Aging-Associated Amyloid-β Plaques and Neuroinflammation in Bottlenose Dolphins (Tursiops truncatus) and Novel Cognitive Health-Supporting Roles of Pentadecanoic Acid (C15:0)
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(8), P. 3746 - 3746
Published: April 16, 2025
There
is
an
urgent
need
to
identify
interventions
that
broadly
target
aging-related
cognitive
decline
and
progression
Alzheimer’s
disease
(AD).
Bottlenose
dolphins
(Tursiops
truncatus)
have
histologic
changes
similar
AD
in
humans,
they
also
develop
shared
age-associated
co-morbidities
identified
as
risk
factors
for
including
type
2
diabetes,
ferroptosis,
iron
overload,
which
can
be
driven
by
nutritional
C15:0
deficiency.
We
hypothesized
(1)
would
amyloid
beta
(Aβ)
plaques
neuroinflammation
paralleled
of
humans
relation
age-related
progression,
quantitative
concentration,
brain
region;
(2)
dose-dependent
activities
relevant
protecting
health.
Quantitative
immunohistochemistry
staining
was
used
assess
68
tissues
from
archived
brains
19
Navy
evaluate
associations
among
region,
sex,
age
group.
Further,
activities,
using
a
third-party
panel
intended
screen
potential
therapeutics,
were
evaluated.
Similar
had
the
highest
Aβ
plaque
density
variation
hippocampus
(90th
percentile
4.95
plaques/mm2),
where
increased
with
(p
=
0.05).
All
measured
markers
detected,
concentrations
activated
microglia
(CD68+)
(0.46
±
0.38
cells/mm2).
inhibitor
two
targets,
fatty
acid
amide
hydrolase
(FAAH)
(IC50
2.5
µM,
89%
maximum
inhibition
at
50
µM
relative
URB597)
monoamine
oxidase
B
(MAO-B)
19.4
70%
R(-)-Deprenyl).
These
demonstrated
efficacy
against
formation
neuroinflammation,
protection
function
hippocampus.
findings
suggest
that,
addition
co-morbidities,
may
play
distinct
role
supporting
health,
especially
higher
concentrations.
Language: Английский
Alzheimer’s Disease Neuropathological Change in Aged Non-Primate Mammals
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(15), P. 8118 - 8118
Published: July 25, 2024
Human
brain
aging
is
characterized
by
the
production
and
deposition
of
β-amyloid
(Aβ)
in
form
senile
plaques
cerebral
amyloid
angiopathy
intracellular
accumulation
hyper-phosphorylated
tau
(Hp-tau)
to
neurofibrillary
tangles
(NFTs)
dystrophic
neurites
plaques.
The
process
progresses
for
years
eventually
manifests
as
cognitive
impairment
dementia
a
subgroup
aged
individuals.
Aβ
produced
deposited
first
neocortex
most
mammals,
including
humans;
it
usually
not
accompanied
altered
behavior
impairment.
Hp-tau
less
frequent
than
pathology,
NFTs
are
rare
mammals.
In
contrast,
familiar
from
middle
age
onward
appear
paleocortex
selected
stem
nuclei.
precede
decades
or
correlate
with
about
5%
individuals
at
65
25%
85.
Based
on
these
comparative
data,
(a)
common
Alzheimer’s
disease
neuropathological
change
(ADNC)
mammals;
(b)
common,
however,
principal
cytoskeletal
pathology
(c)
NFT
humans
starts
nuclei
paleocortical
regions
progressing
parts
other
telencephalon;
(d)
human
unique
among
mammalian
species
due
early
appearance
dramatic
progression
onward,
matching
advanced
cases;
(e)
neither
nor
supports
concept
cascade
hypothesis.
