Nature Communications,
Год журнала:
2018,
Номер
9(1)
Опубликована: Март 26, 2018
Abstract
Microglia
are
highly
motile
glial
cells
that
proposed
to
mediate
synaptic
pruning
during
neuronal
circuit
formation.
Disruption
of
signaling
between
microglia
and
neurons
leads
an
excess
immature
connections,
thought
be
the
result
impaired
phagocytosis
synapses
by
microglia.
However,
until
now
direct
has
not
been
reported
fundamental
questions
remain
about
precise
structures
phagocytic
mechanisms
involved.
Here
we
used
light
sheet
fluorescence
microscopy
follow
microglia–synapse
interactions
in
developing
organotypic
hippocampal
cultures,
complemented
a
3D
ultrastructural
characterization
using
correlative
electron
(CLEM).
Our
findings
define
set
dynamic
interactions,
including
selective
partial
phagocytosis,
or
trogocytosis
(
trogo
-:
nibble),
presynaptic
induction
postsynaptic
spine
head
filopodia
These
allow
us
propose
mechanism
for
facilitatory
role
remodeling
maturation.
Redox Biology,
Год журнала:
2018,
Номер
15, С. 490 - 503
Опубликована: Фев. 3, 2018
The
human
brain
consumes
20%
of
the
total
basal
oxygen
(O2)
budget
to
support
ATP
intensive
neuronal
activity.
Without
sufficient
O2
demands,
activity
fails,
such
that,
even
transient
ischemia
is
neurodegenerative.
While
essentiality
function
clear,
how
oxidative
stress
causes
neurodegeneration
ambiguous.
Ambiguity
exists
because
many
reasons
why
susceptible
remain
obscure.
Many
are
erroneously
understood
as
deleterious
result
adventitious
derived
free
radical
and
non-radical
species
generation.
To
understand
underpin
stress,
one
must
first
re-cast
in
a
positive
light
their
deliberate
generation
enables
achieve
critical
functions
(e.g.
synaptic
plasticity)
through
redox
signalling
(i.e.
functionality).
Using
radicals
derivatives
signal
sensitises
when
goes
awry
negative
advance
mechanistic
understanding,
we
rationalise
13
stress.
Key
include
inter
alia
unsaturated
lipid
enrichment,
mitochondria,
calcium,
glutamate,
modest
antioxidant
defence,
active
transition
metals
neurotransmitter
auto-oxidation.
We
review
RNA
oxidation
an
underappreciated
cause
complex
interplay
between
each
reason
dictates
susceptibility
dynamic
context
neural
identity
dependent
manner.
Our
discourse
sets
stage
for
investigators
interrogate
biochemical
basis
health
disease.
Physiological Reviews,
Год журнала:
2018,
Номер
98(2), С. 813 - 880
Опубликована: Фев. 28, 2018
Neuronal
cell
death
occurs
extensively
during
development
and
pathology,
where
it
is
especially
important
because
of
the
limited
capacity
adult
neurons
to
proliferate
or
be
replaced.
The
concept
used
simple
as
there
were
just
two
three
types,
so
we
had
work
out
which
type
was
involved
in
our
particular
pathology
then
block
it.
However,
now
know
that
are
at
least
a
dozen
ways
for
die,
blocking
mechanism
may
not
prevent
from
dying,
non-neuronal
cells
also
contribute
neuronal
death.
We
review
here
mechanisms
by
intrinsic
extrinsic
apoptosis,
oncosis,
necroptosis,
parthanatos,
ferroptosis,
sarmoptosis,
autophagic
death,
autosis,
autolysis,
paraptosis,
pyroptosis,
phagoptosis,
mitochondrial
permeability
transition.
next
explore
development,
those
induced
axotomy,
aberrant
cell-cycle
reentry,
glutamate
(excitoxicity
oxytosis),
loss
connected
neurons,
aggregated
proteins
unfolded
protein
response,
oxidants,
inflammation,
microglia.
reassess
forms
occur
stroke
Alzheimer’s
disease,
most
pathologies
involving
discuss
why
has
been
difficult
pinpoint
involved,
if
matters,
molecular
overlap
interplay
between
subroutines,
therapeutic
implications
these
multiple
overlapping
