Cannabinoids and cell fate.Conclusion:
Regarding the central nervous
system, most of the experimental evidence indicates that cannabinoids may
protect neurons from toxic
insults such as glutamaergic overstimulation, ischemia and oxidative
Conclusion: Most of the experimental
evidence indicates that cannabinoids may protect normal neurons from toxic
Conclusion: The psychotropic cannabinoid
receptor agonist Δ9tetrahydrocannabinol (THC) and cannabidiol,
(a non-psychoactive constituent of marijuana), both reduced NMDA, AMPA and
kainate receptor mediated neurotoxicities.
Conclusion: Excitotoxic neuronal death
underlies many neurodegenerative disorders. This study demonstrates the
importance of agonist efficacy and the duration of treatment on the
neuroprotective effects of cannabinoids.
Conclusion: In glaucoma, the increased
release of glutamate is the major cause
of retinal ganglion cell death. In conclusion, our results indicate that
lipid peroxidation and ONOO- formation play an important role in NMDA-induced
retinal neurotoxicity and cell loss in the retina, and that THC and CBD, by
reducing the formation of these compounds, are effective neuroprotectants.
Memantine and Δ9
-tetrahydrocannabinol alone were without effect, however, co-administration of
the drugs significantly decreased number of haloperidol-induced jaw movements.
The antitremor activity of the combination was antagonized (i) by injections of
L-glutamate into the dorsal striatum, entopeduncular nucleus, substantia nigra
pars reticulata, globus pallidus, supratrigeminal and trigeminal motor nuclei
but not into the subthalamic and cuneiform nuclei; (ii) by injections of CGS
21680 into the ventrolateral striatum; (iii) by injections of bicuculline into
the rostral part of the parvicellular reticular nucleus. The presented results
identify brain areas influencing parkinsonian-like tremor in rats; these data
can help advance the development of novel treatments for repetitive involuntary
Conclusion: Marijuana users were high
functioning, demonstrating comparable IQs to controls and relatively better
processing speed. Marijuana users demonstrated relative cognitive
impairments in verbal memory, spatial working memory,
spatial planning, and motivated decision making but comorbid use of alcohol,
which was heavier in marijuana users, was unexpectedly found to be associated
with better performance in some of these areas.
Conclusion: At the population level, it
does not appear that current illicit drug use is associated with impaired
cognitive functioning in early middle age.
Smoking marijuana resulted in
intoxication, as assessed by a behavioral rating scale, but did not
significantly alter mean behavioral performance on the attention task. There
was no significant rCBF change in the nucleus accumbens or other reward-related
brain regions, nor in basal ganglia or
have a high density of cannabinoid receptors.
Conclusion: The researchers conclude that
heavy marijuana use produces no irreversible mental deficits.
Conclusion: We conclude that marijuana does
not have a long-term negative impact on global intelligence.
Conclusion: Compared with controls,
marijuana users had significantly less bilateral orbitofrontal gyri volume,
higher functional connectivity in the orbitofrontal cortex (OFC) network, and
higher structural connectivity in tracts that innervate the OFC (forceps minor)
as measured by fractional anisotropy (FA)
Conclusion: We found that the brain-injured
animals treated with the agonist showed a marked recovery.
Conclusion: Cannabinoids inhibit cortical
neuron differentiation and promote glial differentiation. On the other hand,
experiments with differentiated neurons have shown that cannabinoids also
regulate neuritogenesis, axonal growth and synaptogenesis.
Conclusion: When 2-AG was administered
together with additional inactive 2-acyl-glycerols that are normally present in
the brain, functional recovery was significantly enhanced.
Conclusion: An ultralow dose of THC that
lacks any psychotrophic activity protects the brain from
neuroinflammation-induced cognitive damage and might be used as an effective
drug for the treatment of neuroinflammatory conditions, including
Conclusion: Our results suggest that CBC
raises the viability of NSPCs while inhibiting their
astroglia, possibly through up-regulation of ATP and adenosine signalling.
Conclusion: The team found that rats treated
with HU-210 on a regular basis showed neurogenesis the growth of new
brain cells in the hippocampus. This region of the
brain is associated with learning and memory, as well as anxiety and
depression. The effect is the opposite of most legal and illicit drugs such as
alcohol, nicotine, Heroin, and cocaine.
Conclusion: The THC(+) group was compared
with the THC(-) group with respect to injury mechanism, severity, disposition,
and mortality. A positive THC screen is associated with decreased mortality in
adult patients sustaining TBI.
Conclusion: Our findings demonstrate that
CBD exerts robust neuroprotective effects in vivo in HI piglets, modulating
excitotoxicity, oxidative stress and inflammation, and that both CB2
and 5HT1A receptors are implicated in these effects.
