Biomedicines,
Journal Year:
2020,
Volume and Issue:
8(10), P. 421 - 421
Published: Oct. 15, 2020
Neurodegeneration
is
a
highly
complex
process
which
associated
with
variety
of
molecular
mechanisms
related
to
ageing.
Among
neurodegenerative
disorders,
Alzheimer’s
disease
(AD)
the
most
common,
affecting
more
than
45
million
individuals.
The
underlying
involve
amyloid
plaques
and
neurofibrillary
tangles
(NFTs)
deposition,
will
subsequently
lead
oxidative
stress,
chronic
neuroinflammation,
neuron
dysfunction,
neurodegeneration.
current
diagnosis
methods
are
still
limited
in
regard
possibility
accurate
early
detection
diseases.
Therefore,
research
has
shifted
towards
identification
novel
biomarkers
matrices
as
biomarker
sources,
beyond
amyloid-β
tau
protein
levels
within
cerebrospinal
fluid
(CSF),
that
could
improve
AD
diagnosis.
In
this
context,
aim
paper
provide
an
overview
both
conventional
for
found
body
fluids,
including
CSF,
blood,
saliva,
urine,
tears,
olfactory
fluids.
Acta Neuropathologica,
Journal Year:
2020,
Volume and Issue:
140(4), P. 417 - 447
Published: July 29, 2020
Abstract
Tau
and
amyloid
beta
(Aβ)
are
the
prime
suspects
for
driving
pathology
in
Alzheimer’s
disease
(AD)
and,
as
such,
have
become
focus
of
therapeutic
development.
Recent
research,
however,
shows
that
these
proteins
been
highly
conserved
throughout
evolution
may
crucial,
physiological
roles.
Such
functions
be
lost
during
AD
progression
or
unintentionally
disrupted
by
tau-
Aβ-targeting
therapies.
has
revealed
to
more
than
a
simple
stabiliser
microtubules,
reported
play
role
range
biological
processes
including
myelination,
glucose
metabolism,
axonal
transport,
microtubule
dynamics,
iron
homeostasis,
neurogenesis,
motor
function,
learning
memory,
neuronal
excitability,
DNA
protection.
Aβ
is
similarly
multifunctional,
proposed
regulate
angiogenesis,
repair
leaks
blood–brain
barrier,
promote
recovery
from
injury,
act
an
antimicrobial
peptide
tumour
suppressor.
This
review
will
discuss
potential
roles
tau
Aβ,
highlighting
how
changes
contribute
pathology,
well
implications
We
propose
balanced
consideration
both
pathological
essential
design
safe
effective
therapeutics.
Cells,
Journal Year:
2022,
Volume and Issue:
11(13), P. 2091 - 2091
Published: June 30, 2022
Neuroinflammation
is
a
hallmark
of
many
neurodegenerative
diseases
(NDs)
and
plays
fundamental
role
in
mediating
the
onset
progression
disease.
Microglia,
which
function
as
first-line
immune
guardians
central
nervous
system
(CNS),
are
drivers
neuroinflammation.
Numerous
human
postmortem
studies
vivo
imaging
analyses
have
shown
chronically
activated
microglia
patients
with
various
acute
chronic
neuropathological
diseases.
While
microglial
activation
common
feature
NDs,
exact
pathological
states
complex
often
contradictory.
However,
there
consensus
that
play
biphasic
conditions,
detrimental
protective
phenotypes,
overall
response
different
phenotypes
depends
on
nature
duration
inflammatory
insult,
well
stage
disease
development.
This
review
provides
comprehensive
overview
current
research
responses
health,
aging,
special
emphasis
heterogeneous
phenotypic
such
hemorrhagic
stroke
(HS),
Alzheimer's
(AD),
Parkinson's
(PD).
The
primary
focus
translational
preclinical
animal
models
bulk/single-cell
transcriptome
samples.
Additionally,
this
covers
key
receptors
signaling
pathways
potential
therapeutic
targets
to
regulate
during
aging
NDs.
age-,
sex-,
species-specific
differences
will
be
briefly
reviewed.
Cells,
Journal Year:
2021,
Volume and Issue:
10(4), P. 721 - 721
Published: March 24, 2021
Glycogen
synthase
kinase-3
(GSK-3)
is
a
ubiquitously
expressed
serine/threonine
kinase
with
plethora
of
substrates.
