Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
unknown, P. 111338 - 111338
Published: April 1, 2025
Acute
ischemic
stroke
(AIS)
is
a
focal
neurological
deficit
due
to
sudden
occlusion
of
cerebral
vessels
in
the
brain.
AIS-induced
neuronal
injury
and
associated
excite-toxicity
neurodegeneration
affect
synthesis
release
different
neurotrophic
factors
such
as
brain-derived
neurotropic
factor
(BDNF)
its
precursor
proBDNF.
Both
BDNF
proBDNF
act
on
specific
receptors
with
effects.
activates
tropomyosin
receptor
kinase
B
(TrkB)
results
promoting
survival,
synaptic
plasticity,
growth.
However,
p75
neurotrophin
(p75NTR)
sortilin
which
attenuates
plasticity
promotes
apoptosis.
Dysregulation
central
peripheral
expression
proBDNF/BDNF
linked
severity
clinical
outcomes
AIS.
Therefore,
this
review
aims
discuss
alterations
signaling
Findings
from
present
illustrated
that
proBDNF/p75NTR/sortilin
pathway
exaggerated
whereas;
BDNF-TrkB
reduced
AIS
leading
activation
signaling,
inhibition
could
be
promising
therapeutic
strategy
management
Virology Journal,
Journal Year:
2022,
Volume and Issue:
19(1)
Published: Oct. 9, 2022
Most
COVID-19
patients
recovered
with
low
mortality;
however,
some
experienced
long-term
symptoms
described
as
"long-COVID"
or
"Post-COVID
syndrome"
(PCS).
Patients
may
have
persisting
for
weeks
after
acute
SARS-CoV-2
infection,
including
dyspnea,
fatigue,
myalgia,
insomnia,
cognitive
and
olfactory
disorders.
These
last
months
in
patients.
PCS
progress
association
the
development
of
mast
cell
activation
syndrome
(MCAS),
which
is
a
distinct
kind
disorder,
characterized
by
hyper-activation
cells
inappropriate
excessive
release
chemical
mediators.
survivors,
mainly
women,
persistent
severe
fatigue
10
recovery
history
neuropsychiatric
disorders
are
more
prone
to
develop
PCS.
High
D-dimer
levels
blood
urea
nitrogen
were
observed
be
risk
factors
associated
pulmonary
dysfunction
survivors
3
post-hospital
discharge
has
systemic
manifestations
that
resolve
time
no
further
complications.
However,
final
outcomes
chiefly
unknown.
Persistence
inflammatory
reactions,
autoimmune
mimicry,
reactivation
pathogens
together
host
microbiome
alterations
contribute
The
deregulated
mediators
MCAS
produces
extraordinary
during
course
infection
correlated
severity
Therefore,
treated
antihistamines,
inhibition
synthesis
mediators,
mediator
release,
degranulation
cells.
Brain Sciences,
Journal Year:
2022,
Volume and Issue:
12(10), P. 1290 - 1290
Published: Sept. 24, 2022
Alzheimer's
disease
(AD)
was
used
to
describe
pre-senile
dementia
differentiate
it
from
senile
dementia,
which
develops
in
the
adult
age
group
of
more
than
65
years.
AD
is
characterized
by
deposition
amyloid
beta
(Aβ)
plaque
and
tau-neurofibrillary
tangles
(TNTs)
brain.
The
neuropathological
changes
are
related
plaques,
neurofibrillary
tangles,
progression
neuroinflammation,
neuronal
mitochondrial
dysfunction,
autophagy
cholinergic
synaptic
dysfunction.
Statins
one
main
cornerstone
drugs
for
management
cardiovascular
disorders
regardless
dyslipidemia
status.
Increasing
use
statins,
mainly
elderly
groups
primary
secondary
prevention
diseases,
may
affect
their
cognitive
functions.
Extensive
prolonged
statins
functions
healthy
subjects
patients.
Statins-induced
impairments
both
patients
health
providers
had
been
reported
according
post-marketing
survey.
This
survey
depends
on
sporadic
cases,
no
measures
were
used.
Evidence
prospective
observational
studies
gives
robust
conclusion
regarding
beneficial
or
detrimental
effects
Therefore,
this
study
a
narrative
review
aimed
with
evidences
beneficial,
detrimental,
neutral
AD.
Journal of Diabetes,
Journal Year:
2022,
Volume and Issue:
14(12), P. 806 - 814
Published: Nov. 28, 2022
Type
2
diabetes
mellitus
(T2DM)
is
a
chronic
endocrine
disorder
due
to
the
reduction
of
insulin
sensitivity
and
relative
deficiency
secretion.
Growth
differentiation
factor
15
(GDF15)
belongs
transforming
growth
beta
(TGF-β)
superfamily
was
initially
identified
as
macrophage
inhibitory
cytokine-1
(MIC-1).
