Science,
Год журнала:
2011,
Номер
334(6063), С. 1669 - 1675
Опубликована: Дек. 22, 2011
The
rapid
encoding
of
contextual
memory
requires
the
CA3
region
hippocampus,
but
necessary
genetic
pathways
remain
unclear.
We
found
that
activity-dependent
transcription
factor
Npas4
regulates
a
transcriptional
program
in
is
required
for
formation.
was
specifically
expressed
after
learning.
Global
knockout
or
selective
deletion
both
resulted
impaired
memory,
and
restoration
sufficient
to
reverse
deficit
global
mice.
By
recruiting
RNA
polymerase
II
promoters
enhancers
target
genes,
learning-specific
includes
many
well-known
activity-regulated
which
suggests
master
regulator
gene
programs
central
Cell,
Год журнала:
2021,
Номер
184(5), С. 1299 - 1313.e19
Опубликована: Фев. 18, 2021
It
is
unclear
how
binding
of
antidepressant
drugs
to
their
targets
gives
rise
the
clinical
effect.
We
discovered
that
transmembrane
domain
tyrosine
kinase
receptor
2
(TRKB),
brain-derived
neurotrophic
factor
(BDNF)
promotes
neuronal
plasticity
and
responses,
has
a
cholesterol-sensing
function
mediates
synaptic
effects
cholesterol.
then
found
both
typical
fast-acting
antidepressants
directly
bind
TRKB,
thereby
facilitating
localization
TRKB
its
activation
by
BDNF.
Extensive
computational
approaches
including
atomistic
molecular
dynamics
simulations
revealed
site
at
region
dimers.
Mutation
antidepressant-binding
motif
impaired
cellular,
behavioral,
plasticity-promoting
responses
in
vitro
vivo.
suggest
allosteric
facilitation
BDNF
signaling
common
mechanism
for
action,
which
may
explain
why
act
slowly
are
translated
into
mood
recovery.
International Journal of Molecular Sciences,
Год журнала:
2020,
Номер
21(3), С. 1170 - 1170
Опубликована: Фев. 10, 2020
Brain-derived
neurotrophic
factor
(BDNF)
promotes
neuroprotection
and
neuroregeneration.
In
animal
models
of
Parkinson’s
disease
(PD),
BDNF
enhances
the
survival
dopaminergic
neurons,
improves
neurotransmission
motor
performance.
Pharmacological
therapies
PD
are
symptom-targeting,
their
effectiveness
decreases
with
progression
disease;
therefore,
new
therapeutical
approaches
needed.
Since,
in
both
patients
models,
decreased
level
was
found
nigrostriatal
pathway,
it
has
been
hypothesized
that
may
serve
as
a
therapeutic
agent.
Direct
delivery
exogenous
into
patient’s
brain
did
not
relieve
symptoms
disease,
nor
attempts
to
enhance
expression
gene
therapy.
Physical
training
neuroprotective
PD.
This
effect
is
mediated,
at
least
partly,
by
BDNF.
Animal
studies
revealed
physical
activity
increases
tropomyosin
receptor
kinase
B
(TrkB)
expression,
leading
inhibition
neurodegeneration
through
induction
transcription
factors
genes
related
neuronal
proliferation,
survival,
inflammatory
response.
review
focuses
on
evidence
increasing
due
modulation
or
exercise
could
be
considered
adjunctive
therapy
ASN NEURO,
Год журнала:
2010,
Номер
2(5), С. AN20100019 - AN20100019
Опубликована: Авг. 13, 2010
The
production
of
neurons
from
neural
progenitor
cells,
the
growth
axons
and
dendrites
formation
reorganization
synapses
are
examples
neuroplasticity.
These
processes
regulated
by
cell-autonomous
intercellular
(paracrine
endocrine)
programs
that
mediate
responses
cells
to
environmental
input.
Mitochondria
highly
mobile
move
within
between
subcellular
compartments
involved
in
neuroplasticity
(synaptic
terminals,
dendrites,
cell
body
axon).
By
generating
energy
(ATP
NAD(+)),
regulating
Ca(2+)
redox
homoeostasis,
mitochondria
may
play
important
roles
controlling
fundamental
neuroplasticity,
including
differentiation,
neurite
outgrowth,
neurotransmitter
release
dendritic
remodelling.
Particularly
intriguing
is
emerging
data
suggesting
emit
molecular
signals
(e.g.
reactive
oxygen
species,
proteins
lipid
mediators)
can
act
locally
or
travel
distant
targets
nucleus.
Disturbances
mitochondrial
functions
signalling
impaired
neuronal
degeneration
Alzheimer's
disease,
Parkinson's
psychiatric
disorders
stroke.
