Journal of Neuroinflammation,
Journal Year:
2019,
Volume and Issue:
16(1)
Published: Feb. 25, 2019
Neurodegenerative
diseases
such
as
Alzheimer's
disease
(AD),
Parkinson's
dementia
(PDD),
and
frontotemporal
lobar
(FTLD)
are
characterized
by
progressive
neuronal
loss
but
differ
in
their
underlying
pathological
mechanisms.
However,
neuroinflammation
is
commonly
observed
within
these
different
forms
of
dementia.
Recently,
it
has
been
suggested
that
an
altered
sphingolipid
metabolism
may
contribute
to
the
pathogenesis
a
variety
neurodegenerative
conditions.
Especially
ceramide,
precursor
all
complex
sphingolipids,
thought
be
associated
with
pro-apoptotic
cellular
processes,
thereby
propagating
neurodegeneration
neuroinflammation,
although
remains
unclear
what
extent.
The
current
study
therefore
investigates
whether
increased
levels
ceramide
degree
various
disorders.
Immunohistochemistry
was
performed
on
human
post-mortem
tissue
PDD
FTLD
Pick's
cases,
which
well-characterized
cases
subtypes
differing
neuroinflammatory
status,
assess
expression
localization
acid
sphingomyelinase,
synthase
2
5.
In
addition,
we
determined
concentration
sphingosine,
sphingosine-1-phosphate
(S1P),
species
chain-length
brain
homogenates
using
HPLC-MS/MS.
Our
immunohistochemical
analysis
reveals
astrocytes
disease.
Moreover,
increase
correlates
HPLC-MS/MS
shows
shift
under
conditions,
favoring
ceramide.
Together,
findings
suggest
detected
might
common
denominator
diseases.
Translational Neurodegeneration,
Journal Year:
2022,
Volume and Issue:
11(1)
Published: April 21, 2022
Alzheimer's
disease
(AD)
is
a
complex,
heterogeneous,
progressive
and
the
most
common
type
of
neurodegenerative
dementia.
The
prevalence
AD
expected
to
increase
as
population
ages,
placing
an
additional
burden
on
national
healthcare
systems.
There
large
need
for
new
diagnostic
tests
that
can
detect
at
early
stage
with
high
specificity
relatively
low
cost.
development
modern
analytical
tools
has
made
it
possible
determine
several
biomarkers
specificity,
including
pathogenic
proteins,
markers
synaptic
dysfunction,
inflammation
in
blood.
considerable
potential
using
microRNA
(miRNA)
AD,
studies
based
miRNA
panels
suggest
could
potentially
be
determined
accuracy
individual
patients.
Studies
retina
improved
methods
visualization
fundus
are
also
showing
promising
results
diagnosis
disease.
This
review
focuses
recent
developments
blood,
plasma,
ocular
AD.
Alzheimer s & Dementia,
Journal Year:
2021,
Volume and Issue:
17(5), P. 768 - 776
Published: Jan. 6, 2021
Abstract
Introduction
We
investigate
dementia
risk
in
older
adults
with
different
disease
patterns
and
explore
the
role
of
inflammation
apolipoprotein
E
(
APOE
)
genotype.
Methods
A
total
2,478
dementia‐free
participants
two
or
more
chronic
diseases
(ie,
multimorbidity)
part
Swedish
National
study
on
Aging
Care
Kungsholmen
(SNAC‐K)
were
grouped
according
to
their
multimorbidity
followed
detect
clinical
dementia.
The
potential
modifier
effect
C‐reactive
protein
(CRP)
genotype
was
tested
through
stratified
analyses.
Results
People
neuropsychiatric
,
cardiovascular
sensory
impairment/cancer
had
increased
hazards
for
compared
unspecific
(Hazard
ration
(HR)
1.66,
95%
confidence
interval
[CI]
1.13‐2.42;
1.61,
CI
1.17‐2.29;
1.32,
1.10‐1.71,
respectively).
Despite
lack
statistically
significant
interaction,
high
CRP
within
these
patterns,
being
ε4
carriers
heightened
multimorbidity.
Discussion
Individuals
neuropsychiatric,
cardiovascular,
are
at
ε4,
may
further
increase
risk.
Identifying
such
high‐risk
groups
might
allow
tailored
interventions
prevention.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(7), P. 6518 - 6518
Published: March 30, 2023
Alzheimer’s
disease
is
one
of
the
most
commonly
diagnosed
cases
senile
dementia
in
world.
It
an
incurable
process,
often
leading
to
death.
This
multifactorial,
and
factor
this
inflammation.
Numerous
mediators
secreted
by
inflammatory
cells
can
cause
neuronal
degeneration.
Neuritis
may
coexist
with
other
mechanisms
disease,
contributing
progression,
also
directly
underlie
AD.
Although
much
has
been
established
about
processes
pathogenesis
AD,
many
aspects
remain
unexplained.
The
work
devoted
particular
pathomechanism
inflammation
its
role
diagnosis
treatment.
An
in-depth
detailed
understanding
neuroinflammation
help
development
diagnostic
methods
for
early
contribute
new
therapeutic
strategies
disease.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(2), P. 616 - 616
Published: Jan. 6, 2022
Dementia
is
a
neurodegenerative
condition
that
considered
major
factor
contributing
to
cognitive
decline
reduces
independent
function.
Pathophysiological
pathways
are
not
well
defined
for
diseases
such
as
dementia;
however,
published
evidence
has
shown
the
role
of
numerous
inflammatory
processes
in
brain
toward
their
pathology.
