Journal of Alzheimer s Disease Reports,
Journal Year:
2024,
Volume and Issue:
8(1), P. 1339 - 1360
Published: March 1, 2024
Background
Alzheimer's
disease
(AD)
is
a
prevalent,
incurable,
and
chronic
neurodegenerative
condition
characterized
by
the
accumulation
of
amyloid-β
protein
(Aβ),
disrupting
various
bodily
systems.
Despite
lack
cure,
phenolic
compounds
like
cannabidiol
(CBD),
non-psychoactive
component
cannabis,
have
emerged
as
potential
therapeutic
agents
for
AD.
Objective
This
systematic
review
explores
impact
different
types
on
AD,
unveiling
their
neuroprotective
mechanisms.
Methods
The
research
used
PubMed,
Scopus,
Web
Science
databases
with
keywords
“Alzheimer's
disease”
“Cannabidiol.”
Studies
were
evaluated
based
title,
abstract,
relevance
to
treating
AD
CBD.
No
restrictions
type
or
publication
year.
Excluded
hypothesis
papers,
reviews,
books,
unavailable
articles,
etc.
Results
Microsoft
Excel
identified
551
92
included
in
study,
but
only
22
thoroughly
evaluated.
In-vivo
in-silico
studies
indicate
that
CBD
may
disrupt
Aβ
42
,
reduce
pro-inflammatory
molecule
release,
prevent
reactive
oxygen
species
formation,
inhibit
lipid
oxidation,
counteract
Aβ-induced
increases
intracellular
calcium,
thereby
protecting
neurons
from
apoptosis.
Conclusions
In
summary,
study
indicates
its
analogs
production
.
Overall,
these
findings
support
alleviating
underlying
pathology
symptoms
associated
underscoring
crucial
need
further
rigorous
scientific
investigation
elucidate
applications
mechanisms
IntechOpen eBooks,
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 23, 2024
We
assessed
FTY720
and
our
patented-mitochondria-localizing-FTY720-derivative,
FTY720-Mitoxy,
in
mouse
models
of
Parkinson’s
disease
(PD)
MSA.
FTY720-Mitoxy
were
given
by
gavage,
injection,
or
osmotic
pump.
used
symptomatic
transgenic
alpha-Synuclein
(aSyn)
PD
mice
(A53T
aSyn)
MSA
(CNP-aSyn),
as
well
GM2
+/−
mice.
also
tested
toxin
models.
measured
movement,
constipation,
gut
motility,
sweat
ability,
bladder
function.
counted
blood
lymphocytes
24
h
after
FTY720-Mitoxy.
Brain
Derived
Neurotrophic
Factor
(BDNF),
Glial
Cell
Line
(GDNF),
Nerve
Growth
(NGF)
mRNA
protein.
aSyn
insolubility
gut,
brain,
spinal
cord
sequential
protein
extraction
immunoblot.
fecal
genomic
DNA
using
16S
rRNA
sequencing.
In
normalized
body
urinary
function
while
increasing
trophic
factors
eliminating
synucleinopathy.
mitochondrial
function,
improved
microbiota
improve
counteract
As
is
not
immunosuppressive,
it
may
be
safer
for
treating
and/or
Journal of Alzheimer s Disease Reports,
Journal Year:
2024,
Volume and Issue:
8(1), P. 1339 - 1360
Published: March 1, 2024
Background
Alzheimer's
disease
(AD)
is
a
prevalent,
incurable,
and
chronic
neurodegenerative
condition
characterized
by
the
accumulation
of
amyloid-β
protein
(Aβ),
disrupting
various
bodily
systems.
Despite
lack
cure,
phenolic
compounds
like
cannabidiol
(CBD),
non-psychoactive
component
cannabis,
have
emerged
as
potential
therapeutic
agents
for
AD.
Objective
This
systematic
review
explores
impact
different
types
on
AD,
unveiling
their
neuroprotective
mechanisms.
Methods
The
research
used
PubMed,
Scopus,
Web
Science
databases
with
keywords
“Alzheimer's
disease”
“Cannabidiol.”
Studies
were
evaluated
based
title,
abstract,
relevance
to
treating
AD
CBD.
No
restrictions
type
or
publication
year.
Excluded
hypothesis
papers,
reviews,
books,
unavailable
articles,
etc.
Results
Microsoft
Excel
identified
551
92
included
in
study,
but
only
22
thoroughly
evaluated.
In-vivo
in-silico
studies
indicate
that
CBD
may
disrupt
Aβ
42
,
reduce
pro-inflammatory
molecule
release,
prevent
reactive
oxygen
species
formation,
inhibit
lipid
oxidation,
counteract
Aβ-induced
increases
intracellular
calcium,
thereby
protecting
neurons
from
apoptosis.
Conclusions
In
summary,
study
indicates
its
analogs
production
.
Overall,
these
findings
support
alleviating
underlying
pathology
symptoms
associated
underscoring
crucial
need
further
rigorous
scientific
investigation
elucidate
applications
mechanisms