GDF15
considered
cytokine
with
an
anti-inflammatory
effect
increases
sensitivity,
reduces
body
weight,
improves
clinical
outcomes
in
diabetic
patients.
acts
through
stimulation
glial-derived
neurotrophic
(GDNF)
family
receptor
α-like
(GFRAL),
which
highly
expressed
brain
stem
induce
taste
aversion.
Metformin
group
biguanides
that
are
derived
from
plant
Galega
officinalis.
It
interesting
note
metformin
insulin-sensitizing
agent
used
first-line
therapy
for
T2DM
has
been
shown
increase
circulating
level
GDF15.
Thus,
present
review
aims
determine
critical
association
biomarker
how
agents
affect
it.
This
illustrates
activates
expression,
appetite
leads
weight
loss
both
nondiabetic
However,
cannot
give
conclusion
this
regard.
Therefore,
experimental,
preclinical,
studies
warranted
confirm
potential
role
patients.2型糖尿病(T2DM)是一种因胰岛素敏感性降低和胰岛素分泌相对不足而引起的慢性内分泌疾病。生长分化因子15
(GDF15)属于转化生长因子-β
(TGF-β)超家族，最初被鉴定为巨噬细胞抑制因子-1
(MIC)。GDF15被认为是一种具有抗炎作用、增加胰岛素敏感性、减轻体重和改善糖尿病患者临床疗效的细胞因子。GDF15通过刺激脑干高表达的胶质源性神经营养因子(GDNF)家族受体α样(GFRAL)诱导味觉厌恶。二甲双胍属于从大戟属植物中提取的双胍类化合物。二甲双胍是一种胰岛素增敏剂，用于T2DM的一线治疗，已被证明可增加GDF15的循环水平。本综述旨在确定GDF15生物标志物在T2DM中的关键作用以及二甲双胍药物是如何影响它发。综述表明，二甲双胍激活GDF15的表达，降低糖尿病和非糖尿病患者的食欲，诱导体重减轻。然而，目前的研究无法在这方面给出结论。因此，有必要进行实验、临床前和临床研究来确认GDF15在T2DM患者中的潜在作用。.
Cellular and Molecular Neurobiology,
Journal Year:
2023,
Volume and Issue:
43(6), P. 2743 - 2759
Published: April 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.
Diabetes Obesity and Metabolism,
Journal Year:
2024,
Volume and Issue:
26(8), P. 3031 - 3044
Published: May 27, 2024
Abstract
Depression
is
a
mood
disorder
that
may
increase
risk
for
the
development
of
insulin
resistance
(IR)
and
type
2
diabetes
(T2D),
vice
versa.
However,
mechanistic
pathway
linking
depression
T2D
not
fully
elucidated.
The
aim
this
narrative
review,
therefore,
was
to
discuss
possible
link
between
T2D.
coexistence
twice
as
great
compared
occurrence
either
condition
independently.
Hyperglycaemia
dyslipidaemia
promote
incidence
by
enhancing
inflammation
reducing
brain
serotonin
(5‐hydroxytryptamine
[5HT]).
Dysregulation
signalling
in
impairs
5HT
signalling,
leading
depression.
Furthermore,
associated
with
hyperglycaemia
poor
glycaemic
control.
Psychological
stress
In
conclusion,
could
be
potential
factor
through
induction
inflammatory
reactions
oxidative
affect
neurotransmission.
addition,
chronic
induce
dysregulation
hypothalamic–pituitary–adrenal
axis
circulating
cortisol
levels,
which
triggers
IR
Inflammopharmacology,
Journal Year:
2022,
Volume and Issue:
31(1), P. 1 - 7
Published: Nov. 23, 2022
Abstract
In
coronavirus
disease
2019
(Covid-19)
era,
neuroinflammation
may
develop
due
to
neuronal
tropism
of
severe
acute
respiratory
syndrome
type
2
(SARS-CoV-2)
and/or
associated
immune
activation,
cytokine
storm,
and
psychological
stress.
SARS-CoV-2
infection
linked
storm
cause
blood–brain
barrier
(BBB)
injury
through
which
activated
cells
can
pass
into
the
brain
causing
activation
glial
with
subsequent
neuroinflammation.
Different
therapeutic
regimens
were
suggested
alleviate
Covid-19-induced
Since
glibenclamide
has
anti-inflammatory
neuroprotective
effects,
it
could
be
effective
in
mitigation
infection-induced
Glibenclamide
is
a
second-generation
drug
from
sulfonylurea
family,
acts
by
inhibiting
adenosine
triphosphate
(ATP)-sensitive
K
channel
regulatory
subunit
1
receptor
(SUR-1)
pancreatic
β
cells.
reduces
BBB
nod-like
pyrin
3
(NLRP3)
inflammasome,
oxidative
stress,
microglial
activation.
Therefore,
inhibition
NLRP3
stress
attenuate
SARS-CoV-2-mediated
