Revista Master Ensino Pesquisa e Extensão,
Journal Year:
2023,
Volume and Issue:
8(16)
Published: Dec. 14, 2023
Introdução:
Os
benzodiazepínicos
são
as
drogas
psiquiátricas
mais
utilizadas
em
todo
o
mundo
possuindo
propriedades
farmacológicas
com
efeitos
sedativos,
hipnóticos,
ansiolíticos,
anticonvulsivantes
e
relaxantes
musculares.
No
entanto
uso
prolongado
pode
estar
associado
à
demência,
sobretudo
entre
os
idosos.
Objetivo:
Investigar
a
associação
demência
de
Materiais
Métodos:
Foi
feita
uma
revisão
bibliográfica
caráter
narrativo
dos
artigos
publicados
nos
últimos
dez
anos
(2013
2023),
utilizando
bases
dados
SciELO,
PubMed,
BVS
Google
Acadêmico.
Resultados:
O
estudo
das
bibliografias
selecionadas
mostrou
que
idosos
tem
alta
prevalência.
Além
disso,
essa
classe
medicamentos
não
é
recomendada
para
por
idosos,
agravando
suas
consequências
ainda
quando
tratamento
realizado
longo
prazo,
exacerbando
série
eventos
adversos
sem
apresentar
eficácia
nesse
formato
uso.
Grande
parte
estudos
fármacoepidemiológicos
realizados
até
momento
concluíram
usuários
apresentam
maior
risco
desenvolver
mas
permanecem
obscuros
mecanismos
pelos
quais
possivelmente
ocorre
aumento
do
Conclusão:
É
importante
buscar
formas
menos
prejudiciais
sanar
queixas
relação
sono
ansiedade
capacitar
profissionais
saúde,
fim
identificar
recomendado
propor
otimizar
prescrições.
Portanto,
há
necessidade
aprofundados
sobre
assunto,
observar
possíveis
riscos
existentes
no
irracional
benzodiazepínicos.
Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(10)
Published: May 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,
Journal Year:
2023,
Volume and Issue:
20(2), P. 259 - 274
Published: Sept. 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
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Feb. 22, 2024
Abstract
Background
Patients
with
Alzheimer’s
disease
(AD)
are
often
co-morbid
unprovoked
seizures,
making
clinical
diagnosis
and
management
difficult.
Although
it
has
an
important
role
in
both
AD
epilepsy,
abnormal
γ-aminobutyric
acid
(GABA)ergic
transmission
is
recognized
only
as
a
compensative
change
for
glutamatergic
damage.
Neuregulin
1
(NRG1)-ErbB4
signaling
can
promote
GABA
release
suppress
epileptogenesis,
but
its
effects
on
cognition
still
controversial.
Methods
Four-month-old
APPswe/PS1dE9
mice
(APP
mice)
were
used
animal
models
the
early
stage
of
this
study.
Acute/chronic
chemical-kindling
epilepsy
established
pentylenetetrazol.
Electroencephalogram
Racine
scores
performed
to
assess
seizures.
Behavioral
tests
emotion.
Electrophysiology,
western
blot
immunofluorescence
detect
alterations
synapses,
GABAergic
system
components
NRG1-ErbB4
signaling.
Furthermore,
NRG1
was
administrated
intracerebroventricularly
into
APP
then
antiepileptic
cognitive
evaluated.
Results
had
increased
susceptibility
resulting
hippocampal
synaptic
damage
impairment.
Electrophysiological
analysis
revealed
decreased
hippocampus.
This
involved
reduction
number
parvalbumin
interneurons
(PV
+
Ins)
levels
synthesis
transport.
We
also
found
impaired
which
mediated
by
PV
Ins
loss.
And
administration
could
effectively
reduce
seizures
improve
four-month-old
mice.
Conclusion
Our
results
indicated
that
hyperexcitability,
further
excitation/inhibition
imbalance,
promoted
epileptogenesis
AD.
Appropriate
down-regulate
seizure
rescue
function.
study
provided
potential
direction
intervening
co-morbidity
epilepsy.
European journal of medical research,
Journal Year:
2024,
Volume and Issue:
29(1)
Published: Feb. 9, 2024
Abstract
Multiple
sclerosis
(MS)
is
the
most
frequent
inflammatory
and
demyelinating
disease
of
central
nervous
system
(CNS).
The
underlying
pathophysiology
MS
destruction
myelin
sheath
by
immune
cells.
formation
plaques,
inflammation,
injury
neuronal
characterizes
its
neuropathology.
plaques
are
multiple
focal
regions
demyelination
disseminated
in
brain's
white
matter,
spinal
cords,
deep
grey
cerebral
cortex.
Fenofibrate
a
peroxisome
proliferative
activated
receptor
alpha
(PPAR-α)
that
attenuates
reactions
MS.
inhibits
differentiation
Th17
inhibiting
expression
pro-inflammatory
signaling.
According
to
these
findings,
this
review
intended
illuminate
mechanistic
immunoinflammatory
role
fenofibrate
mitigating
In
conclusion,
can
attenuate
neuropathology
modulating
different
pathways,
including
oxidative
stress,
autophagy,
mitochondrial
dysfunction,
inflammatory-signaling
neuroinflammation.