Brain & Neurorehabilitation,
Journal Year:
2024,
Volume and Issue:
17(2)
Published: Jan. 1, 2024
Cerebrolysin
concentrate
is
a
medication
whose
main
active
ingredient
brain-derived
neurotrophic
factor.
It
has
been
reported
to
help
in
the
restoration
of
cognitive
function
and
overall
physical
after
brain
injuries.
We
present
case
72-year-old
man
with
severe
oral
apraxia
due
left
middle
cerebral
artery
ischemic
stroke
involving
insular
cortex.
He
was
being
tube
fed
decline
that
made
it
difficult
for
him
even
imitate
simple
movements.
The
patient
initially
had
impaired
consciousness
function.
also
limited
activity
acute
complications,
such
as
hemorrhagic
transformation
infarction,
required
bed
rest
until
23
days
onset.
received
intravenous
cerebrolysin
addition
intensive
rehabilitation
therapy
from
After
administration
concentrate,
there
marked
recovery
within
short
period
time
point
where
intake
regular
diet
possible,
indicating
significant
improvement
apraxia.
notable
example
potential
therapeutic
effect
post-stroke
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(2), P. 1422 - 1422
Published: Jan. 11, 2023
Excess
body
weight
is
frequently
associated
with
low-grade
inflammation.
Evidence
indicates
a
relationship
between
obesity
and
cancer,
as
well
other
diseases,
such
diabetes
non-alcoholic
fatty
liver
disease,
in
which
inflammation
the
actions
of
various
adipokines
play
role
pathological
mechanisms
involved
these
disorders.
Leptin
mainly
produced
by
adipose
tissue
proportion
to
fat
stores,
but
it
also
synthesized
organs,
where
leptin
receptors
are
expressed.
This
hormone
performs
numerous
brain,
related
control
energy
homeostasis.
It
neurogenesis
neuroprotection,
central
resistance
some
neurological
disorders,
e.g.,
Parkinson’s
Alzheimer’s
diseases.
In
peripheral
tissues,
implicated
regulation
metabolism,
bone
density
muscle
mass.
All
can
be
affected
changes
levels
this
hormone.
review
will
present
recent
advances
molecular
action
their
underlying
roles
situations,
may
interest
for
revealing
new
approaches
treatment
diseases
adipokine
might
compromised.
Neuroprotection/Neuroprotection (Chichester, England. Print),
Journal Year:
2024,
Volume and Issue:
2(2), P. 67 - 78
Published: May 2, 2024
Abstract
Neurodegenerative
diseases,
marked
by
the
gradual
death
of
neurons,
present
a
significant
and
growing
public
health
challenge.
Brain‐derived
neurotrophic
factor
(BDNF)
is
crucial
for
survival,
development,
synaptic
plasticity
neurons.
Studies
have
consistently
demonstrated
that
perturbed
BDNF
communication
pathways
are
associated
with
development
progression
neurodegenerative
conditions,
underscoring
their
potential
as
therapeutic
targets.
This
review
aimed
to
summarize
existing
findings
regarding
expression,
metabolism,
signaling
transduction.
Furthermore,
we
reviewed
intricate
roles
in
elucidating
contributions
disease
onset
progression.
The
latest
advancements
targeting
treatment
including
small
molecules,
nucleic
acid‐based
therapeutics,
antibody‐based
approaches,
were
also
summarized.
Despite
recent
strides,
challenges
persist,
lack
comprehensive
understanding
modulation
across
diverse
contexts
absence
clinically
approved
BDNF‐targeted
drugs.
Neural Regeneration Research,
Journal Year:
2024,
Volume and Issue:
20(3), P. 715 - 724
Published: May 10, 2024
Tropomyosin
receptor
kinase
B
(TrkB)
signaling
plays
a
pivotal
role
in
dendritic
growth
and
spine
formation
to
promote
learning
memory.
The
activity-dependent
release
of
brain-derived
neurotrophic
factor
at
synapses
binds
pre-
or
postsynaptic
TrkB
resulting
the
strengthening
synapses,
reflected
by
long-term
potentiation.
