In
the
previous
chapter,
we
learned
that
circulation
of
CSF
and
interstitial
fluids
throughout
central
nervous
system
is
responsible
for
transport
solutes,
including
nutrients,
drugs,
metabolic
waste.
We
have
also
this
occurs
predominantly
during
sleep
how
privation
can
lead
to
accumulation
first,
will
briefly
review
alterations
in
flow
rate
production
several
pathological
conditions.
Then
learn
flow/turnover
dysfunction
may
play
a
crucial
role
pathogenesis
neurodegenerative
disorders,
tissue
damage
from
stroke
neuroinflammatory
diseases.
The
emerging
knowledge
its
as
CNS
has
significant
implications
human
health.
Neurodegenerative
such
Alzheimer's
disease,
Parkinson's
cerebral
amyloid
angiopathy,
are
thought
be
caused
by
unhealthy
natural
waste
proteins,
which
influenced
impaired
or
degraded
flow.
Additionally,
plays
contributing
local
swelling.
Disruption
glymphatic
clearance
been
noted
those
with
hydrocephalus,
common
outcome
subarachnoid
hemorrhage,
idiopathic
origin.
intracranial
hypertension
leaks
spontaneous
hypotension,
primarily
involved,
while
tumors
usually
consequence.
Finally,
meningitis
autoimmune,
inflammatory
other
groups
diseases
where
clearly
involved
their
pathogenesis.
S S Korsakov Journal of Neurology and Psychiatry,
Год журнала:
2023,
Номер
123(9), С. 31 - 31
Опубликована: Янв. 1, 2023
Selective
and
progressive
death
of
neurons
is
a
characteristic
feature
the
process
neurodegeneration
leads
to
corresponding
neuronal
dysfunctions.
Neurodegenerative
diseases
represent
heterogeneous
group
clinically
distinct
disorders
with
similar
molecular
mechanisms
pathogenesis.
They
are
based
on
processes
abnormal
aggregation
proteins,
formation
fibrillary
insoluble
structures
their
deposition
in
form
histopathological
inclusions
tissues
nervous
system.
Disturbance
homeostatic
functions
that
regulate
ion
energy
metabolism,
biosynthesis
degradation
proteins
nucleotides,
chronic
hypoxia
penetration
toxic
inflammatory
substances
into
brain
from
bloodstream
not
only
cause
metabolic
changes
associated
age
sleep-wake
cycle,
but
also
contribute
development
neurodegenerative
diseases.
In
animal
studies,
clearance
pathways
have
been
identified
which
solutes
specific
tracers
excreted
perivascular
meningeal
lymphatics.
The
glymphatic
pathway
promotes
removal
metabolites,
including
Aβ
amyloid
tau
protein,
parenchymal
extracellular
space
brain.
system
discussed
be
more
efficient
during
natural
sleep,
fluid
dynamics
through
this
exhibit
daily
fluctuations
under
circadian
control.
This
review
systematizes
key
aspects
data
recent
research
role
astroglial
AQP-4
as
its
main
determinant
maintaining
circulation
normal
pathological
conditions,
particular
relation
regulatory
cycle
neurodegeneration.Избирательная
и
прогрессирующая
гибель
нейронов
является
характерной
чертой
процесса
нейродегенерации
приводит
к
соответствующим
нейрональным
дисфункциям.
Нейродегенеративные
заболевания
представляют
гетерогенную
группу
различных
по
клинической
картине
нозологий
со
сходными
молекулярными
механизмами
патогенеза.
В
их
основе
лежат
процессы
аномальной
агрегации
белков,
формирования
фибриллярных
нерастворимых
структур
депонирования
в
виде
гистопатологических
включений
тканях
нервной
системы.
Нарушение
гомеостатических
функций,
регулирующих
нейрональный
ионный
энергетический
обмен,
биосинтез
деградацию
белков
нуклеотидов,
хроническая
гипоксия
проникновение
головной
мозг
из
кровотока
токсических
воспалительных
веществ
не
только
вызывают
метаболические
изменения,
ассоциированные
с
возрастом
нарушениями
цикле
«сон—бодрствование»,
но
способствуют
развитию
нейродегенеративных
процессов.
исследованиях
на
животных
были
выявлены
пути
клиренса,
при
которых
растворенные
вещества
специфические
трассеры
выводятся
периваскулярным
путем
менингеальные
лимфатические
сосуды.
Глимфатическая
сеть
способствует
выведению
метаболитов,
включая
бета-амилоид
тау-белок,
внеклеточного
пространства
головного
мозга.
Обсуждается,
что
глимфатическая
система
более
эффективна
во
время
естественного
сна,
а
гидродинамика
через
этот
путь
демонстрирует
ежедневные
колебания
находится
под
циркадианным
контролем.
