Journal of Food Biochemistry,
Год журнала:
2022,
Номер
46(12)
Опубликована: Сен. 15, 2022
Neurodegenerative
disorders
(NDs)
are
a
cluster
of
progressive,
severe,
and
disabling
that
affect
millions
people
worldwide
on
the
surge.
These
characterized
by
gradual
loss
selectively
vulnerable
group
neurons.
Due
to
complex
pathophysiological
mechanisms
behind
neurodegeneration
despite
enormous
efforts
understanding
occurrence
progression
NDs,
there
is
still
lack
an
effective
treatment
for
such
diseases.
Therefore,
development
new
therapeutic
strategy
NDs
unmet
clinical
need.
Various
natural
compounds
extracted
from
medicinal
plants
or
fruits
have
shown
promising
activities
in
treating
different
types
targeting
multiple
signaling
pathways.
Among
entities,
flavonoids
incited
rise
public
scientific
interest
recent
years
because
their
purported
health-promoting
effects.
Dietary
supplementation
has
been
mitigate
severity
as
Parkinson's
disease
(PD),
Alzheimer's
(AD),
dementia
antioxidant
Naringenin
citrus
flavonoid
known
possess
numerous
biological
like
antioxidant,
anti-proliferative,
anti-inflammatory
activities.
naringenin
emerged
potential
agent
exerts
preventive
curative
effects
several
neurological
disorders.
Increasing
evidence
attained
special
attention
variety
targets
along
with
pathways
naringenin,
which
suggest
its
possible
applications
NDs.
Derived
results
pre-clinical
research
considering
this
compound,
review
focuses
role
pharmacological
management
disease.
The
overall
neuroprotective
underlying
related
discussed.
In
light
substantial
naringenin's
efficacy
experimental
paradigms,
suggests
molecule
should
be
investigated
further
viable
candidate
disease,
emphasis
mechanistic
trials
determine
efficacy.
Practical
flavanone,
aglycone
Naringin,
predominantly
found
actions.
exhibit
remarkable
diseases
various
heart,
liver,
metabolic
Similarly,
it
neurodegenerative
illnesses.
enables
us
better
understand
naringenin.
Also,
provides
indication
manage
symptoms
AD
PD.
Furthermore,
will
useful
field
medicine
active
ingredient
Frontiers in Aging Neuroscience,
Год журнала:
2021,
Номер
13
Опубликована: Июль 13, 2021
The
elderly
population
is
growing
worldwide,
with
important
health
and
socioeconomic
implications.
Clinical
experimental
studies
on
aging
have
uncovered
numerous
changes
in
the
brain,
such
as
decreased
neurogenesis,
increased
synaptic
defects,
greater
metabolic
stress,
enhanced
inflammation.
These
are
associated
cognitive
decline
neurobehavioral
deficits.
Although
not
a
disease,
it
significant
risk
factor
for
functional
worsening,
affective
impairment,
disease
exaggeration,
dementia,
general
susceptibility.
Conversely,
life
events
related
to
mental
stress
trauma
can
also
lead
accelerated
age-associated
disorders
dementia.
Here,
we
review
human
mice
rats,
those
modeling
neurodegenerative
diseases,
that
helped
elucidate
(1)
dynamics
mechanisms
underlying
biological
pathological
of
main
projecting
systems
brain
(glutamatergic,
cholinergic,
dopaminergic)
(2)
effect
defective
glutamatergic,
dopaminergic
projection
disabilities
disorders,
Alzheimer’s
Parkinson’s
diseases.
Detailed
knowledge
age-related
diseases
be
an
element
development
effective
ways
treatment.
In
this
context,
briefly
analyze
which
adverse
glutaminergic
could
targeted
by
therapeutic
strategies
developed
result
our
better
understanding
these
damaging
mechanisms.
World Journal of Psychiatry,
Год журнала:
2022,
Номер
12(1), С. 77 - 97
Опубликована: Янв. 17, 2022
Major
depressive
disorder
is
a
debilitating
affecting
millions
of
people
each
year.
Brain-derived
neurotrophic
factor
(BDNF)
and
inflammation
are
two
prominent
biologic
risk
factors
in
the
pathogenesis
depression
that
have
received
considerable
attention.
Many
clinical
animal
studies
highlighted
associations
between
low
levels
BDNF
or
high
inflammatory
markers
development
behavioral
symptoms
depression.
However,
less
known
about
potential
interaction
inflammation,
particularly
within
central
nervous
system.
Emerging
evidence
suggests
there
bidirectional
regulation
these
with
important
implications
for
anti-depressant
response.