Postsynaptically,
association
density
protein-95
with
enhances
phospholipase
Cγ-Ca2+/calmodulin-dependent
protein
II
phosphatidylinositol
3-kinase-mechanistic
target
rapamycin
required
for
In
this
review,
we
discuss
TrkB-postsynaptic
coupling
as
promising
strategy
magnify
towards
development
novel
therapeutics
specific
neurological
disorders.
A
reduction
has
been
observed
neurodegenerative
disorders,
such
Alzheimer's
disease
Huntington's
disease,
enhancement
could
mitigate
deficiency
neuronal
connectivity
schizophrenia
depression.
Treatment
is
problematic,
due
poor
pharmacokinetics,
low
brain
penetration,
side
effects
from
activation
p75
neurotrophin
truncated
TrkB.T1
isoform.
Although
agonists
antibodies
that
activate
are
being
intensively
investigated,
they
cannot
distinguish
multiple
human
splicing
isoforms
cell
type-specific
functions.
Targeting
provides
an
alternative
approach
specifically
boost
localized
synaptic
sites
versus
global
stimulation
risks
many
adverse
effects.
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
166, P. 115313 - 115313
Published: Aug. 10, 2023
Treatment-resistant
depression
(TRD)
is
a
challenging
issue
to
address.
Repetitive
transcranial
magnetic
stimulation
(rTMS)
commonly
used
but
shows
varying
efficacy,
necessitating
deeper
understanding
of
physiology
and
rTMS
mechanisms.
Notably,
an
increasing
amount
recent
data
has
displayed
the
connection
TRD
its
clinical
outcome
with
chronic
inflammatory
processes.
The
current
study
included
19
patients
undergoing
11
depressed
responding
medication
as
comparison
group.
We
assessed
therapeutic
efficacy
using
MADRS,
HAM-D-17,
GAD-7,
PHQ-9
tests.
Inflammatory
markers,
neurotrophins,
associated
miRNAs
were
measured
in
blood
serum
before
during
treatment.
A
control
group
18
healthy
individuals
provided
baseline
data.
results
our
showed
significantly
higher
levels
pro-inflammatory
interleukins-6
-
8
compared
drug-responders,
which
also
related
more
severe
symptoms
In
addition,
patients,
both
treatment,
exhibited
average
concentrations
interleukin-18
lower
anti-neuroinflammatory
miR-146a-5p
controls.
observed
that
expression
miR-16-5p,
miR-93-5p,
especially
correlated
changes
following
rTMS.
Our
confirmed
possess
status,
while
was
demonstrated
have
considerable
potential
for
predicting
their
treatment
success.
Acta Neurobiologiae Experimentalis,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 13, 2025
In
recent
years,
growing
evidence
suggests
that
lipopolysaccharide
(LPS),
a
bacterial
endotoxin
found
in
the
outer
membrane
of
gram‑negative
bacteria,
can
influence
cognitive
functions,
particularly
memory
formation
and
retrieval.
However,
underlying
mechanisms
through
which
LPS
exerts
its
effects
on
remain
incompletely
understood.
This
review
used
various
electronic
databases,
including
PubMed,
Scopus,
Web
Science,
to
identify
relevant
studies
published
between
2000
2024.
Articles
were
selected
based
their
focus
LPS‑induced
impairments,
experimental
models,
molecular
pathways,
neurochemical
alterations.
administration
has
been
consistently
shown
disrupt
processes
both
animals
humans,
although
magnitude
duration
impairments
might
vary
depending
factors
such
as
dose,
timing,
context
exposure.
Several
potential
have
proposed
explain
deficits,
neuroinflammation,
alterations
synaptic
plasticity,
disruption
neurotransmitter
systems,
dysfunction
blood‑brain
barrier.
Moreover,
activate
immune
signaling
toll‑like
receptors,
interleukins,
microglia,
further
contribute
impairments.
Such
insights
may
pave
way
for
development
targeted
therapeutic
interventions
aimed
at
ameliorating
deficits
associated
with
conditions
involving
exposure,
infections,
sepsis,
neuroinflammatory
disorders.