Conclusion: These results provide
evidence that the
cannabinoid system can serve to protect the brain against
Conclusion: Cannabidiol (CBD), the main
non-psychotomimetic component of the plant Cannabis sativa, exerts
therapeutically promising effects on human mental health such as inhibition of
psychosis, anxiety and depression. However, the
mechanistic bases of CBD action are unclear. Here we investigate the potential
involvement of hippocampal neurogenesis in the anxiolytic effect of CBD
Conclusion: This study provides the first
demonstration of CBD as an in vivo neuroprotectant and shows the efficacy of
lipophilic antioxidants in preventing binge
ethanol induced brain
Conclusion: The endocannabinoid system is
expressed in the intact spinal cord, and it is dramatically upregulated after
Conclusion: Considering that cannabidiol
presents an extremely safe profile and is currently being used clinically,
these results suggest that this compound could be useful in the treatment of
intervertebral disc degeneration.
A recent meta-analysis of 144 animal studies
including 1,473 subjects (rats, mice, and primates), published in the Journal
of Cerebral Blood Flow & Metabolism in December 2014, found that in those
who had suffered an ischemic stroke (temporary or permanent), the amount of the
brain injured as a result was reduced in those subjects that had used
cannabinoid therapies as opposed to those that had not.
Conclusion: Cannabinoids effectively limit
cell damage and provide patients with neuroprotective effects following a
Conclusion: Neuroprotective effects of
cannabinoids could provide the basis for potential therapeutic uses of
cannabinoids and/or endocannabinoids in stroke.
in vivo administration of CBD or BD1063
enhanced morphine-evoked supraspinal antinociception, alleviated NMDA-induced
convulsive syndrome, and reduced the infarct size caused by permanent
unilateral middle cerebral artery occlusion.
Conclusions: CB2R agonist alleviated
neuroinflammation and protected blood-brain barrier permeability in a rat ICH
model. Further molecular mechanisms revealed which is probably mediated by
enhancing the expression of MKP-1, then inhibited MAPKs signal transduction.
Various pathobiological processes contribute
to secondary brain injury closely interact with the
Hence, we summarize the immune response to ICH and recent progress in
treatments targeting the immune system in this
review. The emerging therapeutic strategies that target the
immune system after
ICH are a particular focus and have been summarized.
Conclusion: Phytocannabinoids produce
anticonvulsant effects through the endocannabinoid system, with few adverse
Conclusion: The endocannabinoid system plays
an active role in seizure termination but does not regulate
Conclusion: Our own results confirm the
overall impression from the literature review of better cognitive performance
in the cannabis user group. A majority of the studies report better cognitive
functioning in the cannabis-related schizophrenia and psychosis groups compared
to non-drug groups.
Conclusion: The first small-scale clinical
studies with CBD treatment of patients with psychotic symptoms further confirm
the potential of CBD as an effective, safe and well-tolerated
Conclusion: Experimental studies show that
cannabidiol reduces psychosis-like effects of
Δ9-tetrahydrocannabinol and synthetic analogs.
Conclusion: our data support the view that
inhibition of microglial activation may improve schizophrenia symptoms.
Conclusion: Although data available are
sufficient to suggest a
possible involvement of the endogenous cannabinoid system in the
neurobiology of depression, additional studies should be performed in order to
better elucidate the role of this system in the physiopathology of
Conclusion: These findings indicate
antidepressant-like behavioural properties of both THC and rimonabant in OB
rats although additional studies are required to clarify the relationship
between the chronic effects of cannabinoids in other pre-clinical models and in
Conclusion: CBD induces antidepressant-like
effects comparable to those of imipramine. These effects of CBD were probably
mediated by activation of 5-HT(1A) receptors.
Conclusion: Endocannabinoids (ECBs) such as
anandamide (AEA) act by activating cannabinoid type 1 (CB1) or 2
(CB2) receptors. The anxiolytic effect of drugs that facilitate ECB
effects is associated with increase in AEA levels in several encephalic areas,
including the prefrontal
cortex (PFC). We observed that drugs which interfere with ECB
reuptake/metabolism in both the PL and in the dentate gyrus of the dHIP induced
anxiolytic-like effect, in both the EPM and in the VCT via CB1
receptors, suggesting that CB1 signaling in these brain regions
modulates defensive responses to both innate and learned threatening stimuli.
This data further strengthens previous results indicating modulation of
hippocampal and MPFC activity via CB1 by ECBs, which could be
therapeutically targeted to treat anxiety disorders.Modulation of hippocampal
and MPFC activity via CB1 by ECBs, which could be therapeutically
targeted to treat anxiety disorders.
The cannabinoid receptor type 1
(CB1) antagonist SR141716 (3 mg/kg) caused an increase in
conditioned freezing upon repeated tone presentation on three consecutive days.