настоящем
обзоре
систематизированы
ключевые
аспекты
научные
данные
последних
исследований
о
роли
глимфатического
астроглиального
аквапорина
4-го
типа
как
его
основной
детерминанты
поддержании
гомеостатической
циркуляции
жидкости
мозге
норме
патологии,
частности
взаимосвязи
регулирующей
ролью
цикла
«сон—бодрствование»
развитии
Archives of Plastic Surgery,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 10, 2025
Abstract
The
relatively
recent
discovery
of
a
novel
lymphatic
system
within
the
brain
meninges
has
spurred
interest
in
how
waste
products
generated
by
neurons
and
glial
cells—including
proteins
associated
with
Alzheimer's
disease
(AD)
pathology
such
as
amyloid
beta
(Aβ)
tau—are
disposed
of.
Evidence
is
building
that
suggests
progression
AD
other
cognitive
impairments
could
be
explained
dysfunction
brain's
or
obstruction
drainage.
An
interesting
implication
this
hypothesis
that,
relieving
flow,
reconstruction
along
drainage
pathway
serve
potential
treatment.
Should
concept
prove
true,
it
represent
surgical
solution
to
problem
for
which
only
medical
solutions
have
thus
far
been
considered.
This
study
meant
primer
reconstructive
microsurgeons,
introducing
topic
current
hypotheses
about
role
AD.
A
preview
research
evaluating
feasibility
approach
improving
Aβ
clearance
provided,
aim
inspiring
others
design
robust
preclinical
clinical
investigations
into
intriguing
hypothesis.
Biomedicines,
Год журнала:
2023,
Номер
11(10), С. 2663 - 2663
Опубликована: Сен. 28, 2023
Small
vessel
diseases
(SVD)
is
an
umbrella
term
including
several
entities
affecting
small
arteries,
arterioles,
capillaries,
and
venules
in
the
brain.
One
of
most
relevant
prevalent
SVDs
cerebral
amyloid
angiopathy
(CAA),
whose
pathological
hallmark
deposition
fragments
walls
cortical
leptomeningeal
vessels.
CAA
frequently
coexists
with
Alzheimer’s
Disease
(AD),
both
are
associated
cerebrovascular
events,
cognitive
impairment,
dementia.
AD
share
pathophysiological,
histopathological
neuroimaging
issues.
The
venular
involvement
has
been
neglected,
although
animal
models
human
studies
found
a
beta
venules.
This
review
aimed
to
summarize
available
information
about
CAA,
starting
from
biological
level
putative
pathomechanisms
damage,
passing
through
definition
peculiar
angioarchitecture
cortex
functional
organization
consequences
arteriolar
occlusion,
ending
hypothesized
links
between
main
markers
disease.
Genes and Cells,
Год журнала:
2023,
Номер
18(4), С. 309 - 322
Опубликована: Ноя. 11, 2023
Recently,
the
concept
of
glymphatic
system
as
a
highly
organized
perivascular
network
has
been
formed,
which
by
hydrodynamic
approach,
with
key
participation
aquaporin-4
central
molecule,
connects
cerebrospinal
fluid
lymphatic
vessels
meninges
through
brain
interstitium.
The
latest
scientific
works
demonstrates
potential
role
dysfunction
in
development
neurodegeneration
and
pathological
aging.
Although
precise
molecular
mechanisms
pathway
function
have
not
yet
fully
characterized,
critical
processes
underlying
cerebral
solute
transport
clearance
amyloid
metabolites
largely
elucidated.
complex
interaction
between
number
age-associated
factors,
including
cellular
aging,
disturbances
sleep-wake
cycle
changes
sleep
architecture
quality,
low-grade
systemic
inflammation,
concomitant
diseases,
determines
only
life
expectancy
general,
but
also
forms
basis
healthy
unhealthy
aging
particular.
Imbalances
homeostatic
functions,
activity
blood-brain
barrier
that
support
exchange
solutes
tissue,
can
be
observed
both
normally
physiological
neuropathology,
longitudinal
consequences
ranging
from
disruption
synaptic
signal
transmission
to
onset
neurodegenerative
processes.
This
review
analyzes
current
information
this
area
research,
details
features
glial-mediated
system,
discusses
how
its
plays
fundamental
accumulation
during
brain,
progression
diseases.
Психиатрия психотерапия и клиническая психология,
Год журнала:
2023,
Номер
14(3), С. 291 - 300
Опубликована: Ноя. 28, 2023
Определение
основных
патогенетических
механизмов
развития
наиболее
распространенной
формы
деменции
–
болезни
Альцгеймера,
а
также
поиск
эффективных
решений
для
замедления
и
прекращения
прогрессирования
заболевания
относятся
к
одним
из
приоритетных
направлений
фундаментальной
нейробиологии
практической
медицины.
Гипотеза
бета-амилоида
тау-белка
в
значительной
степени
объясняет
ключевые
патологические
особенности
альцгеймеровского
типа.