Language: Английский
Amyloid-β and phosphorylated tau screening in bottlenose dolphin (Tursiops truncatus) and striped dolphin (Stenella coeruleoalba) brains from Italy reveals distinct immunohistochemical patterns correlating with age and co-morbidity
PLoS ONE,
Journal Year:
2024,
Volume and Issue:
19(11), P. e0314085 - e0314085
Published: Nov. 26, 2024
Cetacean
brains
are
uniquely
adapted
to
diving,
but
can
be
affected
by
diseases
and
exposure
toxins,
triggering
neurodegenerative
processes
that
may
cause
stranding.
Some
species
exhibit
a
significant
post-reproductive
lifespan
(PRLS),
increasing
the
likelihood
of
observing
cumulative
age-related
pathology.
Immunohistochemistry
against
amyloid-β
hyperphosphorylated
tau
proteins
is
increasingly
implemented
assess
Alzheimer’s
Disease-like
neuropathology
in
cetaceans,
comparisons
between
geographically
distinct
populations,
animals
different
age
groups,
sex,
with
concomitant
pathologies
lacking.
We
tested
43
cetaceans’
(30
Tursiops
truncatus
;
13
Stenella
coeruleoalba
)
parietal
cortex,
our
most
consistently
archived
cerebral
tissue,
immunohistochemical
analyses
oligomer
42
(Aβ-42)
(pTau
AT180
AT8)
antibodies.
Aβ-42
antibody
cross-reacted
plaques
three
aged
bottlenose
two
striped
dolphins,
was
more
often
detected
within
neurons,
glia,
blood
vessels
all
dolphins.
Histoscore
dolphins
ages,
sexes,
revealed
correlations
older
age,
viral
infections,
plaque
presence.
Protozoan
cysts
antibody.
pTau
signal
observed
as
single
foci
neurons
neuropil
young
To
knowledge,
this
study
first
its
kind
for
Mediterranean
region
will
help
establish
baseline
understanding
physiological
pathological
expression
associated
human
disease
cetacean
brains.
Language: Английский
Mechanisms of intestinal injury in polychaete Perinereis aibuhitensis caused by low-concentration fluorene pollution: Microbiome and metabonomic analyses
Journal of Hazardous Materials,
Journal Year:
2024,
Volume and Issue:
475, P. 134925 - 134925
Published: June 15, 2024
Language: Английский
Editorial: New insights in the neuroanatomy and neuropathology of marine mammals
Frontiers in Neuroanatomy,
Journal Year:
2024,
Volume and Issue:
18
Published: July 1, 2024
Keywords:
neuroanatomy,
neuropathology,
neurodegenerative
diseases,
marine
mammals,
cetaceans,
toothed
whales,
planetary
health
Language: Английский
Central Nervous System Disorders of Marine Mammals: Models for Human Disease?
Pathogens,
Journal Year:
2024,
Volume and Issue:
13(8), P. 684 - 684
Published: Aug. 14, 2024
This
article
deals
with
Central
Nervous
System
(CNS)
disorders
of
marine
mammals
as
putative
neuropathology
and
neuropathogenesis
models
for
their
human
and,
to
some
extent,
animal
“counterparts”
in
a
dual
“One
Health”
“Translational
Medicine”
perspective.
Within
this
challenging
context,
special
emphasis
is
placed
upon
Alzheimer’s
disease
(AD),
provided
that
AD-like
pathological
changes
have
been
reported
the
brain
tissue
stranded
cetacean
specimens
belonging
different
Odontocete
species.
Further
examples
potential
comparative
pathology
interest
are
represented
by
viral
infections
particular,
“Subacute
Sclerosing
Panencephalitis”
(SSPE),
rare
neurologic
sequela
patients
infected
Measles
virus
(MeV).
Indeed,
Cetacean
morbillivirus
(CeMV)-infected
striped
dolphins
(Stenella
coeruleoalba)
may
also
develop
“brain-only”
form
CeMV
infection,
sharing
neuropathological
similarities
SSPE.
framework,
global
threat
A(H5N1)
avian
influenza
another
major
concern
issue,
severe
meningoencephalitis
occurring
affected
pinnipeds
cetaceans,
similarly
what
seen
beings.
Finally,
role
Brucella
ceti-infected,
neurobrucellosis-affected
cetaceans
counterparts
analyzed
discussed.
