“Cannabinoids have been demonstrated to exert neuroprotective effects on different types of neuronal insults.
Here we have addressed the therapeutic potential of the synthetic cannabinoid HU210 on photoreceptor degeneration, synaptic connectivity and functional activity of the retina in the transgenic P23H rat, an animal model for autosomal dominant retinitis pigmentosa (RP)…
These data suggest that cannabinoids are potentially useful to delay retinal degeneration in RP patients.”
“There is a growing amount of evidence suggesting that cannabinoids may be neuroprotective in central nervous system inflammatory conditions.
Advances in the understanding of the physiology and pharmacology of the cannabinoid system have potentiated the interest in cannabinoids as potential therapeutic targets.
…The effects of cannabinoids on cytokine brain work and on the regulation of neuroinflammatory processes may affect chronic inflammatory demyelinating diseases such as multiple sclerosis.”
“The endocannabinoid system (ECS) is an important modulatory and potentially neuroprotective homeostatic system in the brain.
We have investigated CB1R availability in vivo in patients with AD…
In conclusion, we found no in vivo evidence for a difference in CB1R availability in AD compared to age-matched controls.
Taken together with recently reported in vivo CB1R changes in Parkinson’s and Huntington’s disease, these data suggest that the CB1R is differentially involved in neurodegenerative disorders.”
http://www.ncbi.nlm.nih.gov/pubmed/24189376
“Multiple sclerosis (MS) is a neurodegenerative disease that is characterised by repeated inflammatory/demyelinating events within the central nervous system (CNS). In addition to relapsing-remitting neurological insults, leading to loss of function, patients are often left with residual, troublesome symptoms such as spasticity and pain. These greatly diminish “quality of life” and have prompted some patients to self-medicate with and perceive benefit from cannabis.
Recent advances in cannabinoid biology are beginning to support these anecdotal observations, notably the demonstration that spasticity is tonically regulated by the endogenous cannabinoid system.
Recent clinical trials may indeed suggest that cannabis has some potential to relieve, pain, spasms and spasticity in MS. However, because the CB(1) cannabinoid receptor mediates both the positive and adverse effects of cannabis, therapy will invariably be associated with some unwanted, psychoactive effects.
In an experimental model of MS, and in MS tissue, there are local perturbations of the endocannabinoid system in lesional areas. Stimulation of endocannabinoid activity in these areas either through increase of synthesis or inhibition of endocannabinoid degradation offers the positive therapeutic potential of the cannabinoid system whilst limiting adverse events by locally targeting the lesion.
In addition, CB(1) and CB(2) cannabinoid receptor stimulation may also have anti-inflammatory and neuroprotective potential as the endocannabinoid system controls the level of neurodegeneration that occurs as a result of the inflammatory insults.
Therefore cannabinoids may not only offer symptom control but may also slow the neurodegenerative disease progression that ultimately leads to the accumulation of disability.”
“Ruth Djaldetti, M.D., of Tel Aviv University in Israel, presented the findings of her research at a recent International Congress on Parkinson’s Disease and Movement Disorders. She reported improvement in tremor, pain, rigidity and bradykinesia (slowness of movement). Twenty subjects, all in their mid-sixties, and were rated using the Unified Parkinson’s Disease Rating Scale (UPDRS) both before and after smoking. Their overall “before” scores were over 30 and within 30 minutes of smoking, their scores dropped to 24.. Their tremor scores averaged 7.5 on the UPDRS before and dropped to a score of 3.5 after smoking cannabis. Bradykinesia scores dropped from 13.2 to 8.6 and rigidity went from 7.4 to 6.4. Dr. Djaldetti also saw a marked relief in the pain her subjects were experiencing and this relief of pain led to better sleep and feeling more rested.
This bears out the results of other studies. A study done in Great Britain that was published in 2011 found the principal ingredient in cannabis provided neuroprotection for people with Parkinson’s disease. Its neuroprotective properties included reduction of inflammation and control of spasms, making it an ideal drug for treating Parkinson’s. However, its confusing legal status make it very difficult for people to obtain or consider using and for doctors to even recommend to patients.
