Journal of Alzheimer s Disease,
Год журнала:
2022,
Номер
88(2), С. 619 - 629
Опубликована: Июнь 3, 2022
Despite
the
fact
that
only
modest
adaptive
immune
system
related
approaches
to
treating
Alzheimer's
disease
(AD)
are
available,
an
immunogenomics
approach
study
of
AD
has
not
yet
substantially
advanced.Thus,
we
sought
better
understand
receptor
chemical
features
in
setting.We
characterized
T-cell
alpha
(TRA)
complementarity
determining
region-3
(CDR3)
physicochemical
and
identified
TRA
CDR3
homology
groups,
represented
by
recombination
reads
extracted
from
2,665
AD-related,
blood-
brain-derived
exome
files.We
found
a
higher
isoelectric
value
for
brain
CDR3s
was
associated
with
(clinically
worse)
Braak
stage
number
particular
representing
bloodborne
CDR3s,
were
or
lower
stages.
Lastly,
greater
both
tau,
based
on
recently
described
CDR3-candidate
antigen
scoring
process
(https://adaptivematch.com),
stages.Overall,
data
reported
here
raise
questions
(a)
whether
progression
is
facilitated
response
tau;
(b)
assessment
such
anti-tau
could
potentially
serve
as
basis
related,
risk
stratification?
Frontiers in Immunology,
Год журнала:
2021,
Номер
12
Опубликована: Ноя. 5, 2021
Immune
infiltration
of
peripheral
natural
killer
(NK)
cells
in
the
brain
has
been
observed
Alzheimer’s
disease
(AD).
Immunity-related
genes
(IRGs)
play
an
essential
role
immune
infiltration;
however,
expression
IRGs
and
possible
regulatory
mechanisms
involved
AD
remain
unclear.
The
blood
mononuclear
(PBMCs)
single-cell
RNA
(scRNA)
sequencing
data
from
patients
with
were
analyzed
PBMCs
obtained
ImmPort
database
screened
for
cluster
marker
genes.
IRG
activity
was
calculated
using
AUCell
package.
A
bulk
dataset
tissues
to
explore
common
between
brain.
Relevant
transcription
factors
(TFs)
identified
Human
TFDB
database.
protein-protein
interaction
network
key
TFs
generated
STRING
Eight
clusters
identified,
including
memory
CD4
T,
NKT,
NK,
B,
DC,
CD8
T
cells,
platelets.
NK
significantly
decreased
AD,
while
increased.
DC
exhibited
highest
activity.
GO
KEGG
analyses
scRNA
showed
that
DEGs
focused
on
response.
Seventy
found
both
Seventeen
associated
expression,
PPI
indicated
STAT3,
IRF1,
REL
hub
TFs.
In
conclusion,
we
propose
may
infiltrate
contribute
neuroinflammatory
changes
through
bioinformatic
analysis
data.
Moreover,
STAT3
be
transcriptional
regulation
cells.
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Март 3, 2023
Alzheimer’s
disease
(AD)
is
the
leading
cause
of
dementia
in
United
States.
Sporadic
or
late-onset
AD
remains
incompletely
understood,
with
age
as
current
greatest
risk
factor.
Inflammation
general
and
neutrophils,
a
potent
mediator
inflammation,
have
been
shown
to
exacerbate
associated
dementia.
This
review
explores
latest
research
on
neutrophils
mouse
models
human
cohort
studies
discusses
gaps
needs
for
future
studies.
neutrophil
chemotactic
migration
towards
amyloid
beta
plaques
brain.
Capillary
blood
flow
stalling
decreases
perfusion
brain
regions
demonstrated
that
anti-Ly6G
antibodies
lead
decrease
capillary
memory
improvement.
Several
recent
transcriptomic
tissue
from
persons
an
upregulation
neutrophil-related
genes,
involvement
adhesion,
barrier
breaching,
myeloperoxidase
release,
propensity
extracellular
trap
release
AD.
Neutrophil-derived
inflammation
regulation
are
potential
novel
therapeutic
target
progression.
