CBD for Neuroprotection

One of the many benefits of using CBD is one of its amazing health properties: neuroprotection. As time passes neurons can be damaged by a number of situations. CBD can not only work to help protect neurons but repair them. As a result, CBD is starting to be realized as a key tool in fighting a number of conditions such as multiple sclerosis, Alzheimer’s disease and amyotrophic lateral sclerosis (ALS – also known as Lou Gehrig’s disease).

CBD, or cannabidiol, is one of 113 known cannabinoids (cannabis-based molecules) that are found in cannabis and animals, including humans. CBD has been found to have a number of protective properties including anti-inflammatory, analgesic, and neuroprotective.

Unlike its sibling cannabinoid THC (tetrahydrocannabinol), CBD has no intoxicating effects. Most CBD is derived from a cannabis plant called hemp that has low levels of THC and high levels of CBD.

What Is a Neuron?

A neuron is an electrically excitable cell that communicates with other cells through connections called synapses. Neurons are the main component of nervous tissue.

Neurons are broken down into 3 types based on how they act. The 3 types of neurons are:

  • Sensory neurons respond to touch, sound, or light and affect the cells of the eyes, ears, tongue, skin, and nose (sensory organs), and they send signals to the nervous system and the brain.
  • Motor neurons receive signals from the brain and nervous system to control such actions as muscle contractions to glandular output.
  • Interneurons connect neurons to other neurons within the same region of the brain or nervous system. When these groups connect, they become known as a neural circuit.

To further understand neurons and how CBD can work as a protectant, it’s important to know how neurons work. Neurons consist of 3 parts the soma, dendrites, and the axon.

The soma is the largest part of the cell. It is the body of the cell and contains the cell nucleus, which is the main part of the cell. The cell nucleus produces the molecule ribonucleic acid (RNA). The RNA molecule essential in biological roles such as coding, decoding, regulation, and expression of genes. RNA along with deoxyribonucleic acid (DNA), lipids, proteins, and carbohydrates, constitute the major macromolecules essential for all known forms of life.

Dendrites are parts of a nerve cell that process electrochemical signals that have been received from other neural cells to the soma of a neuron. Electrical stimulation is sent to the dendrites by axons via neural synapses which are located throughout a branch shaped network of neurons called a dendritic tree. Dendrites are responsible for building and incorporating these synaptic inputs and in deciding the extent that electrical signals (action potentials) are created by the neuron.

The axon is a long, slim projection of a neuron that conducts action potentials away from the nerve cell body. In moving these signals away from the cell body, it transmits the information to other neurons, muscles, and glands. In sensory neurons (also known as pseudounipolar neurons), axons are referred to as “afferent nerve fibers” This is because they conduct electrical impulses from the exterior of the cell to the cell body and then onto the nervous system in a different branch within the same axon.

Neurons receive signals from the dendrites and the soma and then send out signals via the axon. Most synapses send signals from the axon of a neuron to the dendrite of another, but this is not always the case as axon can connect to an axon and dendrite can connect to a dendrite.

In many cases, neurons are created by neural stem cells during brain development and childhood. This process called neurogenesis is mostly completed by the time a child reaches adulthood, however, new neurons continue to develop in the hippocampus (which controls memory function and the part of the brain that deals with the sense of smell.

How Do Neurons Get Damaged?

When a neuron is produced in a stem cell, the neuron travels to the portion of the brain or nervous system that it will function. Neurons have been observed to travel by 2 different methods:

  • Radial glia – These are long fibers that extend from the inner layers to the outer layers of the brain.
  • Chemical signals – The surface of a neuron has a special type of molecule called an adhesion molecule that binds with similar molecules or glial cells. These chemical signals guide neurons to these molecules.

But not all neurons reach their proper destination or even get there at all. Out of all the neurons produced, only about 1/3rd reach their destination. Part of the reason is that many die during the process of development.

Of the ones that survive the trip, some wind up not going to the correct place. Thee misguided neurons have been attributed to gene mutations and can cause both misplaced and malformed neurons to pool in the same area. These pools of neurons can cause disorders such as childhood epilepsy, schizophrenia, and dyslexia.

After a body has developed into adulthood, neurons can get damaged by a number of situations. When the neurons get damaged, the result is the body not functioning correctly and results in a medical condition for the person. Among some of the more well-known conditions and their causes are:

  • Spinal cord injury – Since the spinal cord plays a huge role in neural activity, an injury to the spinal cord can be devastating. This type of injury can cause communication between the brain and muscles to stop or be severely inhibited. While the actual neurons may not be affected, the axons within the neuron can no longer send the signals to other nerve fibers.
  • Brain injury – Injury to the brain in the form of a concussion, head trauma or even a stroke can damage neurons and can deprive them of the oxygen and nutrients that they use to fuel themselves and survive, thus causing them to die.
  • Alzheimer’s disease (AD) – In this case, proteins build up around neurons in areas on the neocortex and hippocampus. The proteins then starve the neurons of their oxygen and nutrients causing neuronic death. Because the neocortex and hippocampus are responsible for memory, a person with AD loses their ability to retain memory and complete normal everyday tasks.
  • Parkinson’s disease (PD) – This disease kills off that produce the neurotransmitter dopamine in the basal ganglia. The neurons affected produce dopamine. Among other things, the basal ganglia are responsible for controlling movement. When these neurons are killed off, the person affected can no longer achieve total motor control.
  • Huntington’s disease (HD) – As with Parkinson’s disease, Huntington’s disease originates in the basal ganglia. HD is a genetic mutation that causes over-production of the neurotransmitter glutamate. This overproduction suffocates the neurons and kills them. Because the basal ganglia control motor function, as with PD, HD sufferers loose motor control and will twist and contort uncontrollably.