Системные
механизмы
молекулярные
процессы,
вследствие
которых
такие
белки
накапливаются
приводят
прогрессированию
заболевания,
вызывают
выраженный
научный
практический
интерес,
что
актуализировано
сохранением
терапевтического
пробела
определении
рациональных
вмешательств,
модифицирующих
болезнь,
поиском
доступных
биомаркеров,
высокоинформативных
на
доклинической
стадии
нейродегенеративных
расстройств
у
людей
без
когнитивных
нарушений
определяемых
клинических
симптомов.
Тем
не
менее
недавнее
открытие
аквапорин-зависимого
глимфатического
пути,
управляющего
центральным
клиренсом
растворенных
веществ
головном
мозге,
выявило
новый
механизм,
лежащий
основе
патогенеза
нейродегенерации
нейровоспаления.
Настоящий
обзор
представляет
систематизирует
современные
данные
о
причинно-следственных
связях
дисфункции
глимфатической
системы
мозга
накопления
патологических
белков
с
недостаточным
выведением
токсических
продуктов
метаболизма
функционального
пространства
нейронов,
являющихся
ключевыми
звеньями
развитии
Determination
of
the
main
pathological
mechanisms
development
most
common
form
dementia
Alzheimer’s
disease,
as
well
search
for
effective
solutions
to
slow
down
and
stop
progression
is
one
priority
areas
fundamental
neurobiology
practical
medicine.
The
beta-amyloid
tau
hypothesis
largely
explains
key
features
dementia.
Systemic
molecular
processes,
due
which
such
proteins
accumulate
lead
are
great
scientific
interest,
updated
by
persistence
a
therapeutic
gap
in
definition
rational
disease-modifying
interventions,
available
biomarkers
that
highly
informative
at
preclinical
stage
neurodegenerative
disorders
people
without
cognitive
dysfunction.
However,
recent
discovery
an
aquaporin-dependent
glymphatic
pathway
controls
central
solute
clearance
brain
has
revealed
new
mechanism
underlying
pathogenesis
neurodegeneration
neuroinflammation.
This
review
presents
systematizes
current
data
on
causal
relationships
between
dysfunction
system
accumulation
with
insufficient
excretion
toxic
metabolic
products
from
functional
space
neurons,
links
type.
IBRO Neuroscience Reports,
Год журнала:
2023,
Номер
16, С. 98 - 105
Опубликована: Дек. 23, 2023
A
typical
anatomical
congregate
and
functionally
distinct
multicellular
cerebrovascular
dynamic
confer
diverse
blood-brain
barrier
(BBB)
microstructural
permeabilities
to
conserve
the
health
of
brain
parenchymal
its
microenvironment.
This
equanimity
presupposes
glymphatic
system
that
governs
flow
clearance
metabolic
waste
interstitial
fluids
(IF)
through
venous
circulation.
Following
introduction
concept,
various
studies
have
been
carried
out
on
cerebrospinal
fluid
(CSF)
IF
dynamics.
These
reported
onset
multiple
diseases
can
be
attributed
impairment
in
system,
which
is
newly
referred
as
central
nervous
(CNS)
fluidopathy.
One
such
condition
includes
cerebral
small
vessel
disease
(CSVD)
with
poorly
understood
pathomechanisms.
CSVD
an
umbrella
term
describe
a
chronic
progressive
disorder
affecting
microvasculature
(or
microcirculation)
involving
penetrating
vessels
supply
white
deep
grey
matter.
review
article
proposes
form
"CNS
fluidopathy".
Linking
CNS
fluidopathy
will
open
better
insight
pertaining
perivascular
space
dynamics
pathophysiology.
may
lead
development
treatment
therapeutic
strategies
ameliorate
pathology
adverse
effect
CSVD.
Frontiers in Aging Neuroscience,
Год журнала:
2024,
Номер
16
Опубликована: Май 2, 2024
Objective
This
research
aims
to
investigate
putative
mechanisms
between
glymphatic
activity
and
cognition
in
mild
cognitive
impairment
(MCI)
analyzes
whether
the
relationship
reserve
(CR)
was
mediated
by
activity.
Methods
54
MCI
patients
31
NCs
were
enrolled
evaluate
bilateral
diffusivity
along
perivascular
spaces
acquire
an
index
for
space
(ALPS-index)
on
diffusion
tensor
imaging
(DTI).
The
year
of
education
used
as
a
proxy
CR.
ALPS-index
compared
two
groups
correlation
analyses
among
ALPS-index,
function,
CR
conducted.
Mediation
applied
correlations
CR,
cognition.
Results
group
had
significantly
lower
right
whole
brain
but
higher
y-axis
projection
fiber
area
(Dyproj)
than
NCs.
In
group,
left
Dyproj
negatively
related
test
scores
positively
correlated
with
analysis
demonstrated
that
partially
function.
Conclusion
exhibited
decreased
has
protective
effect
against
decline
MCI,
this
may
be
changes