As
modulator
several
cellular
processes,
GSK-3
has
central
position
in
cell
metabolism
and
signaling,
important
roles
both
physiological
pathological
conditions.
been
associated
number
human
disorders,
such
as
neurodegenerative
diseases
including
Alzheimer's
disease
(AD).
contributes
to
the
hyperphosphorylation
tau
protein,
main
component
neurofibrillary
tangles
(NFTs),
one
hallmarks
AD.
further
involved
regulation
different
neuronal
processes
that
are
dysregulated
during
AD
pathogenesis,
generation
amyloid-β
(Aβ)
peptide
or
Aβ-induced
death,
axonal
transport,
cholinergic
function,
adult
neurogenesis
synaptic
function.
In
this
review,
we
will
summarize
recent
data
about
involvement
these
contributing
pathology,
mostly
focusing
on
crucial
interplay
between
protein.
We
discuss
current
development
potential
therapies
targeting
GSK-3-phosphorylated
tau.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(7), P. 3330 - 3330
Published: March 24, 2021
Alzheimer's
disease
(AD)
is
a
debilitating
neurological
disorder,
and
currently,
there
no
cure
for
it.
Several
pathologic
alterations
have
been
described
in
the
brain
of
AD
patients,
but
ultimate
causative
mechanisms
are
still
elusive.
The
classic
hallmarks
AD,
including
amyloid
plaques
(Aβ)
tau
tangles
(tau),
most
studied
features
AD.
Unfortunately,
all
efforts
targeting
these
pathologies
failed
to
show
desired
efficacy
patients
so
far.
Neuroinflammation
impaired
autophagy
two
other
main
known
It
has
reported
that
exist
long
before
emergence
any
clinical
manifestation
Microglia
inflammatory
cells
considered
by
many
researchers
as
next
hope
finding
viable
therapeutic
target
Interestingly,
it
appears
mitophagy
also
changed
Inside
cells,
inflammation
interact
bidirectional
manner.
In
current
review,
we
briefly
discussed
an
overview
on
then
provided
comprehensive
discussion
role
pathways
microglia
their
involvement
pathogenesis.
Acta Neuropathologica,
Journal Year:
2021,
Volume and Issue:
142(1), P. 57 - 71
Published: April 8, 2021
Abstract
Tauopathies
consist
of
over
25
different
neurodegenerative
diseases
that
include
argyrophilic
grain
disease
(AGD),
progressive
supranuclear
palsy
(PSP),
corticobasal
degeneration
(CBD),
and
Pick’s
(PiD).
are
defined
by
brain
accumulation
microtubule-associated
protein
tau
in
fibrillar
aggregates,
whose
prevalence
strongly
correlates
with
dementia.
Dominant
mutations
cause
diseases,
most
increase
its
aggregation
propensity.
Pathogenesis
tauopathies
may
involve
pathological
conformers
serve
as
templates
to
recruit
native
into
growing
assemblies
also
move
between
cells
progression,
similar
prions.
Prions
adopt
conformations,
termed
“strains,”
stably
propagate
living
systems,
create
unique
patterns
neuropathology.
Data
from
multiple
laboratories
now
suggest
acts
a
prion.
It
propagates
strains
indefinitely
cultured
cells,
when
these
inoculated
mouse
models,
they
neuropathological
patterns,
which
establish
direct
link
conformation
disease.
In
humans,
distinct
fibril
structures
associated
but
causality
has
not
been
established
mice.
Cryo-EM
fibrils
isolated
tauopathy
brains
reveal
cores
across
Interestingly,
the
monomer
unit
within
subtypes
same
patient
appears
relatively
preserved.
This
is
consistent
data
samples
an
ensemble
conformations
act
pathologic
formation
restricted
numbers
strains.
The
propensity
be
linked
local
motifs
expose
amyloidogenic
amino
acid
sequences.
prion
hypothesis,
predicts
structure
dictates
resultant
disease,
proved
particularly
useful
understand
diversity
human
tauopathies.
challenge
develop
methods
rapidly
classify
patients
according
underlying
achieve
more
accurate
diagnosis
effective
therapy.
Chemical Society Reviews,
Journal Year:
2021,
Volume and Issue:
51(2), P. 513 - 565
Published: Dec. 10, 2021
We
discuss
novel
approaches
for
embracing
and
reproducing
complexity
of
Tau
pathology
required
developing
disease-relevant
diagnostics
effective
therapies.
