotransmitter
release
occurs
through
exocytosis
of
synaptic
vesicles.
α-Synuclein's
function
and
dysfunction
in
Parkinson's
disease
other
synucleinopathies
is
thought
to
be
tightly
linked
vesicle
binding.
Age
the
biggest
risk
factor
for
synucleinopathy,
~15%
proteins
have
been
central
nervous
system
diseases.
Yet,
age-
disease-induced
changes
vesicles
remain
unexplored.
Via
systematic
analysis
at
ultrastructural,
protein,
lipid
levels,
we
reveal
specific
populations,
proteins,
lipids
over
age
wild-type
mice
α-synuclein
knockout
with
without
expression
human
α-synuclein.
Strikingly,
find
several
previously
undescribed
lacking
α-synuclein,
suggesting
that
loss
contributes
dysfunction.
These
findings
not
only
provide
insights
into
biology
mechanisms
but
also
serve
as
a
baseline
further
mechanistic
exploration
disease-related
alterations
