Brain,
Год журнала:
2013,
Номер
136(9), С. 2717 - 2726
Опубликована: Июль 17, 2013
White
matter
hyperintensities
and
lacunes
are
among
the
most
frequent
abnormalities
on
brain
magnetic
resonance
imaging.
They
commonly
related
to
cerebral
small
vessel
disease
associated
with
both
stroke
dementia.
We
examined
spatial
relationships
between
incident
white
these
findings
information
vascular
anatomy
study
possible
mechanistic
links
two
lesion
types.
Two
hundred
seventy-six
patients
autosomal
dominant
arteriopathy
subcortical
infarcts
leukoencephalopathy
(CADASIL),
a
genetically
defined
mutations
in
NOTCH3
gene
were
followed
imaging
over
total
of
633
patient
years.
Using
difference
images
Jacobian
maps
from
registered
we
identified
104
lacunes.
The
majority
(n
=
95;
91.3%)
developed
at
edge
hyperintensity
whereas
few
found
develop
fully
within
6;
5.8%)
or
outside
3;
2.9%)
hyperintensities.
Adding
revealed
that
proximal
along
course
perforating
vessels
supplying
respective
region.
further
studied
relationship
prevalent
365
CADASIL
588
elderly
subjects
Austrian
Stroke
Prevention
Study.
results
consistent
for
Lesion
prevalence
different
stages
showed
spread
lesions
towards
regions
cohorts.
Our
suggest
mechanisms
intimately
connected
identify
as
predilection
site
observations
support
refine
concept
penumbra.
Post-stroke
cognitive
impairment
occurs
frequently
in
the
patients
with
stroke.
The
prevalence
of
post-stroke
ranges
from
20%
to
80%,
which
varies
for
difference
between
countries,
races,
and
diagnostic
criteria.
risk
is
related
both
demographic
factors
like
age,
education
occupation
vascular
factors.
underlying
mechanisms
are
not
known
detail.
However,
neuroanatomical
lesions
caused
by
stroke
on
strategic
areas
such
as
hippocampus
white
matter
(WMLs),
cerebral
microbleeds
(CMBs)
due
small
cerebrovascular
diseases
mixed
AD
stroke,
alone
or
combination,
contribute
pathogenesis
impairment.
treatment
may
benefit
only
anti-dementia
drugs,
but
also
manage
measures
diseases.
In
this
review,
we
will
describe
epidemiological
features
impairment,
discuss
promising
management
strategies
these
patients.
ACS Chemical Neuroscience,
Год журнала:
2014,
Номер
6(1), С. 48 - 67
Опубликована: Дек. 30, 2014
Implantable
biosensors
are
valuable
scientific
tools
for
basic
neuroscience
research
and
clinical
applications.
Neurotechnologies
provide
direct
readouts
of
neurological
signal
neurochemical
processes.
These
generally
most
when
performance
capacities
extend
over
months
years
to
facilitate
the
study
memory,
plasticity,
behavior
or
monitor
patients'
conditions.
needs
have
generated
a
variety
device
designs
from
microelectrodes
fast
scan
cyclic
voltammetry
(FSCV)
electrophysiology
microdialysis
probes
sampling
detecting
various
neurochemicals.
Regardless
technology
used,
breaching
blood-brain
barrier
(BBB)
insert
devices
triggers
cascade
biochemical
pathways
resulting
in
complex
molecular
cellular
responses
implanted
devices.
Molecular
changes
microenvironment
surrounding
an
implant
include
introduction
mechanical
strain,
activation
glial
cells,
loss
perfusion,
secondary
metabolic
injury,
neuronal
degeneration.
Changes
tissue
can
dramatically
impact
electrochemical
electrophysiological
sensitivity
stability
time.
This
review
summarizes
magnitude,
variability,
time
course
dynamic
level
neural
induced
by
state-of-the-art
implantable
Studies
show
that
insertion
injuries
foreign
body
response
quality
across
all
central
nervous
system
(CNS)
sensors
varying
degrees
both
acute
(seconds
minutes)
chronic
periods
(weeks
months).
Understanding
underlying
biological
processes
behind
brain
at
leads
intervention
strategies
improving
longevity.
Nature Communications,
Год журнала:
2016,
Номер
7(1)
Опубликована: Май 3, 2016
Microglia
are
the
main
immune
cells
of
brain
and
contribute
to
common
diseases.
However,
it
is
unclear
how
microglia
influence
neuronal
activity
survival
in
injured
vivo.
Here
we
develop
a
precisely
controlled
model
injury
induced
by
cerebral
ischaemia
combined
with
fast
vivo
two-photon
calcium
imaging
selective
microglial
manipulation.
We
show
that
elimination
leads
striking,
60%
increase
infarct
size,
which
reversed
repopulation.
Microglia-mediated
protection
includes
reduction
excitotoxic
injury,
since
an
absence
dysregulated
responses,
overload
increased
death.
Furthermore,
incidence
spreading
depolarization
(SD)
markedly
reduced
microglia.
Thus,
involved
changes
network
SD
after
could
have
important
implications
for
Brain,
Год журнала:
2017,
Номер
140(7), С. 1829 - 1850
Опубликована: Фев. 27, 2017
Sporadic
cerebral
amyloid
angiopathy
is
a
common,
well-defined
small
vessel
disease
and
largely
untreatable
cause
of
intracerebral
haemorrhage
contributor
to
age-related
cognitive
decline.
The
term
'cerebral
angiopathy'
now
encompasses
not
only
specific
cerebrovascular
pathological
finding,
but
also
different
clinical
syndromes
(both
acute
progressive),
brain
parenchymal
lesions
seen
on
neuroimaging
set
diagnostic
criteria—the
Boston
criteria,
which
have
resulted
in
increasingly
detected
during
life.
Over
the
past
few
years,
it
has
become
clear
that,
at
pathophysiological
level,
appears
be
part
protein
elimination
failure
that
this
dysfunction
feed-forward
process,
potentially
leads
worsening
vascular
amyloid-β
accumulation,
activation
injury
pathways
impaired
physiology.
From
standpoint,
characterized
by
individual
focal
(microbleeds,
cortical
superficial
siderosis,
microinfarcts)
large-scale
alterations
(white
matter
hyperintensities,
structural
connectivity,
thickness),
both
subcortical.
This
review
provides
an
interdisciplinary
critical
outlook
various
emerging
changing
concepts
field,
illustrating
mechanisms
associated
with
pathology
neurological
dysfunction.