Elevated
mediators
been
shown
to
reduce
expression
BDNF,
may
play
an
negative
regulatory
role
on
brain.
Understanding
this
more
fully
context
neuropsychiatric
disease
both
developing
fuller
understanding
biological
identifying
novel
therapeutic
opportunities.
Here
we
review
particular
focus
pathogenic
their
interaction.
FEBS Letters,
Год журнала:
2022,
Номер
596(9), С. 1095 - 1110
Опубликована: Янв. 28, 2022
Mitochondria
are
associated
with
various
cellular
activities
critical
to
homeostasis,
particularly
in
the
nervous
system.
The
plastic
architecture
of
mitochondrial
network
and
its
dynamic
structure
play
crucial
roles
ensuring
that
varying
energetic
demands
rapidly
met
maintain
neuronal
axonal
energy
homeostasis.
Recent
evidence
associates
aging
neurodegeneration
anomalous
metabolism
as
age‐dependent
alterations
now
believed
occur
prior
neurodegeneration.
brain
has
a
high
demand,
which
makes
it
sensitive
dysfunction.
Distinct
events
causing
oxidative
stress
or
disruption
homeostasis
can
trigger
neuropathology.
This
review
explores
bioenergetic
hypothesis
for
neurodegenerative
pathomechanisms,
discussing
factors
leading
age‐related
hypometabolism
contribution
cognitive
decline.
research
on
healthy
system
cells,
response
stress,
how
is
affected
by
pathology,
well
current
contributions
novel
therapeutic
approaches
will
be
highlighted.
Nutrients,
Год журнала:
2023,
Номер
15(4), С. 972 - 972
Опубликована: Фев. 15, 2023
It
has
been
reported
that
disordered
Cu
metabolism
is
associated
with
several
neurodegenerative
diseases,
including
Alzheimer's
disease
(AD)
and
Parkinson's
(PD).
However,
the
underlying
mechanism
still
unclear.
In
this
study,
4-week-old
male
mice
were
exposed
to
by
free-drinking
water
for
three
months.
Then,
effects
of
on
cognitive
functions
in
tested
Morris
maze
tests,
potential
mechanisms
investigated
ELISA,
immunochemistry,
TUNEL,
Western
blot
tests.
was
found
exacerbates
learning
memory
impairment,
leads
Cu-overload
brain
urine
mice.
The
results
showed
induces
neuronal
degeneration
oxidative
damage,
promotes
expression
apoptosis-related
protein
Bax,
cuproptosis-related
proteins
FDX1
DLAT
proteotoxic
stress
marker
HSP70,
decreases
Fe-S
cluster
proteins.
addition,
affects
pre-synaptic
post-synaptic
regulatory
through
inhibiting
PSD-95
SYP.
also
suppresses
phosphorylation
levels
CREB
BDNF
TrkB
mouse
hippocampus.
conclusion,
might
mediate
cuproptosis,
damage
synaptic
plasticity
inhibit
CREB/BDNF
pathway
cause
dysfunction
Molecular Psychiatry,
Год журнала:
2022,
Номер
28(1), С. 217 - 229
Опубликована: Окт. 18, 2022
Abstract
Despite
an
ever-growing
prevalence
and
increasing
economic
burden
of
Alzheimer’s
disease
(AD)
Parkinson’s
(PD),
recent
advances
in
drug
development
have
only
resulted
minimally
effective
treatment.
In
AD,
along
with
amyloid
tau
phosphorylation,
there
is
associated
increase
inflammation/glial
activation,
a
decrease
synaptic
function,
astrocyte
state
insulin
resistance.
PD,
α-synuclein
accumulation,
inflammation,
dysfunction,
dopaminergic
neuronal
loss,
some
data
to
suggest
Therapeutic
strategies
for
neurodegenerative
disorders
commonly
targeted
individual
pathological
processes.
An
treatment
might
require
either
utilization
multiple
drugs
which
target
the
processes
underlie
or
use
single
agent
could
influence
Insulin
incretins
are
compounds
effects
on
Preclinical
studies
demonstrated
that
GLP-1
receptor
agonists
reduce
neuroinflammation,
deposition,
improve
memory
formation.
Incretin
mimetics
may
act
through
restoration
signaling
pathways,
inducing
further
neuroprotective
effects.
Currently,
phase
2
3
trials
underway
AD
PD
populations.
Here,
we
provide
comprehensive
review
therapeutic
potential
incretin
PD.
Experimental Gerontology,
Год журнала:
2024,
Номер
195, С. 112539 - 112539
Опубликована: Авг. 8, 2024
Neurodegenerative
diseases
(NDDs)
are
a
class
of
neurological
disorders
marked
by
the
progressive
loss
neurons
that
afflict
millions
people
worldwide.
