Journal of Geriatric Psychiatry and Neurology,
Journal Year:
2021,
Volume and Issue:
35(3), P. 434 - 441
Published: May 26, 2021
Introduction:
Simple
markers
are
required
to
recognize
older
adults
at
higher
risk
for
neurodegenerative
disease.
Mild
behavioural
impairment
(MBI)
and
plasma
β-amyloid
(Aβ)
have
been
independently
implicated
in
the
development
of
incident
cognitive
decline
dementia.
Here
we
studied
associations
between
MBI
Aβ
42
/Aβ
40
.
Methods:
Participants
with
normal
cognition
(n
=
86)
or
mild
53)
were
selected
from
Alzheimer’s
Disease
Neuroimaging
Initiative.
scores
derived
Neuropsychiatric
Inventory
items.
Plasma
ratios
assayed
using
mass
spectrometry.
Linear
regressions
fitted
assess
association
total
score
as
well
domain
Results:
Lower
was
associated
(
p
0.04)
greater
affective
dysregulation
0.04),
but
not
impaired
drive/motivation
0.095)
impulse
dyscontrol
0.29)
domains.
Conclusion:
In
persons
impairment,
low
Incorporating
into
case
detection
may
help
capture
preclinical
prodromal
Molecular Neurodegeneration,
Journal Year:
2022,
Volume and Issue:
17(1)
Published: March 5, 2022
As
the
most
common
dementia,
Alzheimer's
disease
(AD)
exacts
an
immense
personal,
societal,
and
economic
toll.
AD
was
first
described
at
neuropathological
level
in
early
1900s.
Today,
we
have
mechanistic
insight
into
select
aspects
of
pathogenesis
ability
to
clinically
detect
diagnose
underlying
pathologies
living
patients.
These
insights
demonstrate
that
is
a
complex,
insidious,
degenerative
proteinopathy
triggered
by
Aβ
aggregate
formation.
Over
time
pathology
drives
neurofibrillary
tangle
(NFT)
pathology,
dysfunction
virtually
all
cell
types
brain,
ultimately,
overt
neurodegeneration.
Yet,
large
gaps
our
knowledge
pathophysiology
huge
unmet
medical
need
remain.
Though
largely
conceptualize
as
aging,
heritable
non-heritable
factors
impact
brain
physiology,
either
continuously
or
specific
points
during
lifespan,
thereby
alter
risk
for
devolvement
AD.
Herein,
I
describe
lifelong
journey
healthy
from
birth
death
with
AD,
while
acknowledging
many
remain
regarding
understanding
pathogenesis.
To
ensure
current
lexicon
surrounding
changes
inevitable,
incurable,
poorly
manageable
preventable,
curable,
must
address
these
gaps,
develop
therapies
bigger
on
clinical
symptoms
progression
use
interventions
appropriate
stage
disease.
Biomedicines,
Journal Year:
2022,
Volume and Issue:
10(4), P. 850 - 850
Published: April 5, 2022
In
the
115
years
since
discovery
of
Alzheimer’s
disease
(AD),
our
knowledge,
diagnosis,
and
therapeutics
have
significantly
improved.
Biomarkers
are
primary
tools
for
clinical
research,
diagnostics,
therapeutic
monitoring
in
trials.
They
provide
much
insightful
information,
while
they
not
clinically
used
routinely,
help
us
to
understand
mechanisms
this
disease.
This
review
charts
journey
AD
biomarker
development
from
cerebrospinal
fluid
(CSF)
amyloid-beta
1-42
(Aβ42),
total
tau
(T-tau),
phosphorylated
(p-tau)
biomarkers
imaging
technologies
next
generation
biomarkers.
We
also
discuss
advanced
high-sensitivity
assay
platforms
CSF
Aβ42,
T-tau,
p-tau,
blood
analysis.
The
recently
proposed
Aβ
deposition/tau
biomarker/neurodegeneration
or
neuronal
injury
(ATN)
scheme
might
facilitate
definition
biological
status
underpinning
offer
a
common
language
among
researchers
across
biochemical
imaging.
Moreover,
we
highlight
blood-based
that
scalable
alternative
through
cost-saving
reduced
invasiveness,
may
an
understanding
initiation
development.
different
groups
candidates,
their
advantages
limitations,
paths
forward,
identification
analysis
validation.
valid
implementation
future
diagnostics.