Medicinal Research Reviews,
Journal Year:
2024,
Volume and Issue:
44(5), P. 2078 - 2111
Published: March 26, 2024
Abstract
As
the
world
population
ages,
there
will
be
an
increasing
need
for
effective
therapies
aging‐associated
neurodegenerative
disorders,
which
remain
untreatable.
Dementia
due
to
Alzheimer's
disease
(AD)
is
one
of
leading
neurological
diseases
in
aging
population.
Current
therapeutic
approaches
treat
this
disorder
are
solely
symptomatic,
making
new
molecular
entities
acting
on
causes
extremely
urgent.
One
potential
solutions
use
compounds
that
already
market.
The
structures
have
known
pharmacokinetics,
pharmacodynamics,
toxicity
profiles,
and
patient
data
available
several
countries.
Several
drugs
been
used
successfully
different
from
their
original
purposes,
such
as
autoimmunity
peripheral
inflammation.
Herein,
we
divulge
repurposing
area
diseases,
focusing
antineoplastics
dementia
AD
dementia.
We
briefly
touch
upon
shared
pathological
mechanism
between
cancer
drug
strategies,
with
a
focus
artificial
intelligence.
Next,
bring
out
current
status
research
development
drugs,
provide
supporting
evidence
retrospective,
clinical,
preclinical
studies
antineoplastic
use,
areas,
prion‐like
spreading
pathologies
treating
AD.
Neural Regeneration Research,
Journal Year:
2023,
Volume and Issue:
19(4), P. 800 - 806
Published: Sept. 4, 2023
The
onset
of
amyotrophic
lateral
sclerosis
is
usually
characterized
by
focal
death
both
upper
and/or
lower
motor
neurons
occurring
in
the
cortex,
basal
ganglia,
brainstem,
and
spinal
cord,
commonly
involves
muscles
extremities,
bulbar
respiratory
regions.
However,
as
disease
progresses,
it
affects
adjacent
body
regions,
leading
to
generalized
muscle
weakness,
occasionally
along
with
memory,
cognitive,
behavioral,
language
impairments;
dysfunction
occurs
at
final
stage
disease.
has
a
complicated
pathophysiology
currently,
only
riluzole,
edaravone,
phenylbutyrate/taurursodiol
are
licensed
treat
many
industrialized
countries.
TAR
DNA-binding
protein
43
inclusions
observed
97%
those
diagnosed
sclerosis.
This
review
provides
preliminary
overview
potential
effects
pathogenesis
sclerosis,
including
abnormalities
nucleoplasmic
transport,
RNA
function,
post-translational
modification,
liquid-liquid
phase
separation,
stress
granules,
mitochondrial
dysfunction,
oxidative
stress,
axonal
quality
control
system,
non-cellular
autonomous
functions
(e.g.,
glial
cell
prion-like
propagation).
Hormone and Metabolic Research,
Journal Year:
2024,
Volume and Issue:
56(07), P. 482 - 488
Published: Feb. 13, 2024
Abstract
Alzheimer’s
disease
(AD)
is
a
widespread
neurodegenerative
disorder
characterized
by
progressive
memory
and
cognitive
decline,
posing
formidable
public
health
challenge.
This
review
explores
the
intricate
interplay
between
two
pivotal
players
in
AD
pathogenesis:
β-amyloid
(Aβ)
tau
protein.
While
amyloid
cascade
theory
has
long
dominated
research,
recent
developments
have
ignited
debates
about
its
centrality.
Aβ
plaques
NFTs
are
hallmark
pathologies
AD.
Aducanumab
lecanemab,
monoclonal
antibodies
targeting
Aβ,
been
approved,
albeit
amidst
controversy,
raising
questions
therapeutic
efficacy
of
Aβ-focused
interventions.
On
other
hand,
tau,
specifically
hyperphosphorylation,
disrupts
microtubule
stability
contributes
to
neuronal
dysfunction.
Various
post-translational
modifications
drive
aggregation
into
NFTs.
Emerging
treatments
such
as
GSK-3β
CDK5
inhibitors,
shown
promise
preclinical
clinical
studies.
Restoring
equilibrium
protein
kinases
phosphatases,
notably
phosphatase-2A
(PP2A),
promising
avenue
for
therapy,
primarily
regulated
phosphorylation
state.
Activation
tau-specific
phosphatases
offers
potential
mitigating
pathology.
The
evolving
landscape
drug
development
emphasizes
tau-centric
therapies
reevaluation
hypothesis.
Additionally,
exploring
role
neuroinflammation
interaction
with
pathology
present
research
directions.
EMBO Reports,
Journal Year:
2024,
Volume and Issue:
25(2), P. 745 - 769
Published: Jan. 17, 2024
Abstract
Pho85
is
a
multifunctional
CDK
that
signals
to
the
cell
when
environmental
conditions
are
favorable.
It
has
been
connected
cycle
control,
mainly
in
Start
where
it
promotes
G1/S
transition.
Here
we
describe
repressor
Whi7
key
target
of
regulation
entry.
The
phosphorylation
by
inhibits
and
explains
most
contribution
activation
Start.
Mechanistically,
downregulates
protein
levels
through
control
stability
WHI7
gene
transcription.
also
restrains
intrinsic
ability
associate
with
promoters.
Furthermore,
although
Whi5
main
normal
cycling
cells,
absence
Pho85,
becomes
major
leading
G1
arrest.
Overall,
our
results
reveal
novel
mechanism
which
at
multiple
levels,
may
confer
functional
specialization
connect
response
adverse
control.
Journal of Advanced Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Feb. 1, 2024
One
of
the
hallmarks
Parkinsońs
Disease
(PD)
is
oxidative
distress,
leading
to
mitochondrial
dysfunction
and
neurodegeneration.
Insulin-like
growth
factor
II
(IGF-II)
has
been
proven
have
antioxidant
neuroprotective
effects
in
some
neurodegenerative
diseases,
including
PD.
Consequently,
there
growing
interest
understanding
different
mechanisms
involved
effect
this
hormone.
To
clarify
mechanism
action
IGF-II
protective
The
present
study
was
carried
out
on
a
cellular
model
PD
based
incubation
dopaminergic
cells
(SN4741)
culture
with
toxic
1-methyl-4-phenylpyridinium
(MPP+),
presence
IGF-II.
This
undertakes
proteomic
analyses
order
understand
which
molecular
cell
pathways
might
be
most
important
proteins
found
were
tested
by
Western
blot,
colorimetric
enzymatic
activity
assay
immunocytochemistry.
Along
study,
morphology
function
also
studied
transmission
electron
microscopy
oxygen
consumption
rate.
cycle
analysed
using
7AAd/BrdU
staining,
flow
cytometry.
results
obtained
indicate
that
MPP+,
MPP++IGF-II
treatment
IGF-II,
when
compared
control,
modified
expression
197,
246
207
respectively.
Some
these
structure
function,
regulation.
Including
medium
prevents
damage
induced
recovering
dysregulation,
thereby
decreasing
apoptosis.
improves
dynamics
promoting
association
Mitofilin
mitochondria,
regaining
redox
homeostasis.
It
rebalances
cycle,
reducing
amount
apoptosis
death
regulation
transcription
factors,
such
as
Checkpoint
kinase
1.
