International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(21), P. 11353 - 11353
Published: Oct. 22, 2024
Alzheimer's
disease
(AD)
is
a
devasting
neurodegenerative
afflicting
mainly
glutamatergic
neurons
together
with
massive
neuroinflammation
mediated
by
the
transcription
factor
NF-κB.
A
65%-plus
increase
in
patients
2050
might
be
major
threat
to
society.
Hallmarks
of
AD
are
neurofibrillary
tangles
(NFTs)
composed
hyperphosphorylated
tau
and
amyloid
beta
(Aβ)
plaques.
Here,
we
review
potential
involvement
NF-κB
hereditary
mutations
tumor
necrosis
pathway
patients.
One
greatest
genetic
risk
factors
Entropy,
Journal Year:
2024,
Volume and Issue:
26(6), P. 481 - 481
Published: May 31, 2024
Many
studies
on
memory
emphasize
the
material
substrate
and
mechanisms
by
which
data
can
be
stored
reliably
read
out.
Here,
I
focus
complementary
aspects:
need
for
agents
to
dynamically
reinterpret
modify
memories
suit
their
ever-changing
selves
environment.
Using
examples
from
developmental
biology,
evolution,
synthetic
bioengineering,
in
addition
neuroscience,
propose
that
a
perspective
as
preserving
salience,
not
fidelity,
is
applicable
many
phenomena
scales
cells
societies.
Continuous
commitment
creative,
adaptive
confabulation,
molecular
behavioral
levels,
answer
persistence
paradox
it
applies
individuals
whole
lineages.
also
speculate
substrate-independent,
processual
view
of
life
mind
suggests
memories,
patterns
excitable
medium
cognitive
systems,
could
seen
active
sense-making
process.
explore
diverse
set
embodied
perspectives—nested
who
interpret
each
other’s
own
past
messages
actions
best
they
(polycomputation).
This
synthesis
unifying
symmetries
across
disciplines,
relevance
research
programs
Diverse
Intelligence
engineering
novel
minds.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 26, 2024
Genome
editing
is
poised
to
revolutionize
treatment
of
genetic
diseases,
but
poor
understanding
and
control
DNA
repair
outcomes
hinders
its
therapeutic
potential.
especially
understudied
in
nondividing
cells
like
neurons,
which
must
withstand
decades
damage
without
replicating.
This
lack
knowledge
limits
the
efficiency
precision
genome
clinically
relevant
cells.
To
address
this,
we
used
induced
pluripotent
stem
(iPSCs)
iPSC-derived
neurons
examine
how
postmitotic
human
Cas9-induced
damage.
We
discovered
that
can
take
weeks
fully
resolve
this
damage,
compared
just
days
isogenic
iPSCs.
Furthermore,
Cas9-treated
upregulated
unexpected
genes,
including
factors
canonically
associated
with
replication.
Manipulating
response
chemical
or
perturbations
allowed
us
direct
neuronal
toward
desired
outcomes.
By
studying
cells,
uncovered
unforeseen
challenges
opportunities
for
precise
editing.
Frontiers in Medical Technology,
Journal Year:
2024,
Volume and Issue:
6
Published: Sept. 9, 2024
When
faced
with
the
prospect
of
death,
some
people
would
prefer
a
form
long-term
preservation
that
may
allow
them
to
be
restored
healthy
life
in
future,
if
technology
ever
develops
point
this
is
feasible
and
humane.
Some
believe
we
have
capacity
perform
type
experimental
today-although
it
has
never
been
proven-using
contemporary
methods
preserve
structure
brain.
The
idea
morphomolecular
organization
brain
encodes
information
required
for
psychological
properties
such
as
personality
memories.
If
these
structures
can
maintained
intact
over
time,
could
theoretically
provide
bridge
access
restorative
technologies
future.
To
consider
hypothesis,
first
describe
possible
metrics
used
assess
structural
quality.
We
next
explore
several
brain,
including
traditional
cryonics
method
cryopreservation,
well
aldehyde-stabilized
cryopreservation
fluid
preservation.
focus
in-depth
on
preservation,
which
relies
aldehyde
fixation
induce
chemical
gel
formation
wide
set
biomolecules
appears
cost-effective
method.
two
theoretical
recovery
technologies,
alongside
ethical
legal
complexities
all
will
require
prudent
approach.
non-negligible
chance
allowing
successful
restoration
future
deserves
serious
research
efforts
by
scientific
community.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 9, 2025
The
5’-3’
exonuclease
phospholipase
D3
(PLD3)
is
a
single-pass
transmembrane
protein
undergoing
sequential
post-translational
modifications
(PTM)
by
N
-glycosylation,
AMPylation
and
proteolytic
cleavage.
substrates
of
PLD3
activity
are
single-stranded
DNAs
RNAs,
which
act
as
ligands
for
Toll-like
receptors
(TLRs)
trigger
downstream
pro-inflammatory
response.
Although
has
primarily
been
studied
in
immune
cells,
recent
findings
indicate
its
enrichment
neurons,
where
it
plays
role
regulating
axonal
fitness
Alzheimer’s
disease
(AD).
However,
the
regulatory
mechanisms
governing
processing
into
catalytically
active
soluble
form
functional
roles
both
neuronal
cells
remain
unclear.
Here,
we
describe
implications
AMPylation,
direct
interaction
with
adenylyltransferase
FICD,
changes
Parkinson’s
(PD)
patient-derived
neurons.
We
identified
sites
within
proteins’
region
show
that
mutation
these
lead
to
loss
catalytic
activity.
FICD
AMP-transferase
accelerates
degradation
induces
cellular
stress
Furthermore,
depletion
two
human
AMP-transferases
SelO
point
towards
complex
network
AMPylation.
Together,
our
demonstrate
critical
regulation
provide
new
insights
protein’s
transport
localization
lysosomes.
observation
PD-derived
neurons
altered
compared
healthy
further
highlights
neurodegenerative
diseases.
A
fluorescent
thymine
analogue,
ThexT,
enables
visualisation
of
immunostimulatory
CpG
oligonucleotides
in
macrophages.
Its
incorporation
site
affects
TLR9
activation,
offering
insights
into
immune
response
modulation
and
intracellular
DNA
tracking.
