Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 4
Published: Dec. 22, 2024
ALSUntangled
reviews
alternate
and
off-label
treatments
prompted
by
patient
interest.
Here,
we
review
psilocybin,
a
chemical
derived
from
mushrooms
belonging
in
the
category
of
drugs
known
as
psychedelics.
Psilocybin
has
plausible
mechanisms
for
slowing
ALS
progression
because
its
ability
to
cross
blood
brain
barrier
effect
neurogenesis
inflammation.
Currently,
there
are
no
pre-clinical
models,
case
reports,
or
trials
psilocybin
context
disease
modifying
therapy.
Depending
on
dosing,
can
be
high
risk
psychological
side
effects
including
hallucinations
physical
harm.
Based
above
information,
do
not
currently
support
use
means
slow
progression.
International Journal of Biological Macromolecules,
Journal Year:
2024,
Volume and Issue:
280, P. 135826 - 135826
Published: Sept. 23, 2024
Neurodegenerative
diseases
(NDDs)
are
increasingly
prevalent
with
global
aging,
demanding
effective
treatments.
Exosomes,
which
contain
biological
macromolecules
such
as
RNA
(including
miRNAs)
and
proteins
like
α-synuclein,
tau,
amyloid-beta,
gaining
attention
innovative
therapeutics.
This
comprehensive
review
systematically
explores
the
potential
roles
of
exosomes
in
NDDs,
a
particular
focus
on
their
role
synaptic
dysfunction.
We
present
pathophysiology
NDDs
discuss
mechanisms
exosome
formation,
secretion,
action.
Subsequently,
we
different
types
Alzheimer's
disease
Parkinson's
disease,
special
regulation
function.
In
addition,
explore
use
biomarkers,
well
challenges
opportunities
clinical
application.
provide
perspectives
future
research
directions
development
trends
to
more
understanding
guidance
for
application
treatment
NDDs.
conclusion,
rich
macromolecules,
novel
therapeutic
strategy,
have
opened
up
new
possibilities
brought
hope
patients.
Chronobiology International,
Journal Year:
2023,
Volume and Issue:
40(10), P. 1395 - 1403
Published: Oct. 2, 2023
ABSTRACTChronobiology,
which
studies
biological
rhythms
and
their
impacts
on
health,
presents
a
potential
avenue
for
treating
amyotrophic
lateral
sclerosis.
Clock
gene-related
therapies,
focusing
genes
responsible
regulating
rhythms,
may
hold
promise
in
the
treatment.
Among
these
clock
genes,
nuclear
receptor
subfamily
1
Group
D
member
(NR1D1)
plays
vital
role
neurodegenerative
diseases.
In
this
particular
study,
it
was
aimed
to
investigate
of
FDA-approved
drugs
commonly
used
sclerosis
treatment
melatonin,
hormone
known
its
sleep-wake
cycles,
as
ligands
therapy.
The
were
subjected
molecular
docking
dynamics
simulation
methods
against
NR1D1
gene.
These
results
suggested
that
combining
melatonin
with
medications
might
yield
positive
outcomes.
This
study
provides
preliminary
data
lays
groundwork
future
investigations
involving
vitro
(laboratory-based)
vivo
(animal
or
human-based)
research
chronotherapy.
summary,
highlights
therapy
utilizing
conjunction
treatment,
offering
insights
into
novel
strategies.
findings
underscore
need
further
explore
effectiveness
hypothetical
approach
experimental
clinical
settings.KEYWORDS:
Amyotrophic
sclerosisNR1D1melatoninmolecular
dockingmolecular
dynamicschronotherapy
Disclosure
statementNo
conflict
interest
reported
by
author(s).Data
availability
statementAll
are
available
tables
figures
manuscript
http://dx.doi.org/10.1080/07420528.2023.226547.Additional
informationFundingThe
author(s)
there
is
no
funding
associated
work
featured
article.
Frontiers in Neurology,
Journal Year:
2024,
Volume and Issue:
15
Published: May 3, 2024
Introduction
The
pathogenesis
of
amyotrophic
lateral
sclerosis
(ALS),
a
fatal
neurodegenerative
disease
caused
by
the
demise
motor
neurons
has
been
linked
to
excitotoxicity
excessive
calcium
influx
via
N-methyl-D-aspartate
receptors
(NMDARs),
suggesting
that
uncompetitive
NMDAR
antagonism
could
be
strategy
attenuate
neuron
degeneration.
REL-1017,
dextro-isomer
racemic
methadone,
is
low-affinity
antagonist.
Importantly,
in
humans
REL-1017
shown
excellent
tolerability
clinical
trials
for
major
depression.
Methods
Here,
we
tested
if
improves
phenotypes
G93A
SOD1
mouse,
well-established
model
familial
ALS,
examining
survival
and
functions,
as
well
expression
genes
proteins
involved
neuroplasticity.
Results
We
found
sex-dependent
effect
mice.
A
delay
ALS
symptom
onset,
assessed
10%-decrease
body
weight
(
p
<
0.01
vs.
control
untreated
mice)
an
extension
lifespan
0.001
was
observed
male
Female
mice
treated
with
showed
improvement
muscle
strength
mice).
Both
males
females
decrease
hind
limb
clasping.
