Human Brain Mapping,
Год журнала:
2024,
Номер
46(1)
Опубликована: Дек. 29, 2024
Abstract
Despite
transverse
relaxation
rate
(R
2
)
being
one
of
the
fundamental
contrasts
in
MRI,
most
investigations
brain
R
and
cognition
have
been
cross‐sectional
conducted
predominantly
non‐Latino
White
adults.
We
investigated
profile
as
related
to
212
older
African
Americans
(~75
years
age)
with
longitudinal
3T
MRI
scans
cognitive
test
data
determine
how
changes
are
associated
cognition.
For
each
participant,
slopes
global
five
domain
scores
were
separately
combined
voxel‐specific
whole
voxelwise
analyses.
Participants
less
negative
rates
change
within
left
basal
ganglia
centrum
semiovale,
bilateral
hippocampal
complex
temporal
gyri,
parietooccipital
white
matter,
well
posterior
cingulate
displayed
Similar
associations
seen
for
regional
episodic
memory
(most
robustly
hippocampi)
semantic
(left
greater
than
right
hemisphere
involvement).
Results
suggest
a
relatively
wide
distribution
between
Americans;
that
became
more
regionally
specific
when
considering
individual
domains.
Relative
preservation
tissue
integrity
across
grey
key
regions
domains,
is
slower
decline
Americans.
These
results
may
lay
foundation
directed
work
support
healthy
aging
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.
CNS Drugs,
Год журнала:
2024,
Номер
38(7), С. 507 - 532
Опубликована: Июнь 3, 2024
Numerous
physiological
processes
happening
in
the
human
body,
including
cerebral
development
and
function,
require
participation
of
biometal
ions
such
as
iron,
copper,
zinc.
Their
dyshomeostasis
may,
however,
contribute
to
onset
Alzheimer's
disease
(AD)
potentially
other
neurodegenerative
diseases.
Chelation
is
therefore
a
therapeutic
strategy
against
AD.
This
review
provides
survey
natural
synthetic
chelating
agents
that
are
or
could
be
used
target
metal
hypothesis
Since
not
only
pathological
aspect
AD,
nature
this
disorder
very
complex
multifactiorial,
most
efficient
therapeutics
should
many
neurotoxic
factors
possible.
Various
coumarin
derivatives
match
description
apart
from
being
able
chelate
ions,
they
exhibit
capacity
inhibit
cholinesterases
(ChEs)
monoamine
oxidase
B
(MAO-B)
while
also
possessing
antioxidant,
anti-inflammatory,
numerous
beneficial
effects.
Compounds
based
on
scaffold
represent
desirable
class
anti-AD
therapeutics.
Frontiers in Aging Neuroscience,
Год журнала:
2025,
Номер
17
Опубликована: Фев. 25, 2025
Alzheimer's
disease
(AD)
is
a
severe
neurodegenerative
characterized
mainly
by
the
formation
of
amyloid
beta
(Aβ)
plaques
and
abnormal
phosphorylation
tau.
In
recent
years,
an
imbalance
in
iron
homeostasis
has
been
recognized
to
play
key
role
pathological
process
AD.
Abnormal
accumulation
can
activate
various
kinases
such
as
glycogen
synthase
kinase-3β,
cyclin-dependent
kinase
5,
mitogen-activated
protein
kinase,
leading
tau
precursor
protein,
accelerating
Aβ
neurofibrillary
tangles.
addition,
iron-mediated
oxidative
stress
not
only
triggers
neuronal
damage,
but
also
exacerbates
dysfunction
altering
N-methyl-D-aspartate
receptors
γ-aminobutyric
acid
type
A
receptors.
Iron
affects
status
tyrosine
hydroxylase,
rate-limiting
enzyme
for
dopamine
synthesis,
interfering
with
signaling
pathway.
On
other
hand,
transport
metabolism
brain
regulating
transferrin,
further
disrupting
homeostasis.
Therapeutic
strategies
targeting
show
promise
reducing
accumulation,
inhibiting
stress,
proteins.
This
article
reviews
molecular
mechanisms
modifications
mediated
AD,
discusses
potential
interventions
that
regulate
related
pathways,
providing
new
theoretical
basis
treatment
Ageing and Neurodegenerative Diseases,
Год журнала:
2025,
Номер
5(1)
Опубликована: Март 10, 2025
Aim:
Melatonin
has
been
found
to
inhibit
the
induced
Tau
hyperphosphorylation
in
cellular
and
animal
models.
However,
underlying
mechanisms
are
not
fully
understood,
especially
with
respect
ability
of
melatonin
control
Tau-related
pathologies
neuronal
damage.
Methods:
6-month-old
male
P301S
mice
were
employed
evaluate
effects
intranasally
administered
(10
mg/kg)
on
tauopathy
progression
ferroptosis.
HT22
D1A
cells
also
further
uncover
mechanism
iron
metabolism.
Results:
We
verified
that
intranasal
administration
effectively
improved
via
modulating
activity
several
kinases,
accompanied
by
a
stifling
synaptic
loss,
degeneration,
neuroinflammation,
oxidative
damage
transgenic
mice.
Moreover,
restoration
ferroptosis-related
indicators
such
as
accumulation
hippocampal
neurons,
metabolism,
activating
Nrf2/GPX4
signaling
contributed
which
supplementation
ameliorated
behavioral
deficits
Interestingly,
we
treatment
may
stimulate
astrocytes
secrete
hepcidin
vitro,
turn
helps
alleviate
efflux
stressed
conditions.
Conclusion:
These
findings
provide
compelling
evidence
plays
role
improving
tauopathies
ferroptosis
neurodegenerative
disease.
