Journal of Biomedical Science,
Journal Year:
2019,
Volume and Issue:
26(1)
Published: May 9, 2019
Alzheimer’s
disease
(AD)
is
the
most
common
type
of
dementia
and
typically
manifests
through
a
progressive
loss
episodic
memory
cognitive
function,
subsequently
causing
language
visuospatial
skills
deficiencies,
which
are
often
accompanied
by
behavioral
disorders
such
as
apathy,
aggressiveness
depression.
The
presence
extracellular
plaques
insoluble
β-amyloid
peptide
(Aβ)
neurofibrillary
tangles
(NFT)
containing
hyperphosphorylated
tau
protein
(P-tau)
in
neuronal
cytoplasm
remarkable
pathophysiological
cause
patients’
brains.
Approximately
70%
risk
developing
AD
can
be
attributed
to
genetics.
However,
acquired
factors
cerebrovascular
diseases,
diabetes,
hypertension,
obesity
dyslipidemia
increase
development.
aim
present
minireview
was
summarize
mechanism
main
for
AD.
As
complement,
some
protective
associated
with
lower
incidence,
reserve,
physical
activity
diet
will
also
addressed.
The Journal of Experimental Medicine,
Journal Year:
2015,
Volume and Issue:
212(7), P. 991 - 999
Published: June 15, 2015
The
central
nervous
system
(CNS)
is
considered
an
organ
devoid
of
lymphatic
vasculature.
Yet,
part
the
cerebrospinal
fluid
(CSF)
drains
into
cervical
lymph
nodes
(LNs).
mechanism
CSF
entry
LNs
has
been
unclear.
Here
we
report
surprising
finding
a
vessel
network
in
dura
mater
mouse
brain.
We
show
that
dural
vessels
absorb
from
adjacent
subarachnoid
space
and
brain
interstitial
(ISF)
via
glymphatic
system.
Dural
transport
deep
(dcLNs)
foramina
at
base
skull.
In
transgenic
model
expressing
VEGF-C/D
trap
displaying
complete
aplasia
vessels,
macromolecule
clearance
was
attenuated
dcLNs
abrogated.
Surprisingly,
ISF
pressure
water
content
were
unaffected.
Overall,
these
findings
indicate
flow
directly
network,
which
may
be
important
for
macromolecules
Importantly,
results
call
reexamination
role
CNS
physiology
disease.
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.
