Abstract
Background
The
consequences
of
trace
element
exposure
on
cognitive
function
in
elderly
adults
have
been
recognized
as
primarily
attributed
to
the
inflammatory
response.
It
is
noteworthy
that
diet
can
either
exacerbate
or
reduce
Despite
this,
there
limited
studies
about
effects
relationship
between
and
function.
Methods
A
cross-sectional
study
utilized
data
from
2011–2014
NHANES
survey
explore
association
adults.
enrolled
1726
participants,
generalized
linear
regression
model
(GLM),
Bayesian
kernel
machine
(BKMR),
weighted
quantile
sum
(WQS),
g-computation
analysis
(Qg-comp)
were
conducted
assess
impact
five
elements
(lead,
cadmium,
mercury,
manganese,
selenium)
blood
under
anti-inflammatory
pro-inflammatory
diet.
Results
GLM
showed
a
positive
correlation
selenium
(Se)
both
instant
recall
test
(IRT)
digit
symbol
substitution
(DSST)
(β
=
2.06,
95%
CI:
0.70
~
3.41;
β
6.41,
2.35
10.46,
respectively).
In
contrast,
cadmium
(Cd)
was
negatively
associated
with
DSST
-1.17,
-2.13~
-0.22),
lead
(Pb)
IRT
-0.47,
-0.82~
-0.11).
For
animal
fluency
(AFT),
highest
quartile
manganese
(Mn)
lowest
-0.72,
-1.34~-0.10),
while
mercury
(Hg)
no
significant
associations
tests.
Subgroup
revealed
Cd
Se
Furthermore,
BKMR
an
inverted
U-shaped
curve
negative
mixtures
linearly
trend
Among
them,
emphasized
most
potent
risk
factor,
vital
protective
factor
for
WQS
Qg-comp
analysis.
Conclusions
suggests
high-quality
might
alleviate
adverse
DSST.
High
levels
also
better
scores
These
findings
provide
valuable
insights
into
connection
diet,
exposure,
Journal of Clinical Medicine,
Год журнала:
2024,
Номер
13(8), С. 2381 - 2381
Опубликована: Апрель 19, 2024
Changes
in
trace
element
concentrations
are
being
wildly
considered
when
it
comes
to
neurodegenerative
disorders,
such
as
Alzheimer’s
disease
and
Parkinson’s
disease.
This
study
aims
present
the
role
that
elements
play
central
nervous
system.
Moreover,
we
reviewed
mechanisms
involved
their
neurotoxicity.
Low
zinc
concentrations,
well
high
levels
of
copper,
manganese,
iron,
activate
signalling
pathways
inflammatory,
oxidative
nitrosative
stress
response.
Neurodegeneration
occurs
due
association
between
metals
proteins,
which
is
then
followed
by
aggregate
formation,
mitochondrial
disorder,
and,
ultimately,
cell
death.
In
disease,
low
Zn
suppress
neurotoxicity
induced
β-amyloid
through
selective
precipitation
aggregation
intermediates.
High
iron
manganese
cause
intracellular
α-synuclein,
results
synaptic
dysfunction
axonal
transport
disruption.
caused
accumulation
Fe
midbrain
dopaminergic
nucleus,
pathogenesis
multiple
sclerosis
derives
from
deficiency,
leading
an
imbalance
T
functions.
Aluminium
disturbs
homeostasis
other
a
rise
production
oxygen
reactive
forms,
leads
cellular
Selenium,
with
plays
distinct
process
ferroptosis.
Outlining
influence
have
on
oxidoreduction
processes
crucial
recognising
pathophysiology
diseases
may
provide
possible
new
methods
for
both
avoidance
therapy.
Neuroglia,
Год журнала:
2025,
Номер
6(1), С. 4 - 4
Опубликована: Янв. 6, 2025
Overexposure
of
humans
to
heavy
metals
and
essential
poses
a
significant
risk
for
the
development
neurological
neurodevelopmental
disorders.
The
mechanisms
through
which
these
exert
their
effects
include
generation
reactive
oxygen
species,
mitochondrial
dysfunction,
activation
inflammatory
pathways,
disruption
cellular
signaling.
function
glial
cells
in
brain
maintenance
homeostasis
cannot
be
overlooked.
are
particularly
susceptible
metal-induced
neurotoxicity.