Future
should
further
investigate
functionality
In
addition,
other
aspects
may
impact
including
microbiome
APOE4
allele
be
studied.
Alzheimer s & Dementia,
Год журнала:
2023,
Номер
19(9), С. 3965 - 3976
Опубликована: Апрель 26, 2023
Low
hemoglobin
and
anemia
are
associated
with
cognitive
impairment
Alzheimer's
disease
(AD).
However,
the
associations
of
other
blood
cell
indices
incident
dementia
risk
underlined
mechanisms
unknown.
Nature Communications,
Год журнала:
2023,
Номер
14(1)
Опубликована: Март 9, 2023
Abstract
Systemic
immunity
supports
lifelong
brain
function.
Obesity
posits
a
chronic
burden
on
systemic
immunity.
Independently,
obesity
was
shown
as
risk
factor
for
Alzheimer’s
disease
(AD).
Here
we
show
that
high-fat
obesogenic
diet
accelerated
recognition-memory
impairment
in
an
AD
mouse
model
(5xFAD).
In
obese
5xFAD
mice,
hippocampal
cells
displayed
only
minor
diet-related
transcriptional
changes,
whereas
the
splenic
immune
landscape
exhibited
aging-like
CD4
+
T-cell
deregulation.
Following
plasma
metabolite
profiling,
identified
free
N
-acetylneuraminic
acid
(NANA),
predominant
sialic
acid,
linking
to
increased
immune-suppressive
mice.
Single-nucleus
RNA-sequencing
revealed
visceral
adipose
macrophages
potential
source
of
NANA.
vitro,
NANA
reduced
proliferation,
tested
both
and
human.
vivo,
administration
standard
diet-fed
mice
recapitulated
effects
T
We
suggest
accelerates
manifestation
via
exhaustion.
Cellular and Molecular Life Sciences,
Год журнала:
2023,
Номер
80(7)
Опубликована: Июнь 24, 2023
Abstract
Ageing
is
characterized
by
the
progressive
loss
of
cellular
homeostasis,
leading
to
an
overall
decline
organism’s
fitness.
In
brain,
ageing
highly
associated
with
cognitive
and
neurodegenerative
diseases.
With
rise
in
life
expectancy,
characterizing
brain
process
becomes
fundamental
for
developing
therapeutic
interventions
against
increased
incidence
age-related
diseases
aim
increase
human
span
and,
more
importantly,
health
span.
this
review,
we
start
introducing
molecular/cellular
hallmarks
their
impact
on
cell
populations.
Subsequently,
assess
emerging
evidence
how
systemic
translates
into
ageing.
Finally,
revisit
mainstream
novel
rejuvenating
strategies,
discussing
most
successful
ones
delaying
related
Biomedicines,
Год журнала:
2023,
Номер
11(10), С. 2793 - 2793
Опубликована: Окт. 14, 2023
Many
potential
immune
therapeutic
targets
are
similarly
affected
in
adult-onset
neurodegenerative
diseases,
such
as
Alzheimer's
(AD)
disease,
Parkinson's
disease
(PD),
amyotrophic
lateral
sclerosis
(ALS),
and
frontotemporal
dementia
(FTD),
well
a
seemingly
distinct
Niemann-Pick
type
C
with
primarily
juvenile
onset.
This
strongly
argues
for
an
overlap
pathogenic
mechanisms.
The
commonly
researched
include
various
cell
subsets,
microglia,
peripheral
macrophages,
regulatory
T
cells
(Tregs);
the
complement
system;
other
soluble
factors.
In
this
review,
we
compare
these
diseases
from
clinical
point
of
view
highlight
common
pathways
mechanisms
protein
aggregation,
neurodegeneration,
and/or
neuroinflammation
that
could
potentially
lead
to
shared
treatment
strategies
overlapping
dysfunctions
diseases.
These
approaches
but
not
limited
immunisation,
cascade
blockade,
microbiome
regulation,
inhibition
signal
transduction,
Treg
boosting,
stem
transplantation.
