Cannabinoids in treatment of amyotrophic lateral sclerosis
August 29, 20222 min read
Lou Gehrig’s Disease, also known as motor neuron (or neurone) disease, or amyotrophic lateral sclerosis (‘ALS’), is characterised by progressive degeneration of motor neurons in the brain and spinal cord.
The disease involves a number of abnormal physiological processes at once. Addressing them all would require a drug regimen that included glutamate antagonists, antioxidants, a centrally acting anti-inflammatory agent, microglial cell modulators (which would need to include TNF-α inhibitors), an antiapoptotic agent, some number of neurotrophic growth factors, and some form of mitochondrial function-enhancing agent. Cannabinoids, or some of them at least, appear to have activity in all of those areas.
Most of the studies showing thatcannabinoids can sometimes delay disease progression and prolong survival in ALS have so far been performed in animal models. The few clinical trials that have investigatedcannabinoid-based intervention focus only on alleviation of symptoms, not on control of the disease.
At this point, in other words, the significant research is still laboratory-based. Data deriving from transgenic mice does support the idea that the endocannabinoid signaling system, in particular at the CB2 receptor, may point to an avenue for development of a neuroprotective therapy in TDP-43-related disorders. TDP-43 is a DNA-binding protein. Targeting glial cannabinoid CB2 receptors does delay the progression of the pathological phenotype in TDP-43 (A315T) transgenic mice, a model of amyotrophic lateral sclerosis. This appears to derive from activation of the receptors in astrocytes and reactive microglia in the spinal dorsal and ventral horns. There is some evidence in one ALS mouse model that this strategy could possibly prolong survival time. Other studies investigating this strategy have high risks of bias, and are very heterogeneous in nature, so consolidating results that are meaningful in this theoretical mode of intervention is not yet possible. A standardized way of testing specific cannabinoids is necessary before evaluating therapeutic potential of cannabinoids in human patients with ALS.
The variety of particular cannabinoids used in extant studies is still small. The CB2 agonist AM-1241 is one. This has prolonged survival in a transgenic mouse model when initiated at symptom onset. In gingival stromal cells in vitro, cannabidiol (CBD) has modulated genes linked with ALS. And a 2018 study showed benefits with VCE-003.2 in SOD1G93A transgenic mice, supporting PPAR-γ as an additional neuroprotective target available for cannabinoids in ALS. All of these findings still need to be validated in other ALS models prior to being translated to the clinical level.
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