Acta Neuropathologica Communications,
Год журнала:
2021,
Номер
9(1)
Опубликована: Сен. 9, 2021
Abstract
In
this
review,
we
discuss
the
synaptic
aspects
of
Tau
pathology
occurring
during
Alzheimer’s
disease
(AD)
and
how
may
relate
to
memory
impairment,
a
major
hallmark
AD.
Whilst
clinical
diagnosis
AD
patients
is
loss
working
long-term
declarative
memory,
histological
presence
neurofibrillary
tangles
hyperphosphorylated
Amyloid-beta
plaques.
spreads
through
synaptically
connected
neurons
impair
function
preceding
formation
tangles,
loss,
axonal
retraction
cell
death.
Alongside
pathology,
recent
data
suggest
that
has
physiological
roles
in
pre-
or
post-
compartments.
Thus,
have
seen
shift
research
focus
from
as
microtubule-stabilising
protein
axons,
with
accelerating
spine
formation,
dendritic
elongation,
plasticity
coordinating
pathways.
We
collate
here
myriad
emerging
interactions
Tau,
current
evidence
contributes
Journal of Neuroinflammation,
Год журнала:
2020,
Номер
17(1)
Опубликована: Окт. 6, 2020
Abstract
Alzheimer’s
disease
(AD)
is
the
most
common
type
of
dementia
and
a
neurodegenerative
disorder
characterized
by
memory
deficits
especially
forgetting
recent
information,
recall
ability
impairment,
loss
time
tracking,
problem-solving,
language,
recognition
difficulties.
AD
also
globally
important
health
issue
but
despite
all
scientific
efforts,
treatment
still
challenge.
Sleep
has
roles
in
learning
consolidation.
Studies
have
shown
that
sleep
deprivation
(SD)
insomnia
are
associated
with
pathogenesis
may
an
impact
on
symptoms
development.
Thus,
disorders
decisive
effects
AD;
this
association
deserves
more
attention
research,
diagnostics,
treatment,
knowing
relation
can
help
to
prevent
through
screening
proper
management
disorders.
This
study
aimed
show
potential
role
SD
progression
AD.
Frontiers in Cell and Developmental Biology,
Год журнала:
2021,
Номер
9
Опубликована: Июль 28, 2021
Tau
is
a
protein
that
associates
with
microtubules
(MTs)
and
promotes
their
assembly
stability.
The
loses
its
ability
to
bind
MTs
in
tauopathies,
detached
tau
can
misfold
induce
the
pathological
changes
characterize
Alzheimer’s
disease
(AD).
A
growing
body
of
evidence
indicates
tauopathies
spread
between
cells
or
connected
regions.
Pathological
transmission
brain
patients
AD
other
due
various
species
along
neuroanatomically
regions
“prion-like”
manner.
This
complex
process
involves
multiple
steps
secretion,
cellular
uptake,
transcellular
transfer,
and/or
seeding,
but
precise
mechanisms
pathology
propagation
remain
unclear.
review
summarizes
current
on
nature
propagative
possible
involved
spread,
including
detachment
from
MTs,
degradations,
discusses
different
underlying
pathology.
Frontiers in Neuroscience,
Год журнала:
2021,
Номер
15
Опубликована: Дек. 14, 2021
Autophagy
is
an
important
cellular
self-digestion
and
recycling
pathway
that
helps
in
maintaining
homeostasis.
Dysregulation
at
various
steps
of
the
autophagic
endolysosomal
has
been
reported
several
neurodegenerative
disorders
such
as
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
Huntington
(HD)
cited
a
critically
feature
for
central
nervous
system
(CNS)
proteostasis.
Recently,
another
molecular
target,
namely
transcription
factor
EB
(TFEB)
explored
globally
to
treat
disorders.
This
TFEB,
key
regulator
autophagy
lysosomal
biogenesis
pathway.
Multiple
research
studies
suggested
therapeutic
potential
by
targeting
TFEB
human
diseases
involving
autophagy-lysosomal
dysfunction,
especially
A
common
observation
all
their
poor
efficacy
clearing
recycle
toxic
aggregated
proteins
damaged
organelles
due
impairment
dysfunction
characterized
accumulation
protein
aggregates
leads
progressive
loss
structural
integrity/functionality
neurons
may
even
result
neuronal
death.
In
recent
years
biogenesis,
received
considerable
attention.
It
emerged
target
numerous
like
AD
PD.
neurobiology
animal
models,
found
ameliorate
neurotoxicity
rescue
neurodegeneration.
Since
master
transcriptional
plays
crucial
role
defining
activation.
Studies
have
done
understand
mechanisms
which
yield
insights
into
how
might
be
targeted
used
strategy
develop
treatment
process
with
extensive
application
this
review,
we
explore
different
factor-based
therapy
some
natural
compounds
PD
special
emphasis
on
TFEB.
International Journal of Molecular Sciences,
Год журнала:
2020,
Номер
21(8), С. 3028 - 3028
Опубликована: Апрель 24, 2020
Alterations
in
autophagy
and
the
ubiquitin
proteasome
system
(UPS)
are
commonly
implicated
protein
aggregation
toxicity
which
manifest
a
number
of
neurological
disorders.
In
fact,
both
UPS
alterations
bound
to
aggregation,
spreading
so-called
prionoid
proteins,
including
alpha
synuclein
(α-syn),
amyloid-beta
(Aβ),
tau,
huntingtin,
superoxide
dismutase-1
(SOD-1),
TAR-DNA-binding
43
kDa
(TDP-43)
fused
sarcoma
(FUS).
Recent
biochemical
morphological
studies
add
this
scenario,
focusing
on
coordinated,
either
synergistic
or
compensatory,
interplay
that
occurs
between
UPS.
pathways
such
as
mammalian
target
rapamycin
(mTOR),
transcription
factor
EB
(TFEB),
Bcl2-associated
athanogene
1/3
(BAG3/1)
glycogen
synthase
kinase
beta
(GSk3β),
widely
explored
potential
targets
neurodegenerative
proteinopathies,
operate
at
crossroad
These
steps
key
orchestrating
specificity
magnitude
two
degradation
systems
for
effective
homeostasis,
while
intermingling
with
intracellular
secretory/trafficking
inflammatory
pathways.
The
findings
discussed
present
manuscript
supposed
novel
viewpoints
may
further
enrich
our
insight
complex
interactions
occurring
cell-clearing
systems,
misfolding
propagation.
Discovering
mechanisms
enabling
cross-talk
is
expected
provide
molecular
proteinopathies.
Acta Neuropathologica Communications,
Год журнала:
2021,
Номер
9(1)
Опубликована: Сен. 9, 2021
Abstract
In
this
review,
we
discuss
the
synaptic
aspects
of
Tau
pathology
occurring
during
Alzheimer’s
disease
(AD)
and
how
may
relate
to
memory
impairment,
a
major
hallmark
AD.
Whilst
clinical
diagnosis
AD
patients
is
loss
working
long-term
declarative
memory,
histological
presence
neurofibrillary
tangles
hyperphosphorylated
Amyloid-beta
plaques.
spreads
through
synaptically
connected
neurons
impair
function
preceding
formation
tangles,
loss,
axonal
retraction
cell
death.
Alongside
pathology,
recent
data
suggest
that
has
physiological
roles
in
pre-
or
post-
compartments.
Thus,
have
seen
shift
research
focus
from
as
microtubule-stabilising
protein
axons,
with
accelerating
spine
formation,
dendritic
elongation,
plasticity
coordinating
pathways.
We
collate
here
myriad
emerging
interactions
Tau,
current
evidence
contributes