Acta Neuropathologica Communications,
Journal Year:
2013,
Volume and Issue:
1(1)
Published: July 11, 2013
Abstract
Background
Tau
is
a
microtubule
stabilizing
protein
and
mainly
expressed
in
neurons.
aggregation
into
oligomers
tangles
considered
an
important
pathological
event
tauopathies,
such
as
frontotemporal
dementia
(FTD)
Alzheimer’s
disease
(AD).
Tauopathies
are
also
associated
with
deficits
synaptic
plasticity
long-term
potentiation
(LTP),
but
the
specific
role
of
tau
manifestation
these
deficiencies
not
well-understood.
We
examined
long
lasting
forms
JNPL3
(BL6)
mice
expressing
mutant
that
identified
some
inherited
FTDs.
Results
found
aged
(>12
months)
exhibit
enhanced
hippocampal
late-phase
(L-LTP),
while
young
(age
6
displayed
normal
L-LTP.
This
L-LTP
was
rescued
GABA
A
R
agonist,
zolpidem,
suggesting
loss
GABAergic
function.
Indeed,
we
reduction
interneurons.
Finally,
expression
led
to
severe
sensorimotor-gating
hippocampus-dependent
memory
mice.
Conclusions
show
for
first
time
function
impaired
by
protein,
leading
altered
deficits.
Increased
understanding
molecular
mechanisms
underlying
failure
AD
FTD
critical
identifying
targets
therapies
restore
cognitive
tauopathies.
Journal of Alzheimer s Disease,
Journal Year:
2016,
Volume and Issue:
57(4), P. 975 - 999
Published: Aug. 27, 2016
Amyloid-beta
(Aβ)
and
hyperphosphorylated
tau
are
hallmark
lesions
of
Alzheimer's
disease
(AD).
However,
the
loss
synapses
dysfunctions
neurotransmission
more
directly
tied
to
severity.
The
role
these
in
pathoetiological
progression
remains
contested.
Biochemical,
cellular,
molecular,
pathological
studies
provided
several
lines
evidence
improved
our
understanding
how
Aβ
accumulation
may
harm
alter
neurotransmission.
In
vitro
suggests
that
have
both
direct
indirect
cytotoxic
effects
affect
neurotransmission,
axonal
transport,
signaling
cascades,
organelle
function,
immune
response
ways
lead
synaptic
neurotransmitter
release.
Observations
preclinical
models
autopsy
support
findings,
suggesting
while
pathoetiology
positive
elusive,
their
removal
reduce
severity
progression.
purpose
this
article
is
highlight
need
for
further
investigation
its
interactions
with
neurotransmitters
alike.
Biomolecules,
Journal Year:
2019,
Volume and Issue:
10(1), P. 59 - 59
Published: Dec. 30, 2019
Quercetin
is
a
flavonoid
with
notable
pharmacological
effects
and
promising
therapeutic
potential.
It
widely
distributed
among
plants
found
commonly
in
daily
diets
predominantly
fruits
vegetables.
Neuroprotection
by
quercetin
has
been
reported
several
vitro
studies.
shown
to
protect
neurons
from
oxidative
damage
while
reducing
lipid
peroxidation.
In
addition
its
antioxidant
properties,
it
inhibits
the
fibril
formation
of
amyloid-β
proteins,
counteracting
cell
lyses
inflammatory
cascade
pathways.
this
review,
we
provide
synopsis
recent
literature
exploring
relationship
between
cognitive
performance
Alzheimer’s
disease
potential
as
lead
compound
clinical
applications.
Alzheimer s & Dementia,
Journal Year:
2014,
Volume and Issue:
10(3S)
Published: June 1, 2014
Cigarette
smoking
has
been
linked
with
both
increased
and
decreased
risk
for
Alzheimer's
disease
(AD).
This
is
relevant
the
US
military
because
prevalence
of
in
approximately
11%
higher
than
civilians.
Frontiers in Aging Neuroscience,
Journal Year:
2013,
Volume and Issue:
5
Published: Jan. 1, 2013
Traumatic
brain
injury
(TBI)
results
in
significant
disability
due
to
cognitive
deficits
particularly
attention,
learning
and
memory
higher-order
executive
functions.
The
role
of
TBI
chronic
neurodegeneration
the
development
neurodegenerative
diseases
including
Alzheimer's
disease
(AD),
Parkinson's
(PD),
Amyotrophic
Lateral
Sclerosis
(ALS)
most
recently
traumatic
encephalopathy
(CTE)
is
particular
importance.
However,
despite
effort
very
few
therapeutic
options
exist
prevent
or
reverse
impairment
following
TBI.
In
this
review
we
present
experimental
evidence
known
secondary
mechanisms
which
contribute
neuronal
cell
loss,
axonal
synaptic
dysfunction
hence
both
acutely
chronically
focus
on
linking
two
forms
dementia:
AD
CTE.
We
provide
potential
molecular
involved
modulating
Aβ
Tau
these
pathology.
Additionally
propose
a
mechanism
by
generated
as
direct
result
capable
exacerbating
thereby
establishing
neurotoxic
cascade
that
leads
neurodegeneration.
Scientific Reports,
Journal Year:
2015,
Volume and Issue:
5(1)
Published: Oct. 15, 2015
Abstract
The
possibility
that
Alzheimer’s
disease
(AD)
has
a
microbial
aetiology
been
proposed
by
several
researchers.
Here,
we
provide
evidence
tissue
from
the
central
nervous
system
(CNS)
of
AD
patients
contain
fungal
cells
and
hyphae.
Fungal
material
can
be
detected
both
intra-
extracellularly
using
specific
antibodies
against
fungi.
Different
brain
regions
including
external
frontal
cortex,
cerebellar
hemisphere,
entorhinal
cortex/hippocampus
choroid
plexus
material,
which
is
absent
in
control
individuals.
Analysis
sections
ten
additional
reveals
all
are
infected
with
infection
also
observed
blood
vessels,
may
explain
vascular
pathology
frequently
patients.
Sequencing
DNA
extracted
frozen
CNS
samples
identifies
species.
Collectively,
our
findings
compelling
for
existence
patients,
but
not
Journal of Alzheimer s Disease,
Journal Year:
2017,
Volume and Issue:
57(4), P. 1049 - 1069
Published: Feb. 17, 2017
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disease,
characterized
by
the
loss
of
memory,
multiple
cognitive
impairments
and
changes
in
personality
behavior.
Several
decades
intense
research
have
revealed
that
cellular
are
involved
process,
including
synaptic
damage,
mitochondrial
abnormalities
inflammatory
responses,
addition
to
formation
accumulation
amyloid-β
(Aβ)
phosphorylated
tau.
Although
tremendous
progress
has
been
made
understanding
impact
neurotransmitters
progression
pathogenesis
AD,
we
still
do
not
drug
molecule
associated
with
neurotransmitter(s)
can
delay
process
elderly
individuals
and/or
restore
functions
AD
patients.
The
purpose
our
article
assess
latest
developments
using
cell
mouse
models
AD.
We
also
updated
current
status
clinical
trials
neurotransmitters'
agonists/antagonists
