Circulation,
Journal Year:
2017,
Volume and Issue:
136(8), P. 719 - 728
Published: June 7, 2017
Cerebral
hypoperfusion
has
previously
been
associated
with
mild
cognitive
impairment
and
dementia
in
various
cross-sectional
studies,
but
whether
precedes
neurodegeneration
is
unknown.
We
prospectively
determined
the
association
of
cerebral
perfusion
subsequent
decline
development
dementia.Between
2005
2012,
we
measured
blood
flow
by
2-dimensional
phase-contrast
magnetic
resonance
imaging
participants
population-based
Rotterdam
Study
without
dementia.
(mL/100mL/min)
risk
(until
2015)
using
a
Cox
model,
adjusting
for
age,
sex,
demographics,
cardiovascular
factors,
apolipoprotein
E
genotype.
repeated
analyses
Alzheimer
disease
accounting
stroke.
used
linear
regression
to
determine
change
performance
during
2
consecutive
examination
rounds
relation
perfusion.
Finally,
investigated
associations
were
modified
baseline
severity
white
matter
hyperintensities.Of
4759
(median
age
61.3
years,
55.2%
women)
median
follow-up
6.9
123
developed
(97
disease).
Lower
was
higher
(adjusted
hazard
ratio,
1.31;
95%
confidence
interval
per
standard
deviation
decrease,
1.07-1.61),
similar
only,
unaltered
Risk
increasing
hyperintensities
(with
severe
hyperintensities;
1.54;
interval,
1.11-2.14).
At
reexamination
after
on
average
5.7
lower
accelerated
cognition
(global
cognition:
β=-0.029,
P=0.003),
which
excluding
those
incident
dementia,
again
most
profound
individuals
volume
(P
value
interaction=0.019).Cerebral
an
increased
general
population.
Physiological Reviews,
Journal Year:
2018,
Volume and Issue:
99(1), P. 21 - 78
Published: Oct. 3, 2018
The
blood-brain
barrier
(BBB)
prevents
neurotoxic
plasma
components,
blood
cells,
and
pathogens
from
entering
the
brain.
At
same
time,
BBB
regulates
transport
of
molecules
into
out
central
nervous
system
(CNS),
which
maintains
tightly
controlled
chemical
composition
neuronal
milieu
that
is
required
for
proper
functioning.
In
this
review,
we
first
examine
molecular
cellular
mechanisms
underlying
establishment
BBB.
Then,
focus
on
physiology,
endothelial
pericyte
transporters,
perivascular
paravascular
transport.
Next,
discuss
rare
human
monogenic
neurological
disorders
with
primary
genetic
defect
in
BBB-associated
cells
demonstrating
link
between
breakdown
neurodegeneration.
review
effects
genes
inheritance
and/or
increased
susceptibility
Alzheimer's
disease
(AD),
Parkinson's
(PD),
Huntington's
disease,
amyotrophic
lateral
sclerosis
(ALS)
relation
to
other
pathologies
deficits.
We
next
how
dysfunction
relates
deficits
majority
sporadic
AD,
PD,
ALS
cases,
multiple
sclerosis,
neurodegenerative
disorders,
acute
CNS
such
as
stroke,
traumatic
brain
injury,
spinal
cord
epilepsy.
Lastly,
BBB-based
therapeutic
opportunities.
conclude
lessons
learned
future
directions,
emphasis
technological
advances
investigate
functions
living
brain,
at
level,
address
key
unanswered
questions.
Science,
Journal Year:
2016,
Volume and Issue:
353(6301), P. 777 - 783
Published: Aug. 18, 2016
Neurodegenerative
diseases
such
as
Alzheimer's
disease,
Parkinson's
amyotrophic
lateral
sclerosis,
and
frontotemporal
lobar
dementia
are
among
the
most
pressing
problems
of
developed
societies
with
aging
populations.
Neurons
carry
out
essential
functions
signal
transmission
network
integration
in
central
nervous
system
main
targets
neurodegenerative
disease.
In
this
Review,
I
address
how
neuron's
environment
also
contributes
to
neurodegeneration.
Maintaining
an
optimal
milieu
for
neuronal
function
rests
supportive
cells
termed
glia
blood-brain
barrier.
Accumulating
evidence
suggests
that
neurodegeneration
occurs
part
because
is
affected
during
disease
a
cascade
processes
collectively
neuroinflammation.
These
observations
indicate
therapies
targeting
glial
might
provide
benefit
those
afflicted
by
disorders.
Molecular Neurodegeneration,
Journal Year:
2020,
Volume and Issue:
15(1)
Published: July 16, 2020
Abstract
Alzheimer’s
disease
(AD)
is
the
most
common
neurodegenerative
disorder
seen
in
age-dependent
dementia.
There
currently
no
effective
treatment
for
AD,
which
may
be
attributed
part
to
lack
of
a
clear
underlying
mechanism.
Studies
within
last
few
decades
provide
growing
evidence
central
role
amyloid
β
(Aβ)
and
tau,
as
well
glial
contributions
various
molecular
cellular
pathways
AD
pathogenesis.
Herein,
we
review
recent
progress
with
respect
Aβ-
tau-associated
mechanisms,
discuss
dysfunction
emphasis
on
neuronal
receptors
that
mediate
Aβ-induced
toxicity.
We
also
other
critical
factors
affect
pathogenesis,
including
genetics,
aging,
variables
related
environment,
lifestyle
habits,
describe
potential
apolipoprotein
E
(APOE),
viral
bacterial
infection,
sleep,
microbiota.
Although
have
gained
much
towards
understanding
aspects
this
devastating
disorder,
greater
commitment
research
mechanism,
diagnostics
will
needed
future
research.
