Journal of Cellular and Molecular Medicine,
Год журнала:
2024,
Номер
28(11)
Опубликована: Июнь 1, 2024
Abstract
Cyclin‐dependent
kinase
5
(Cdk5)
is
a
protein
expressed
in
postmitotic
neurons
the
central
nervous
system
(CNS).
Cdk5
activated
by
p35
and
p39
which
are
neuron
regulatory
subunits.
Cdk5/p35
complex
calpain
protease
to
form
has
neuroprotective
effect
regulating
synaptic
plasticity
memory
functions.
However,
exaggerated
implicated
different
types
of
neurodegenerative
diseases
including
Parkinson
disease
(PD).
Therefore,
modulation
signalling
may
mitigate
PD
neuropathology.
aim
present
review
was
discuss
critical
role
pathogenesis
PD,
how
inhibitors
effectual
management
PD.
In
conclusion,
overactivated
involved
development
neurodegeneration,
Cdk5/calpain
such
as
statins,
metformin,
fenofibrates
rosiglitazone
can
attenuate
progression
Journal of Cellular and Molecular Medicine,
Год журнала:
2024,
Номер
28(10)
Опубликована: Май 1, 2024
Parkinson's
disease
(PD)
is
a
neurodegenerative
disorder
of
the
brain
and
manifested
by
motor
non-motor
symptoms
because
degenerative
changes
in
dopaminergic
neurons
substantia
nigra.
PD
neuropathology
associated
with
mitochondrial
dysfunction,
oxidative
damage
apoptosis.
Thus,
modulation
apoptosis
growth
factors
could
be
novel
boulevard
management
PD.
Brain-derived
neurotrophic
factor
(BDNF)
its
receptor
tropomyosin
kinase
type
B
(TrkB)
are
chiefly
involved
neuropathology.
BDNF
promotes
survival
nigra
enhances
functional
activity
striatal
neurons.
Deficiency
TrkB
triggers
degeneration
accumulation
α-Syn
As
well,
BDNF/TrkB
signalling
reduced
early
phase
Targeting
specific
activators
may
attenuate
this
review
aimed
to
discuss
potential
role
against
In
conclusion,
decreased
linked
severity
long-term
complications.
Activation
Autophagy,
Год журнала:
2023,
Номер
20(2), С. 259 - 274
Опубликована: Сен. 15, 2023
Multiple
sclerosis
(MS)
is
a
chronic
progressive
demyelinating
disease
of
the
central
nervous
system
(CNS)
due
to
an
increase
abnormal
peripherally
auto-reactive
T
lymphocytes
which
elicit
autoimmunity.
The
main
pathophysiology
MS
myelin
sheath
damage
by
immune
cells
and
defect
in
generation
oligodendrocytes.
Macroautophagy/autophagy
critical
degradation
process
that
eliminates
dysfunctional
or
superfluous
cellular
components.
Autophagy
has
property
double-edged
sword
it
may
have
both
beneficial
detrimental
effects
on
neuropathology.
Therefore,
this
review
illustrates
protective
harmful
autophagy
with
regard
disease.
prevents
progression
reducing
oxidative
stress
inflammatory
disorders.
In
contrast,
over-activated
associated
neuropathology
case
use
inhibitors
alleviate
pathogenesis
MS.
Furthermore,
provokes
activation
different
supporting
play
intricate
role
functions
modulation
regulating
cell
proliferation
related
demyelination
remyelination.
enhances
remyelination
increasing
activity
oligodendrocytes,
astrocytes.
However,
induces
activating
microglia
cells.
conclusion,
specific
autophagic
activators
astrocytes,
dendritic
(DCs),
induce
against
Pharmacology Research & Perspectives,
Год журнала:
2023,
Номер
11(2)
Опубликована: Фев. 22, 2023
Parkinson's
disease
(PD)
is
the
second
most
frequent
neurodegenerative
brain
(NBD)
after
Alzheimer's
(AD).
Statins
are
common
lipid-lowering
agents
used
in
management
of
dyslipidemia
and
prevention
primary
secondary
cardiovascular
diseases
(CVD)
events.