2-AG fear-promoting effects depended on CB1 signaling in GABAergic
neurons, while an involvement of glutamatergic neurons remained inconclusive
due to the high freezing shown by vehicle-treated
amyotrophic lateral sclerosis
Conclusion: Based on the currently available
scientific data, it is reasonable to think that cannabis might significantly
slow the progression of ALS,
potentially extending life expectancy and substantially reducing the overall
burden of the disease.
Conclusion: Although the small number of
people with ALS that reported
using cannabis limits the interpretation of the survey findings, the results
indicate that cannabis may be moderately effective at reducing symptoms of
appetite loss, depression, pain, spasticity, and drooling.
Conclusion: There is evidence that
nabiximols oromucosal spray may reduce subjective symptoms of spasticity and
that dronabinol is effective against neuropathic pain in patients with MS.
Conclusion: Smoked cannabis was superior to
placebo in symptom and pain reduction in
participants with treatment-resistant spasticity.
Conclusion: Cannabinoids inhibit
neurodegeneration in models of multiple sclerosis. In addition
to symptom management, cannabis may also slow the neurodegenerative processes
that ultimately lead to chronic disability in multiple sclerosis
Conclusion: Our results suggest that JWH-133
acts at CB2 receptors, most likely within the dorsal horn of the
spinal cord, to suppress the hypersensitivity associated with
Conclusion: Parkinson's disease (PD) has a
progressive course and is characterized by the degeneration of
dopaminergic neurons. Although no
neuroprotective treatments for PD have been found to date, the endocannabinoid
system has emerged as a promising target. Our findings point to a possible
effect of CBD in improving quality of life measures in PD patients with
no psychiatric comorbidities
Conclusion: Significant improvement of sleep
and pain scores. No significant adverse effects of the drug were observed. The
study suggests that cannabis might have a place in the therapeutic
armamentarium of PD.
Conclusion: Given its antioxidant properties
and its ability to activate CB2 but to block CB1
receptors, Δ9-THCV has a promising pharmacological profile for
delaying disease progression in PD and also for ameliorating parkinsonian
Conclusion: Our results support the view of
a potential neuroprotective action of cannabinoids against the in vivo and in
vitro toxicity of 6-hydroxydopamine, which might be relevant for PD. Our data
indicated that these neuroprotective effects might be due, among others, to the
antioxidant properties of certain plant-derived cannabinoids, or exerted
through the capability of cannabinoid agonists to modulate glial function, or
produced by a combination of both mechanisms.
Conclusion: We have demonstrated
up-regulation of the CB1 receptor in direct response to
neuronal injury in a human PD cell
culture model, and a direct neuronal protective effect of
Δ9-THC that may be mediated through PPAR? activation.
Conclusion: These sets of data strongly
suggest that THC could be a potential therapeutic treatment option for
through multiple functions and pathways.
(AD) is characterized by enhanced ß-amyloid peptide (ßA) deposition
along with glial activation in senile plaques, selective neuronal loss, and
cognitive deficits. Cannabinoids are neuroprotective agents against
excitotoxicity in vitro and acute brain damage in vivo. Recent studies on
therapeutic strategies for neurodegenerative diseases such as Parkinson's
disease and AD have focused on the neuroprotective properties (e.g., slowing
the ongoing neurodegeneration) rather than just on palliating symptoms of the
diseases (Dawson and Dawson, 2002). Because cannabinoids combine both
anti-inflammatory and neuroprotective actions, our findings may set the basis
for the use of these compounds as a therapeutic approach for AD.
disease is the leading cause of
dementia among the elderly, and with the ever-increasing size of this
population, cases of Alzheimer's
disease are expected to triple over the next 50 years. AChE inhibitors such
as THC and its analogues may provide an improved therapeutic for
augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing
Aß amalgamation, thereby simultaneously treating both the symptoms and
progression of Alzheimer's
Conclusion: Alzheimer's disease (AD) brain
shows an ongoing inflammatory condition and
anti-inflammatories diminish the risk of
neurologic disease. Cannabinoids are neuroprotective and anti-inflammatory
agents with therapeutic potential. We have shown that chronically administered
cannabinoid showed marked beneficial effects concomitant with inflammation
reduction and increased Aß clearance.
Conclusion: Currently, the treatment of
Tourette's syndrome (TS) is unsatisfactory. A single-dose, cross-over study in
12 patients, as well as a 6-week, randomised trial in 24 patients, demonstrated
that Δ9-tetrahydrocannabinol (THC), the most psychoactive
ingredient of cannabis, reduces tics in TS patients. No serious adverse effects
occurred and no impairment on neuropsychological performance was