Extremely low levels of delta-9-tetrahydrocannabinol (THC), the
active compound in marijuana, may offer a novel and viable treatment for
Alzheimer's disease (AD), preliminary research suggests.
Investigators
at the University of South Florida in Tampa found that THC both
decreases the production of amyloid beta (Aβ) and inhibits its
aggregation in cell cultures. In addition, it does so at extremely
safe doses.
These observations have implications for a potentially
new therapeutic approach to the treatment of Alzheimer's disease (AD),
as researchers suggest.
"Our group believes that amyloid
aggregation is the initiator of AD, so we wanted to see if THC can
inhibit amyloid beta aggregation in vitro," study investigator Chuanhai
Cao, PhD, a neuroscientist at the Byrd Alzheimer's Institute, College
of Pharmacy, University of South Florida, told Medscape Medical News.
"And in our in vitro cell cultures, we
discovered that THC inhibits amyloid beta production as well as
aggregation at extremely low doses and that it enhances mitochondrial
function as well. These observations suggest that THC has
anti-Alzheimer's activity."
The study was published online August 27 in the Journal of Alzheimer’ Disease.
Amyloid Lowering
For the study, investigators incubated THC
together with a variant of Aβ protein precursor cells and assayed the
culture for the presence of Aβ levels at the 6-, 24-, and 48-hour time
points.
TCH was also tested for synergy with caffeine to see
whether the combination of the 2 led to greater reductions in the Aβ
levels of these Aβ protein precursor cells in vitro.
"From the
results, we have discovered THC to be effective at lowering Aβ levels in
[Aβ protein precursor cells] at extremely low concentrations in a
dose-dependent manner," the investigators report.
However, the
combination of TCH and caffeine did not prove to be synergistic,
inasmuch as there was no additive effect on Aβ levels when the 2
compounds were combined in vitro.
Investigators also observed that
the same active compound in marijuana directly interacts with Aβ
peptide, thereby inhibiting its aggregation. Low doses of THC can
enhance mitochondria function as well.
Mitochondria function
helps supply energy, transmit signals, and maintain a healthy brain, all
of which decrease with age, said Dr. Cao. Previous research by this
team has shown that Aβ migrates into the mitochondria with age,
impairing its function.
"Thus, if THC can inhibit amyloid beta
aggregation and reduce its production, it is going to enhance
mitochondria function." Dr. Cao said.
Neuroprotective Effect
Concerns about memory impairment are
frequently raised in the context of any research associated with
potential therapeutic benefits of THC.
However, Dr. Chao
emphasized, memory impairment is only observed at "abuse" concentrations
of THC, which are more than a thousand times higher than the doses used
in their own in vitro experiments.
Newer research also suggests
that such ultra-low doses of TCH have a neuroprotective effect and are
not harmful, as has been previously suggested.
"This research is no excuse to smoke marijuana to prevent AD," Dr. Cao said.
"But
we have provided some evidence of how TCH works in terms of its
anti-Alzheimer's potential, and we feel that patients particularly in
the earlier stages of Alzheimer's could benefit from this natural
compound, provided we use the compound properly."
Both early-onset
familial AD as well as late-onset sporadic AD are characterized by
extracellular Aβ peptide and by amyloid plaques along with
tau-containing neurofibrillary tangles.
The continuous aggregation
of Aβ peptides along with hyperphosphorylation of the tau protein
inside the cell causing neurofibrillary tangle formation are generally
accepted as the major etiologic factors behind the neuronal cell death
associated with AD progression.
"Large Leap"
Commenting on the findings for Medscape Medical News,
Barbara Koppel, MD, chief of neurology and professor of clinical
neurology, New York Medical College, in Valhalla, said it was a "large
leap" to say that the use of THC clinically might slow progression of
AD.
"Nevertheless," she noted, "the series of in vitro experiments
conducted by Dr. Cao and colleagues that measured a lowering of levels
of production and aggregation of amyloid beta suggests there is a
connection between the function of the endocannabinoid system found in
the normal brain and the destruction of neurons by toxic amyloid
deposition."
Dr. Koppel added that the exact mechanism behind this
connection is complicated, and even with the other experiments
described by the investigators, the interrelationship between
neurodegeneration and the role of cannabinoids is intricate and complex.
"Of
course, translation to patients with minor cognitive impairment or AD
will require studies of the best route for efficacy and minimization of
toxicity in patients who may already suffer from cognitive impairment
from their underlying condition," she said.
"But given the fact
that the THC 'dose' used in these experiments is much less than what is
used recreationally, there is a possible place for cannabinoid therapy
in this otherwise progressive neurodegenerative disease."
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