Accumulation
promotes
microglial
activation,
triggering
responses
that
can
coincide
with
other
neurotoxicity,
inducing
alteration
synaptic
transmission,
cognitive
deficit,
neuronal
damage.
In
this
review,
we
highlighted
role
dysfunction
some
selected
neurodegenerative
diseases
We
further
dive
into
how
exposure
such
as
nickel,
manganese,
methyl
mercury,
cadmium,
iron,
arsenic,
lead
affect
functions
microglia,
astrocytes,
oligodendrocytes
they
on
relation
Potential
therapeutic
interventions
use
new
improved
chelating
agents
antioxidant
therapies
might
approach
alleviating
perturbations.
Journal of Alzheimer s Disease,
Год журнала:
2024,
Номер
97(4), С. 1581 - 1588
Опубликована: Янв. 26, 2024
The
possibility
that
Alzheimer's
disease
and
related
dementias
(ADRD)
is
a
modern
arises
from
the
minimal
mention
of
advanced
cognitive
decline
by
ancient
Greeks
Romans,
who
were
mainly
concerned
with
physical
frailties
older
ages.
Ecotoxicology and Environmental Safety,
Год журнала:
2024,
Номер
273, С. 116155 - 116155
Опубликована: Фев. 27, 2024
Excessive
exposure
to
manganese
in
the
environment
or
workplace
is
strongly
linked
neurodegeneration
and
cognitive
impairment,
but
precise
pathogenic
mechanism
preventive
measures
are
still
not
fully
understood.
The
study
aimed
investigate
-induced
oxidative
damage
nervous
system
from
an
epigenetic
perspective,
focusing
on
H3K36ac-dependent
antioxidant
pathway.
Additionally,
it
sought
examine
potential
of
curcumin
preventing
manganese-induced
damage.
Histopathology
transmission
electron
microscopy
revealed
that
apoptosis
necrosis
neurons
mitochondrial
ultrastructure
were
observed
striatum
manganese-exposed
rats.
suppressed
expression
genes,
leading
rats'
SH-SY5Y
cells.
With
higher
doses
manganese,
levels
histone
acetyltransferase
lysine
2
A
(KAT2A)
H3K36ac
level
decreased.
ChIP-qPCR
confirmed
enrichment
promoter
regions
genes
SOD2,
PRDX3,
TXN2
was
reduced
cells
after
exposure,
decreased
these
genes.
Overexpression
KAT2A
confirms
attenuates
by
regulating
levels,
which
turn
controls
cell
model.
Furthermore,
might
control
influencing
expression,
boosting
reducing
In
conclusion,
regulation
stress
acetylation
may
be
important
neurotoxicity.
This
could
achieved
near
region
mitochondrial-associated
via
KAT2A.
Curcumin
mitigates
mitochondria
plays
a
crucial
protective
role
injury
system.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(3), С. 1004 - 1004
Опубликована: Янв. 24, 2025
Alzheimer’s
disease
(AD)
is
a
major
neurodegenerative
dementia,
with
its
complex
pathophysiology
challenging
current
treatments.
Recent
advancements
have
shifted
the
focus
from
traditionally
dominant
amyloid
hypothesis
toward
multifactorial
understanding
of
disease.
Emerging
evidence
suggests
that
while
amyloid-beta
(Aβ)
accumulation
central
to
AD,
it
may
not
be
primary
driver
but
rather
part
broader
pathogenic
process.
Novel
hypotheses
been
proposed,
including
role
tau
protein
abnormalities,
mitochondrial
dysfunction,
and
chronic
neuroinflammation.
Additionally,
gut–brain
axis
epigenetic
modifications
gained
attention
as
potential
contributors
AD
progression.
The
limitations
existing
therapies
underscore
need
for
innovative
strategies.
This
study
explores
integration
machine
learning
(ML)
in
drug
discovery
accelerate
identification
novel
targets
candidates.
ML
offers
ability
navigate
AD’s
complexity,
enabling
rapid
analysis
extensive
datasets
optimizing
clinical
trial
design.
synergy
between
these
themes
presents
promising
future
more
effective
