Биохимия,
Journal Year:
2024,
Volume and Issue:
89(6), P. 1015 - 1030
Published: Dec. 25, 2024
Alzheimer’s
disease
(AD)
is
a
severe
neurodegenerative
that
affects
millions
of
people
around
the
world.
The
increasing
prevalence
AD
correlates
with
life
expectancy
and
aging
populations
in
developed
countries.
Since
multifactorial
includes
various
pathological
processes,
such
as:
synaptic
dysfunction,
neuroinflammation,
oxidative
stress,
protein
misfolding,
etc.,
an
integrated
approach
aimed
simultaneously
at
several
targets
may
be
effective
slow
down
progression
disease.
Cell
therapy
its
further
development
form
transplantation
cellular
vesicles
especially
mitochondria
are
very
promising
for
treatment
neurodegeneration.
use
synaptosomes,
due
to
uniqueness
their
content,
become
new
stage
complex
diseases
particular.
This
review
discusses
preparation
composition
as
well
possibilities
advantages
transporters
delivery
other
biologically
active
substances
brain.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(1), P. 364 - 364
Published: Jan. 3, 2025
This
review
describes
our
current
understanding
of
the
role
mitochondria
in
repurposing
anti-diabetes
drugs
metformin,
gliclazide,
GLP-1
receptor
agonists,
and
SGLT2
inhibitors
for
additional
clinical
benefits
regarding
unhealthy
aging,
long
COVID,
mental
neurogenerative
disorders,
obesity.
Metformin,
most
prominent
these
diabetes
drugs,
has
been
called
“Drug
Miracles
Wonders,”
as
trials
have
found
it
to
be
beneficial
human
patients
suffering
from
maladies.
To
promote
viral
replication
all
infected
cells,
SARS-CoV-2
stimulates
liver
cells
produce
glucose
export
into
blood
stream,
which
can
cause
COVID
patients,
reduces
levels
blood,
was
shown
cut
incidence
rate
half
recovering
SARS-CoV-2.
Metformin
leads
phosphorylation
AMP-activated
protein
kinase
AMPK,
accelerates
import
via
transporter
GLUT4
switches
starvation
mode,
counteracting
virus.
Diabetes
also
stimulate
unfolded
response
thus
mitophagy,
is
healthy
aging
health.
were
mimic
exercise
help
reduce
body
weight.
Cells,
Journal Year:
2025,
Volume and Issue:
14(3), P. 195 - 195
Published: Jan. 28, 2025
Focal
swellings
of
dendrites
(“dendritic
blebbing”)
together
with
structural
damage
mitochondria
and
the
endoplasmic
reticulum
(ER)
are
morphological
hallmarks
glutamate
neurotoxicity,
also
known
as
excitotoxicity.
These
pathological
alterations
generally
thought
to
be
caused
by
so-called
“overactivation”
N-methyl-D-aspartate
receptors
(NMDARs).
Here,
we
demonstrate
that
activation
extrasynaptic
NMDARs,
specifically
when
forming
a
protein–protein
complex
TRPM4,
drives
these
traits.
In
contrast,
strong
synaptic
NMDARs
fails
induce
cell
despite
evoking
plateau-type
calcium
signals
comparable
those
generated
NMDAR/TRPM4
complex,
indicating
high
intracellular
levels
per
se
not
toxic
neurons.
Using
confocal
laser
scanning
microscopy
transmission
electron
microscopy,
show
disrupting
using
recently
discovered
small-molecule
TwinF
interface
inhibitor
FP802
inhibits
NMDA-induced
neurotoxicity-associated
dendritic
blebbing
ER.
It
prevents,
at
least
in
part,
disruption
ER–mitochondria
contact
sites.
findings
establish
trigger
for
organelles
associated
They
suggest
addition
inducing
high-amplitude,
signals,
generates
second
signal
required
neurotoxicity
(“two-hit
hypothesis”).
As
organelles,
particularly
mitochondria,
is
common
feature
many
human
neurodegenerative
diseases,
including
Alzheimer’s
disease
amyotrophic
lateral
sclerosis
(ALS),
inhibitors
have
potential
provide
neuroprotection
across
broad
spectrum
diseases.
Molecular Brain,
Journal Year:
2023,
Volume and Issue:
16(1)
Published: Oct. 17, 2023
The
major
neuropathologic
feature
of
Parkinson's
disease
is
the
presence
widespread
intracellular
inclusions
α-synuclein
known
as
Lewy
bodies.
Evidence
suggests
that
these
misfolded
protein
spread
through
brain
with
progression.
Changes
in
synaptic
function
precede
neurodegeneration,
and
this
extracellular
can
affect
transmission.
However,
whether
how
spreading
aggregates
modulates
before
neuronal
loss
remains
unknown.
In
present
study,
we
investigated
effect
intrastriatal
injection
preformed
fibrils
(PFFs)
on
activity
somatosensory
cortex
using
a
combination
whole-cell
patch-clamp
electrophysiology,
histology,
Golgi-Cox
staining.
Intrastriatal
PFF
was
followed
by
formation
phosphorylated
layer
5
cortex,
leading
to
decrease
synapse
density,
dendritic
spines,
spontaneous
excitatory
post-synaptic
currents,
without
apparent
loss.
Additionally,
three-dimensional
reconstruction
microglia
confocal
imaging
showed
an
increase
engulfment
synapses.
Collectively,
our
data
indicate
propagation
neural
networks
causes
abnormalities
structure
dynamics
prior