Microglia
central
nervous
system
(CNS)
principal
components
brain’s
immune
defence
and
can
detect
harmful
or
external
pathogens.
When
stimulated,
cells
trigger
neuroinflammatory
responses
by
releasing
proinflammatory
chemokines,
cytokines,
reactive
oxygen
species,
nitrogen
species
order
preserve
cell’s
microenvironment.
These
markers
include
cytokines
IL-1,
IL-6,
TNFα
chemokines
CCR3
CCL2
CCR5.
Microglial
may
produce
prolonged
response
that,
some
circumstances,
indicated
promotion
diseases.
The
present
review
focused
on
involvement
microglial
cell
activation
throughout
conditions
link
between
dementia.
Journal of Neuroinflammation,
Journal Year:
2022,
Volume and Issue:
19(1)
Published: Sept. 8, 2022
Multifactorial
diseases
are
characterized
by
inter-individual
variation
in
etiology,
age
of
onset,
and
penetrance.
These
tend
to
be
relatively
common
arise
from
the
combined
action
genetic
environmental
factors;
however,
parsing
convoluted
mechanisms
underlying
these
gene-by-environment
interactions
presents
a
significant
challenge
their
study
management.
For
neurodegenerative
disorders,
resolving
this
is
imperative,
given
enormous
health
societal
burdens
they
impose.
The
which
effects
may
act
concert
destabilize
homeostasis
elevate
risk
has
become
major
research
focus
disease.
Emphasis
further
being
placed
on
determining
extent
unifying
biological
principle
account
for
progressively
diminishing
capacity
system
buffer
disease
phenotypes,
as
increases.
Data
emerging
studies
common,
providing
insights
pragmatically
connect
that
previously
seemed
disparate.
In
review,
we
discuss
evidence
positing
inflammation
homeostatic
destabilization
affecting
risk,
progression
diseases.
Specifically,
how
associated
with
Alzheimer
Parkinson
contribute
pro-inflammatory
responses,
such
predisposition
exacerbated
insults,
theme
leveraged
ongoing
search
effective
therapeutic
interventions.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(22), P. 16288 - 16288
Published: Nov. 14, 2023
The
blood-brain
barrier
(BBB)
is
a
unique
and
selective
feature
of
the
central
nervous
system's
vasculature.
BBB
dysfunction
has
been
observed
as
an
early
sign
Alzheimer's
Disease
(AD)
before
onset
dementia
or
neurodegeneration.
intricate
relationship
between
pathogenesis
AD,
especially
in
context
neurovascular
coupling
overlap
pathophysiology
neurodegenerative
cerebrovascular
diseases,
underscores
urgency
to
understand
BBB's
role
more
deeply.
Preserving
restoring
function
emerges
potentially
promising
strategy
for
mitigating
progression
severity
AD.
Molecular
genetic
changes,
such
isoform
ε4
apolipoprotein
E
(ApoEε4),
significant
risk
factor
promoter
dysfunction,
have
shown
mediate
disruption.
Additionally,
receptors
transporters
like
low-density
lipoprotein
receptor-related
protein
1
(LRP1),
P-glycoprotein
(P-gp),
receptor
advanced
glycation
end
products
(RAGEs)
implicated
AD's
pathogenesis.
In
this
comprehensive
review,
we
endeavor
shed
light
on
pathogenic
therapeutic
connections
AD
BBB.
We
also
delve
into
latest
developments
pioneering
strategies
targeting
interventions,
addressing
its
potential
carrier.
By
providing
integrative
perspective,
anticipate
paving
way
future
research
treatments
focused
exploiting
therapy.
Frontiers in Neuroscience,
Journal Year:
2019,
Volume and Issue:
13
Published: Feb. 4, 2019
Alzheimer's
disease
(AD)
is
a
devastating
neurological
condition
associated
with
abnormal
protein
modification,
inflammation
and
memory
impairment.
Aggregated
amyloid
beta
(Aβ)
phosphorylated
tau
proteins
are
medical
diagnostic
features
but
detected
only
after
the
has
progressed
to
advanced
stages.
The
loss
of
in
AD
been
central
cholinergic
dysfunction
basal
forebrain,
where
circuitry
projects
cerebral
cortex
hippocampus.
Current
medications
target
acetylcholine
metabolism
stabilize
decline.
Various
reports
link
progression
declining
activity
forebrain
neurons.
neurotrophin,
nerve
growth
factor
(NGF),
enhances
survival
effects
neurons,
which
retrogradely
transported
from
hippocampus
forebrain.
Recent
studies
have
shown
that
NGF
plays
role
aging
as
well
age-related
diseases
such
AD,
since
can
interact
pre-existing
abnormalities
trophic
signalling
trigger
cognitive
decline
observed
AD.
Further,
gradual
dysregulation
neurotrophic
factors
brain
derived
(BDNF)
during
development
thus
intensifying
further
research
targeting
these
modifying
therapies
against
Today,
there
no
cure
available
for
symptomatic
treatment
like
cholinesterase
inhibitors
(ChEIs)
memantine
transient
moderate.
Although
many
carried
out,
yet
breakthrough
new
highly
needed.
Therefore
need
review
advancements
its
potential
therapeutic
implications
In
this
review,
we
will
put
emphasis
on
focus
encapsulated
biodelivery
(ECB)
therapy
method
summary,
hope
describe
experimental
clinical
data,
demonstrating
important
roles
treatment,
an
efficient