Notwithstanding
above,
much
more
work
needed
before
drawing
conclusion
mammal
CNS
mirror
“analogues”.
Language: Английский
Perivascular phosphorylated TDP‐43 inclusions are associated with Alzheimer's disease pathology and loss of CD146 and Aquaporin‐4
Brain Pathology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 9, 2024
Abstract
The
majority
of
patients
with
Alzheimer's
disease
(AD)
exhibit
aggregates
Trans‐active
response
DNA
binding
protein
43
(TDP‐43)
in
their
hippocampus,
which
is
associated
a
more
aggressive
progression.
TDP‐43
inclusions
are
commonly
found
neurons,
but
also
astrocytes.
impact
the
astrocytes
less
known.
In
current
study,
we
investigate
presence
phosphorylated
(pTDP‐43)
astrocytic
endfeet
and
potential
association
blood–brain
barrier
(BBB)
damage,
glymphatic
system
dysfunction,
AD
pathology.
By
staining
postmortem
hippocampal
sections
from
non‐demented
controls
against
pTDP‐43
together
markers
glial
fibrillary
acidic
(GFAP),
marker
Aquaporin‐4
(AQP4),
for
BBB
alterations
(CD146)
leakiness
(Immunoglobulin
A),
demonstrate
close
between
perivascular
or
GFAP
AQP4.
These
were
prominent
correlated
severity
loss
CD146
findings
indicate
relationship
accumulation
may
contribute
to
downstream
pathological
events
seen
Language: Английский
Neurodegenerative Diseases: What Can Be Learned from Toothed Whales?
Neuroscience Bulletin,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 1, 2024
Neurodegeneration
involves
a
wide
range
of
neuropathological
alterations
affecting
the
integrity,
physiology,
and
architecture
neural
cells.
Many
studies
have
demonstrated
neurodegeneration
in
different
animals.
In
case
Alzheimer's
disease
(AD),
spontaneous
animal
models
should
display
two
neurohistopathological
hallmarks:
deposition
β-amyloid
arrangement
neurofibrillary
tangles.
However,
no
natural
that
fulfill
these
conditions
been
reported
most
research
into
AD
has
performed
using
transgenic
rodents.
Recent
also
toothed
whales
-
homeothermic,
long-lived,
top
predatory
marine
mammals
show
signs
AD-like
pathology.
The
hallmarks
cetaceans
could
help
to
better
understand
their
endangered
health
as
well
neurodegenerative
diseases
humans.
This
systematic
review
analyzes
all
literature
published
date
on
this
trending
topic
proposed
causes
for
iconic
are
approached
context
One
Health/Planetary
Health
translational
medicine.
Language: Английский
Evaluation of cyanotoxin L-BMAA effect on α-synuclein and TDP43 proteinopathy
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: March 26, 2024
The
complex
interplay
between
genetic
and
environmental
factors
is
considered
the
cause
of
neurodegenerative
diseases
including
Parkinson’s
disease
(PD)
Amyotrophic
Lateral
Sclerosis
(ALS).
Among
factors,
toxins
produced
by
cyanobacteria
have
received
much
attention
due
to
significant
increase
in
growth
worldwide.
In
particular,
L-BMAA
toxin,
diverse
taxa
cyanobacteria,
dinoflagellates
diatoms,
has
been
extensively
correlated
neurodegeneration.
molecular
mechanism
neurotoxicity
still
cryptic
far
from
being
understood.
this
research
article,
we
investigated
pathways
altered
exposure
cell
systems,
highlighting
a
specific
stress
an
impairment
autophagic
processes.
Interestingly,
these
changes
lead
accumulation
both
α-synuclein
TDP43,
which
are
with
PD
ALS
proteinopathy,
respectively.
Finally,
were
able
demonstrate
alterations
TDP43
WT
or
pathological
mutants
respect
protein
accumulation,
aggregation
cytoplasmic
translocation,
some
typical
features
sporadic
familial
ALS.
Language: Английский