These
illnesses
affect
brain
connection,
impairing
memory,
cognition,
behavior,
sensory
perception,
and
motor
function.
Alzheimer's,
Parkinson's,
Huntington's
examples
common
NDDs,
which
frequently
include
buildup
misfolded
proteins.
Cognitive-behavioral
impairments
early
markers
neurodevelopmental
disorders,
emphasizing
importance
detection
intervention.
Neurotrophins
such
as
brain-derived
neurotrophic
factor
(BDNF)
critical
for
neuron
survival
synaptic
plasticity,
is
required
learning
memory.
NDDs
have
been
associated
with
decreased
BDNF
levels.
Physical
exercise,
non-pharmacological
intervention,
benefits
health
increasing
levels,
lowering
cognitive
deficits,
slowing
degradation.
Exercise
advantages
increased
well-being,
reduced
depression,
improved
skills,
neuroprotection
amyloid
accumulation,
oxidative
stress,
neuroinflammation.
This
study
examines
effects
physical
exercise
on
cognitive-behavioral
deficits
levels
in
limbic
system
impacted
neurodegeneration.
The
findings
highlight
necessity
including
into
NDD
treatment
to
improve
structure,
function,
total
As
research
advances,
becoming
increasingly
acknowledged
an
important
technique
treating
decline
neurodegenerative
disorders.
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
Trends in Biochemical Sciences,
Год журнала:
2024,
Номер
49(5), С. 445 - 456
Опубликована: Март 2, 2024
TrkB
(neuronal
receptor
tyrosine
kinase-2,
NTRK2)
is
the
for
brain-derived
neurotrophic
factor
(BDNF)
and
a
critical
regulator
of
activity-dependent
neuronal
plasticity.
The
past
few
years
have
witnessed
an
increasing
understanding
structure
function
TrkB,
including
its
transmembrane
domain
(TMD).
interacts
with
membrane
cholesterol,
which
bidirectionally
regulates
signaling.
Additionally,
has
recently
been
recognized
as
binding
target
antidepressant
drugs.
A
variety
different
antidepressants,
typical
rapid-acting
well
psychedelic
compounds,
act
allosteric
potentiators
BDNF
signaling
through
TrkB.
This
suggests
that
common
compounds.
Although
more
research
needed,
current
knowledge
promising
further
drug
development.
CNS Neuroscience & Therapeutics,
Год журнала:
2024,
Номер
30(3)
Опубликована: Март 1, 2024
Parkinson's
disease
(PD)
is
a
progressive
neurodegenerative
brain
due
to
degeneration
of
dopaminergic
neurons
(DNs)
presented
with
motor
and
non-motor
symptoms.
PD
symptoms
are
developed
in
response
the
disturbance
diverse
neurotransmitters
including
γ-aminobutyric
acid
(GABA).
GABA
has
neuroprotective
effect
against
neuropathology
by
protecting
DNs
substantia
nigra
pars
compacta
(SNpc).
It
been
shown
that
GABAergic
linked
progression
neurotransmission
necessary
pathway
for
normal
sleep
patterns,
thus
deregulation
could
be
potential
cause
disorders
PD.
Cell Communication and Signaling,
Год журнала:
2025,
Номер
23(1)
Опубликована: Янв. 3, 2025
Oxidative
stress
and
neuroinflammation
are
recognized
as
key
factors
in
the
development
of
neurodegenerative
diseases,
yet
effective
interventions
biomarkers
to
address
oxidative
these
conditions
limited.
Uric
acid
(UA),
traditionally
associated
with
gout,
is
now
gaining
prominence
a
potential
target
diseases.
Soluble
UA
stands
out
one
most
vital
antioxidant
compounds
produced
by
human
body,
accounting
for
up
55%
extracellular
capacity
neutralize
free
radicals.
While
there
increasing
evidence
supporting
neuroprotective
properties
Parkinson's
disease
Alzheimer's
disease,
gaps
knowledge
still
exist
regarding
underlying
mechanisms
how
effectively
translate
benefits
into
clinical
practice.
Moreover,
current
elevation
therapy
exhibits
unstable
properties,
individual
variability,
even
adverse
effects,
limiting
its
applications.
This
review
consolidates
recent
advancements
understanding
exerts
effects
on
diseases
emphasizes
dual
roles
managing
neuroinflammation.
Additionally,
elucidates
through
which
confers
neuroprotection.
Based
this,
underscores
significance
biomarker
aims
provide
comprehensive
therapeutic
target,
while
also
addressing
possible
challenges
implementation.