Cold Spring Harbor Perspectives in Biology,
Journal Year:
2019,
Volume and Issue:
11(4), P. a035063 - a035063
Published: Feb. 11, 2019
David
L.
Prole
and
Colin
W.
Taylor
Department
of
Pharmacology,
University
Cambridge,
Cambridge
CB2
1PD,
United
Kingdom
Correspondence:
cwt1000{at}cam.ac.uk
Molecular Neurodegeneration,
Journal Year:
2020,
Volume and Issue:
15(1)
Published: May 29, 2020
Abstract
Alzheimer’s
disease
(AD)
is
one
of
the
most
prevalent
neurodegenerative
diseases,
characterized
by
impaired
cognitive
function
due
to
progressive
loss
neurons
in
brain.
Under
microscope,
neuronal
accumulation
abnormal
tau
proteins
and
amyloid
plaques
are
two
pathological
hallmarks
affected
brain
regions.
Although
detailed
mechanism
pathogenesis
AD
still
elusive,
a
large
body
evidence
suggests
that
damaged
mitochondria
likely
play
fundamental
roles
AD.
It
believed
healthy
pool
not
only
supports
activity
providing
enough
energy
supply
other
related
mitochondrial
functions
neurons,
but
also
guards
minimizing
oxidative
damage.
In
this
regard,
exploration
multitude
mechanisms
altered
constitutes
novel
promising
therapeutic
targets
for
disease.
review,
we
will
summarize
recent
progress
underscores
essential
role
dysfunction
discuss
underlying
with
focus
on
structural
functional
integrity
including
biogenesis
dynamics,
axonal
transport,
ER-mitochondria
interaction,
mitophagy
proteostasis.
Science,
Journal Year:
2019,
Volume and Issue:
367(6477), P. 528 - 537
Published: Dec. 13, 2019
Microglia
are
the
main
immune
cells
in
brain
and
have
roles
homeostasis
neurological
diseases.
Mechanisms
underlying
microglia-neuron
communication
remain
elusive.
Here,
we
identified
an
interaction
site
between
neuronal
cell
bodies
microglial
processes
mouse
human
brain.
Somatic
junctions
a
specialized
nanoarchitecture
optimized
for
purinergic
signaling.
Activity
of
mitochondria
was
linked
with
junction
formation,
which
induced
rapidly
response
to
activation
blocked
by
inhibition
P2Y12
receptors.
Brain
injury-induced
changes
at
somatic
triggered
receptor-dependent
neuroprotection,
regulating
calcium
load
functional
connectivity.
Thus,
these
could
potentially
monitor
protect
functions.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: June 30, 2023
Abstract
Amyloid
β
protein
(Aβ)
is
the
main
component
of
neuritic
plaques
in
Alzheimer’s
disease
(AD),
and
its
accumulation
has
been
considered
as
molecular
driver
pathogenesis
progression.
Aβ
prime
target
for
development
AD
therapy.
However,
repeated
failures
Aβ-targeted
clinical
trials
have
cast
considerable
doubt
on
amyloid
cascade
hypothesis
whether
drug
followed
correct
course.
recent
successes
targeted
assuaged
those
doubts.
In
this
review,
we
discussed
evolution
over
last
30
years
summarized
application
diagnosis
modification.
particular,
extensively
pitfalls,
promises
important
unanswered
questions
regarding
current
anti-Aβ
therapy,
well
strategies
further
study
more
feasible
approaches
optimization
prevention
treatment.