Sex-dependent
effects
were
also
detected
molecular
markers
neuronal
plasticity
(PSD95
SYN1)
spinal
cord
GluN1
subunit
quadricep
muscles.
Conclusion
In
conclusion,
this
study
provides
preclinical
vivo
evidence
supporting
evaluation
ALS.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(13), P. 7059 - 7059
Published: June 27, 2024
Amyotrophic
lateral
sclerosis
(ALS)
is
an
extremely
complex
neurodegenerative
disease
involving
different
cell
types,
but
motoneuronal
loss
represents
its
main
pathological
feature.
Moreover,
compensatory
plastic
changes
taking
place
in
parallel
to
neurodegeneration
are
likely
affect
the
timing
of
ALS
onset
and
progression
and,
interestingly,
they
might
represent
a
promising
target
for
disease-modifying
treatments.
Therefore,
simplified
animal
model
mimicking
without
other
aspects
has
been
established
by
means
intramuscular
injection
cholera
toxin-B
saporin
(CTB-Sap),
which
targeted
neurotoxin
able
kill
motoneurons
retrograde
suicide
transport.
Previous
studies
employing
mouse
CTB-Sap
have
proven
that
spontaneous
motor
recovery
possible
after
subtotal
removal
spinal
pool.
Although
these
kinds
not
enough
counteract
functional
effects
progressive
motoneuron
degeneration,
it
would
nevertheless
treatments
aiming
postpone
and/or
delay
progression.
Herein,
used
test
efficacy
mitochondrial
division
inhibitor
1
(Mdivi-1)
as
tool
toxicity
promote
neuroplasticity.
The
homeostasis
fission/fusion
dynamics
indeed
important
integrity,
could
be
affected
during
neurodegeneration.
Lesioned
mice
were
treated
with
Mdivi-1
then
examined
series
behavioral
histological
analyses.
results
shown
drug
may
capable
reducing
deficits
lesion
promoting
synaptic
plasticity
neuroprotection,
thus
representing
putative
translational
approach
disorders.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: March 24, 2023
Summary
Cytoplasmic
mislocalization
and
aggregation
of
the
RNA-binding
protein
TDP-43
is
a
pathological
hallmark
motor
neuron
(MN)
disease
amyotrophic
lateral
sclerosis
(ALS).
Furthermore,
while
mutations
in
TARDBP
gene
(encoding
TDP-43)
have
been
associated
with
ALS,
pathogenic
consequences
these
remain
poorly
understood.
Using
CRISPR/Cas9,
we
engineered
two
homozygous
knock-in
iPSC
lines
carrying
encoding
A382T
G348C
,
common
yet
understudied
ALS
variants.
MNs
differentiated
from
iPSCs
had
normal
viability
displayed
no
significant
changes
subcellular
localization,
phosphorylation,
solubility,
or
compared
isogenic
control
MNs.
However,
our
results
highlight
synaptic
impairments
both
MN
cultures,
as
reflected
synapse
abnormalities
alterations
spontaneous
neuronal
activity.
Collectively,
findings
suggest
that
dysfunction
may
precede
occurrence
pathology
neurodegeneration
further
implicate
excitability
defects
pathobiology
this
disease.
Neurology Clinical Practice,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Dec. 11, 2024
Amyotrophic
lateral
sclerosis
(ALS)
is
a
neurodegenerative
disease
leading
to
the
loss
of
motor
function
and
muscle
strength.
Nonpharmacologic
neuromodulative
therapeutic
approaches
such
as
active
exercise
may
contribute
preserve
functions
in
ALS,
but
this
hypothesis
remains
debated.
The
present
meta-analysis
first
aimed
evaluate
effect
on
strength
preservation.
Moreover,
since
responsiveness
induced
neuroplasticity
patients
with
ALS
being
discussed,
second
objective
was
review
analogous
effects
noninvasive
brain
stimulation
(NIBS).
Following
PRISMA
guidelines,
we
systematically
reviewed
PubMed,
CENTRAL,
NIH
PMC,
PEDro,
ScienceDirect,
Web
Science
databases
from
period
between
January
10
July
1,
2023.
Criteria
limited
inclusion
randomized
controlled
trials
comparing
(aerobic
or
resistance)
usual
care
NIBS
sham.
primary
outcome
assessed
based
functional
assessment
scores
reported
validated
clinical
scales,
secondary
analysis
included
neurophysiologic
changes.
Methodologic
quality
selected
studies
using
Physiotherapy
Evidence-Based
(PEDro)
scale.
Relative
risk
(RR)
heterogeneity
(I2)
were
calculated
Revman
software,
evidence
estimated
by
GRADE
Thirteen
included.
Analysis
involved
393
among
whom
164
underwent
155
received
care,
41
33
sham
stimulations.
nature
consistent
across
varied
frequency.
parameters
for
sites
session
Function
significantly
preserved
5
9
2
4
trials.
Meta-analysis
scales
indicated
moderate
effectiveness
exercises
(RR
=
0.61
[0.18,
1.04]
I2
69%)
compared
very
low
-1.41
[-0.44,
3.26]
89%).
Only
1
study
revealed
neuroplastic
changes
brain.
Active
likely
slows
need
further
investigation
support
their
neuroprotective
effectiveness.
both
interventions
require
elucidate
neuroplasticity.
This
has
been
registered
PROSPERO
(CRD42023408121).
