NeuroImage Clinical,
Journal Year:
2018,
Volume and Issue:
19, P. 240 - 251
Published: Jan. 1, 2018
Alzheimer's
disease
(AD)
is
marked
by
cognitive
dysfunction
emerging
from
neuropathological
processes
impacting
brain
function.
AD
affects
dynamics
at
the
local
level,
such
as
changes
in
balance
of
inhibitory
and
excitatory
neuronal
populations,
well
long-range
to
global
network.
Individual
differences
these
they
relate
behaviour
are
poorly
understood.
Here,
we
use
a
multi-scale
neurophysiological
model,
"The
Virtual
Brain
(TVB)",
based
on
empirical
multi-modal
neuroimaging
data,
study
how
correlate
with
individual
cognition.
In
particular,
modeled
resting-state
functional
activity
124
individuals
across
behavioural
spectrum
healthy
aging,
amnesic
Mild
Cognitive
Impairment
(MCI),
AD.
The
model
parameters
required
accurately
simulate
imaging
data
correlated
significantly
cognition,
exceeded
predictive
capacity
connectomes.
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.
Nutrition Reviews,
Journal Year:
2016,
Volume and Issue:
74(10), P. 624 - 634
Published: Sept. 15, 2016
It
has
been
hypothesized
that
alterations
in
the
composition
of
gut
microbiota
might
be
associated
with
onset
certain
human
pathologies,
such
as
Alzheimer
disease,
a
neurodegenerative
syndrome
cerebral
accumulation
amyloid-β
fibrils.
shown
bacteria
populating
can
release
significant
amounts
amyloids
and
lipopolysaccharides,
which
play
role
modulation
signaling
pathways
production
proinflammatory
cytokines
related
to
pathogenesis
disease.
Additionally,
nutrients
have
affect
well
formation
aggregation
amyloid-β.
This
suggests
modulating
microbiome
amyloidogenesis
through
specific
nutritional
interventions
prove
an
effective
strategy
prevent
or
reduce
risk
review
examines
possible
dissemination
amyloids,
regulation
gut–brain
axis,
potential
amyloidogenic
properties
bacteria,
impact
on
amyloid
relation
Journal of Neurochemistry,
Journal Year:
2016,
Volume and Issue:
138(6), P. 785 - 805
Published: June 23, 2016
Abstract
Synapses
are
essential
components
of
neurons
and
allow
information
to
travel
coordinately
throughout
the
nervous
system
adjust
behavior
environmental
stimuli
control
body
functions,
memories,
emotions.
Thus,
optimal
synaptic
communication
is
required
for
proper
brain
physiology,
slight
perturbations
synapse
function
can
lead
disorders.
In
fact,
increasing
evidence
has
demonstrated
relevance
dysfunction
as
a
major
determinant
many
neurological
diseases.
This
notion
led
concept
synaptopathies
diseases
with
defects
shared
pathogenic
features.
this
review,
which
was
initiated
at
13th
International
Society
Neurochemistry
Advanced
School,
we
discuss
basic
concepts
structure
function,
provide
critical
view
how
aberrant
physiology
may
contribute
neurodevelopmental
disorders
(autism,
Down
syndrome,
startle
disease,
epilepsy)
well
neurodegenerative
(Alzheimer
Parkinson
disease).
We
finally
appropriateness
potential
implications
gathering
under
single
term.
Understanding
common
causes
intrinsic
differences
in
disease‐associated
could
offer
novel
clues
toward
synapse‐based
therapeutic
intervention
neuropsychiatric
image
Review,
(
ISN
)
(Alzheimer's
Parkinson's
diseases),
gathered
together
term
synaptopathies.
Read
Editorial
Highlight
article
on
page
783
.
Journal of Experimental Neuroscience,
Journal Year:
2016,
Volume and Issue:
10s1
Published: Jan. 1, 2016
In
the
mammalian
central
nervous
system,
reactive
oxygen
species
(ROS)
generation
is
counterbalanced
by
antioxidant
defenses.
When
large
amounts
of
ROS
accumulate,
mechanisms
become
overwhelmed
and
oxidative
cellular
stress
may
occur.
Therefore,
are
typically
characterized
as
toxic
molecules,
oxidizing
membrane
lipids,
changing
conformation
proteins,
damaging
nucleic
acids,
causing
deficits
in
synaptic
plasticity.
High
concentrations
associated
with
a
decline
cognitive
functions,
observed
some
neurodegenerative
disorders
age-dependent
decay
neuroplasticity.
Nevertheless,
controlled
production
provides
optimal
redox
state
for
activation
transductional
pathways
involved
changes.
Since
regulate
neuronal
activity
elicit
negative
effects
at
same
time,
distinction
between
beneficial
deleterious
consequences
unclear.
this
regard,
review
assesses
current
research
describes
main
sources
neurons,
specifying
their
involvement
plasticity
distinguishing
physiological
pathological
processes
implicated.
Frontiers in Neuroscience,
Journal Year:
2019,
Volume and Issue:
12
Published: Jan. 13, 2019
Cross-talk
between
adipose
tissue
and
central
nervous
system
(CNS)
underlies
the
increased
risk
of
obese
people
to
develop
brain
diseases
such
as
cognitive
mood
disorders.
Detailed
mechanisms
for
how
peripheral
changes
caused
by
accumulation
in
obesity
impact
CNS
cause
dysfunction
are
poorly
understood.
Adipokines
a
large
group
substances
secreted
white
regulate
wide
range
homeostatic
processes
including,
but
not
limited
to,
energy
metabolism
immunity.
Obesity
is
characterized
generalized
change
levels
circulating
adipokines
due
abnormal
tissue.
Altered
adipokine
underlie
complications
well
development
obesity-related
comorbidities
type
2
diabetes,
cardiovascular
neurodegenerative
diseases.
Here,
we
review
literature
role
key
mediators
communication
periphery
health
disease.
We
will
focus
on
actions
leptin
adiponectin,
two
most
abundant
studied
adipokines,
brain,
with
particular
emphasis
altered
signaling
these
may
lead
augmented
Alzheimer's
A
better
understanding
biology
disorders
prove
major
relevance
diagnostic,
prevention
therapy.
