International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(16), P. 8413 - 8413
Published: Aug. 5, 2021
Neonicotinoids
are
a
class
of
insecticides
that
exert
their
effect
through
specific
action
on
neuronal
nicotinic
acetylcholine
receptors
(nAChRs).
The
success
these
is
due
to
this
mechanism
action,
since
they
act
as
potent
agonists
insect
nAChRs,
presenting
low
affinity
for
vertebrate
which
reduces
potential
toxic
risk
and
increases
safety
non-target
species.
However,
although
neonicotinoids
considered
safe,
presence
in
the
environment
could
increase
exposure
toxicity.
On
other
hand,
have
mammalian
large
quantity,
variety,
ubiquity
receptors,
combined
with
its
diversity
functions,
raises
question
what
effects
can
produce
In
present
systematic
review,
we
investigate
available
evidence
biochemical
behavioral
nervous
system.
general,
at
an
early
age
alters
correct
development,
decreases
neurogenesis
alterations
migration,
induces
neuroinflammation.
adulthood,
induce
neurobehavioral
toxicity,
being
associated
modulating
consequent
neurochemical
alterations.
These
include
decreased
expression
modifications
acetylcholinesterase
activity,
significant
changes
function
nigrostriatal
dopaminergic
All
lead
activation
series
intracellular
signaling
pathways
generate
oxidative
stress,
neuroinflammation
and,
finally,
death.
Neonicotinoid-induced
nAChR
be
responsible
most
observed
different
studies.
European Journal of Neuroscience,
Journal Year:
2020,
Volume and Issue:
53(1), P. 151 - 171
Published: March 9, 2020
Abstract
Some
recent
clinical
and
preclinical
evidence
suggests
that
neuroinflammation
is
a
key
factor
interacts
with
the
three
neurobiological
correlates
of
major
depressive
disorder:
depletion
brain
serotonin,
dysregulation
hypothalamus–pituitary–adrenal
(HPA)
axis
alteration
continuous
production
adult‐generated
neurons
in
dentate
gyrus
hippocampus.
This
review
discusses
main
players
immunity
as
well
how
inflammation
above
mechanisms.
It
reported
kynurenine
(KYN)
pathway
favour
its
excitotoxic
component
HPA
have
common
effect
increasing
extracellular
glutamate
levels
neurotransmission,
which
can
impact
hippocampal
neurogenesis.
pathophysiological
cascade
appears
to
be
triggered
or
sustained
reinforced
by
any
chronic
inflammatory
condition
involving
increased
circulating
markers
are
able
cross
blood–brain
barrier
activate
microglia;
it
also
consequence
primary
neuroinflammation,
such
neurodegenerative
disorders
early
manifestations
frequently
symptoms.
Further
data
indicate
microglial
activation
may
result
from
direct
stress
on
vascular
function.
The
intricated
dynamic
crosstalk
between
other
relevant
depression
add
therapeutic
target
for
future
strategies
disorder.
Proceedings of the National Academy of Sciences,
Journal Year:
2020,
Volume and Issue:
117(17), P. 9180 - 9182
Published: April 13, 2020
The
blood–brain
barrier
(BBB)
presents
a
significant
challenge
for
treating
brain
disorders.
hippocampus
is
key
target
novel
therapeutics,
playing
an
important
role
in
Alzheimer’s
disease
(AD),
epilepsy,
and
depression.
Preclinical
studies
have
shown
that
magnetic
resonance
(MR)-guided
low-intensity
focused
ultrasound
(FUS)
can
reversibly
open
the
BBB
facilitate
delivery
of
targeted
therapeutics.
We
report
initial
clinical
trial
results
evaluating
safety,
feasibility,
reversibility
opening
with
FUS
treatment
entorhinal
cortex
(EC)
patients
early
AD.
Six
subjects
tolerated
total
17
treatments
no
adverse
events
neither
cognitive
nor
neurological
worsening.
Post-FUS
contrast
MRI
revealed
immediate
sizable
hippocampal
parenchymal
enhancement
indicating
opening,
followed
by
closure
within
24
h.
average
was
95%
volume,
which
corresponds
to
29%
overall
volume.
demonstrate
safely,
noninvasively,
transiently,
reproducibly,
focally
mediate
hippocampus/EC
humans.
This
provides
unique
translational
opportunity
investigate
therapeutic
AD
other
conditions.
Cell stem cell,
Journal Year:
2021,
Volume and Issue:
28(10), P. 1805 - 1821.e8
Published: May 24, 2021
Neural
stem
cells
residing
in
the
hippocampal
neurogenic
niche
sustain
lifelong
neurogenesis
adult
brain.
Adult
(AHN)
is
functionally
linked
to
mnemonic
and
cognitive
plasticity
humans
rodents.
In
Alzheimer's
disease
(AD),
process
of
generating
new
neurons
at
impeded,
yet
mechanisms
involved
are
unknown.
Here
we
identify
miR-132,
one
most
consistently
downregulated
microRNAs
AD,
as
a
potent
regulator
AHN,
exerting
cell-autonomous
proneurogenic
effects
neural
their
progeny.
Using
distinct
AD
mouse
models,
cultured
human
primary
established
cells,
patient
material,
demonstrate
that
AHN
directly
affected
by
pathology.
miR-132
replacement
hippocampus
restores
relevant
memory
deficits.
Our
findings
corroborate
significance
models
reveal
possible
therapeutic
potential
targeting
neurodegeneration.