Another interesting study done in 2010 found that cannabinoid receptors are located in many parts of the brain and that cannabinoids are produced naturally in the brain. People with Parkinson’s have even higher levels of endocannabinoids (cannabinoids produced within the brain). The main ingredient in cannabis, Tetrahydrcannibol (THC) actually increases dopamine production temporarily. Cannabidiol (CBD) another component of cannabis, also provides neuroprotective properties and has been shown to reduce dystonias . CDB could be a very vital improvement for treating Parkinson’s, and a recent study has shown it useful in treating certain cancers as well.
While there have been many, many people reporting the anecdotal benefits of smoking cannabis, clinical trials are lagging behind. Laboratory and animal studies have shown many benefits, but perplexing issues around the legality of cannabis are slowing the efforts and impeding progress.”
“Cannabinoids such as Δ9-tetrahydrocannabinol (Δ9-THC) are neuroprotective in animal and cell culture models of Parkinson’s disease (PD).
In a PD cell culture model we recently demonstrated that Δ9-THC is neuroprotective through activation of the nuclear receptor peroxisomal proliferator-activated receptor γ (PPARγ)…
Here we investigate the effect of Δ9-THC and pioglitazone on mitochondrial biogenesis…
Even though Δ9-THC and pioglitazone are both protective against MPP+ only Δ9-THC induces PPARγ dependent mitochondrial biogenesis, a mechanism that may be beneficial for the treatment of PD.”
http://jnnp.bmj.com/content/84/11/e2.58
“The endocannabinoid system has recently emerged as a promising therapeutic target for MS. The protective mechanisms of cannabinoids are thought to be mediated by activation of cannabinoid receptor 1 (CB1) and 2 (CB2)…
activation of CB1 receptors contributes significantly to the anti-inflammatory and neuroprotective effects of cannabinoids on MS.”
“The clinical use of neurotrophic factors is difficult due to side effects and elevated costs, but other molecules might be effective and more easily obtained. Among them, some are derived from Cannabis sativa.
Cannabidiol (CBD) is the major non-psychotropic component found on the surface of such plant leaves.
The present study aimed to investigate the neuroprotective potential of CBD…
The present results show that CBD possesses neuroprotective characteristics that may, in turn, be promising for future clinical use.”
“Traumatic brain injury (TBI) and its consequences represent one of the leading causes of death in young adults. This lesion mediates glial activation and the release of harmful molecules and causes brain edema, axonal injury, and functional impairment. Since glial activation plays a key role in the development of this damage, it seems that controlling it could be beneficial and could lead to neuroprotective effects. Recent studies show that minocycline suppresses microglial activation, reduces the lesion volume, and decreases TBI-induced locomotor hyperactivity up to 3 months. The endocannabinoid system (ECS) plays an important role in reparative mechanisms and inflammation under pathological situations by controlling some mechanisms that are shared with minocycline pathways. We hypothesized that the ECS could be involved in the neuroprotective effects of minocycline. To address this hypothesis, we used a murine TBI model in combination with selective CB1 and CB2 receptor antagonists (AM251 and AM630, respectively). The results provided the first evidence for the involvement of ECS in the neuroprotective action of minocycline on brain edema, neurological impairment, diffuse axonal injury, and microglial activation, since all these effects were prevented by the CB1 and CB2 receptor antagonists.”
“Cannabidiol, the main nonpsychotropic constituent of Cannabis sativa, possesses a large number of pharmacological effects including anticonvulsive, sedative, hypnotic, anxiolytic, antipsychotic, anti-inflammatory, and neuroprotective, as demonstrated in clinical and preclinical studies.
Many neurodegenerative disorders involve cognitive deficits, and this has led to interest in whether cannabidiol could be useful in the treatment of memory impairment associated to these diseases…
We used an animal model of cognitive impairment induced by iron overload in order to test the effects of cannabidiol in memory-impaired rats…
A single acute injection of cannabidiol at the highest dose was able to recover memory in iron-treated rats. Chronic cannabidiol improved recognition memory in iron-treated rats. Acute or chronic cannabidiol does not affect memory in control rats.
The present findings provide evidence suggesting the potential use of cannabidiol for the treatment of cognitive decline associated with neurodegenerative disorders.
Further studies, including clinical trials, are warranted to determine the usefulness of cannabidiol in humans suffering from neurodegenerative disorders.”