In
addition,
there
a
controversial
point
regarding
role
serum
lipids
pathogenesis
PD.
this
bargain,
as
statins
reduce
cholesterol
so
they
affect
PD
neuropathology
bidirectional
ways
either
protective
or
harmful.
not
PD,
but
frequently
disorders
commonly
associated
with
elderly
population.
Therefore,
use
that
population
may
outcomes.
Concerning
potential
on
neuropathology,
conflicts
controversies
against
development
harmful
by
increasing
risk
for
review
aimed
to
clarify
precise
pros
cons
from
published
studies.
Many
studies
suggest
through
modulation
inflammatory
lysosomal
signaling
pathways.
Nevertheless,
other
observations
statin
therapy
increase
diverse
mechanisms
including
reduction
CoQ10.
conclusion,
strong
neuropathology.
retrospective
prospective
necessary
regard.
Cellular and Molecular Neurobiology,
Год журнала:
2023,
Номер
43(6), С. 2743 - 2759
Опубликована: Апрель 19, 2023
Abstract
Parkinson’s
disease
(PD)
is
one
of
the
most
common
degenerative
brain
disorders
caused
by
loss
dopaminergic
neurons
in
substantia
nigra
(SN).
Lewy
bodies
and
-synuclein
accumulation
SN
are
hallmarks
neuropathology
PD.
Due
to
lifestyle
changes
prolonged
L-dopa
administration,
patients
with
PD
frequently
have
vitamin
deficiencies,
especially
folate,
B6,
B12.
These
augment
circulating
levels
Homocysteine
development
hyperhomocysteinemia,
which
may
contribute
pathogenesis
Therefore,
this
review
aimed
ascertain
if
hyperhomocysteinemia
play
a
part
oxidative
inflammatory
signaling
pathways
that
development.
Hyperhomocysteinemia
implicated
neurodegenerative
disorders,
including
triggers
progression
different
mechanisms,
stress,
mitochondrial
dysfunction,
apoptosis,
endothelial
dysfunction.
Particularly,
linked
high
systemic
disorders.
induces
immune
activation
stress.
In
turn,
activated
response
promotes
hyperhomocysteinemia.
hyperhomocysteinemia-induced
immunoinflammatory
abnormal
aggravate
PD,
leading
more
severity.
Also,
like
nuclear
factor
kappa
B
(NF-κB)
nod-like
receptor
pyrin
3
(NLRP3)
inflammasome
other
intricate
conclusion,
involved
either
directly
via
induction
degeneration
or
indirectly
pathways.
Diabetology & Metabolic Syndrome,
Год журнала:
2023,
Номер
15(1)
Опубликована: Май 13, 2023
Abstract
Human
Islet
amyloid
polypeptide
(hIAPP)
from
pancreatic
β
cells
in
the
islet
of
Langerhans
has
different
physiological
functions
including
inhibiting
release
insulin
and
glucagon.
Type
2
diabetes
mellitus
(T2DM)
is
an
endocrine
disorder
due
to
relative
insufficiency
resistance
(IR)
associated
with
increased
circulating
hIAPP.
Remarkably,
hIAPP
structural
similarity
beta
(Aβ)
can
engage
pathogenesis
T2DM
Alzheimer’s
disease
(AD).
Therefore,
present
review
aimed
elucidate
how
acts
as
a
link
between
AD.
IR,
aging
low
cell
mass
increase
expression
which
binds
membrane
leading
aberrant
Ca
2+
activation
proteolytic
enzymes
series
events
causing
loss
cells.
Peripheral
plays
major
role
AD,
high
level
AD
risk
patients.
However,
there
no
hard
evidence
for
brain-derived
Nevertheless,
oxidative
stress,
mitochondrial
dysfunction,
chaperon-mediated
autophagy,
heparan
sulfate
proteoglycan
(HSPG),
immune
response,
zinc
homeostasis
could
be
possible
mechanisms
induction
aggregation
risk.
In
conclusion,
increasing
levels
patients
predispose
them
development
progression
Dipeptidyl
peptidase
4
(DPP4)
inhibitors
glucagon-like
peptide-1
(GLP-1)
agonists
attenuate
by
deposition
hIAP.