Case Studies

For the last few decades, CBD has been touted as a neuroprotectant. This, however, can’t be observed in real-world situations. This must be observed in a laboratory setting and done through clinical studies. Since the 1980s many CBD studies have been done. Some of these studies were done specifically to evaluate the neuroprotective properties of CBD and some found the neuroprotective properties, as a result, examining some other aspect of CBD.

One such study from 2006 dealt with the use of CBD for patients with diabetes in an effort to stave off the effects of diabetic retinopathy. The study involved “the protective effects of a nonpsychotropic cannabinoid, cannabidiol (CBD), were examined in streptozotocin-induced diabetic rats after 1, 2, or 4 weeks. Retinal cell death was determined by terminal dUTP nick-end labeling assay; BRB function by quantifying extravasation of bovine serum albumin-fluorescein; and oxidative stress by assays for lipid peroxidation, dichlorofluorescein fluorescence, and tyrosine nitration. Experimental diabetes-induced significant increases in oxidative stress, retinal neuronal cell death, and vascular permeability.” The study went on to find that “CBD treatment significantly reduced oxidative stress; decreased the levels of tumor necrosis factor-α, vascular endothelial growth factor, and intercellular adhesion molecule-1; and prevented retinal cell death and vascular hyperpermeability in the diabetic retina. Consistent with these effects, CBD treatment also significantly inhibited p38 MAP kinase in the diabetic retina. These results demonstrate that CBD treatment reduces neurotoxicity, inflammation, and BRB breakdown in diabetic animals through activities that may involve inhibition of p38 MAP kinase.” It further concluded that “The nonpsychotropic CBD is a promising candidate for anti-inflammatory and neuroprotective therapeutics.” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592672/)

A 2017 study that involved CBD and epilepsy in rats had some interesting results. The study looked at “the behavioral, electrophysiological, and neuropathological effects of cannabidiol (CBD), a major non-psychotropic constituent of Cannabis sativa, in the intrahippocampal pilocarpine-induced status epilepticus (SE) rat model.” The study found that “[the] findings demonstrate anticonvulsant and neuroprotective effects of CBD preventive treatment in the intrahippocampal pilocarpine epilepsy model, either as single or multiple administrations, reinforcing the potential role of CBD in the treatment of epileptic disorders.” The study further concluded that “this study showed that CBD treatment reduces the behavioral severity and oscillatory electrographic changes of SE, the post-ictal lethargy, and the neuronal loss associated with the pilocarpine-induced SE rat model. More studies are needed to understand the specific mechanisms of action related to the neuroprotective and anticonvulsant effects of CBD in epilepsy” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355474/)

A study from 2013 looked at CBD and neurodegeneration due to excessive alcohol use. The premise of the study was “aimed to advance the preclinical development of transdermal delivery of cannabidiol (CBD) for the treatment of alcohol-induced neurodegeneration.” Several concentrations of CBD were used, but the success was found with both the 2.5% and 5% (the highest in the study) concentrations of CBD. The results found that “The 5.0% CBD gel resulted in a 48.8% reduction in neurodegeneration in the entorhinal cortex assessed by Fluoro-Jade B (FJB), which trended to statistical significance. Treatment with the 5.0% CBD gel resulted in day 3 CBD plasma concentrations of ~100.0 ng/mL so this level was used as a target concentration for the development of an optimized gel formulation. Experiment 2 tested a next-generation 2.5% CBD gel formulation, which was compared to CBD administration by intraperitoneal injection (IP). This experiment found similar magnitudes of neuroprotection following both routes of administration; transdermal CBD decreased FJB+ cells in the entorhinal cortex by 56.1%, while IP CBD resulted in a 50.6% reduction in FJB+ cells. These results demonstrate the feasibility of using CBD transdermal delivery systems for the treatment of alcohol-induced neurodegeneration.” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4096899/)

An interesting study from 2018 looked at the adverse impacts of marijuana on the hippocampus. The study worked on the premise that CBD can essentially block the effects of its cannabinoid sibling THC (tetrahydrocannabinol), the substance that causes a person to get high when consuming marijuana. The goal was to see if CBD could “reverse or reduce the characteristic hippocampal harms associated with chronic cannabis use.” The study found that “a restorative effect of CBD on hippocampal substructures in cannabis users, even within the context of continued cannabis use. In the absence of ongoing use, as might occur in a motivated treatment-seeking sample, greater neurotherapeutic benefit may be expected. During the trial, participants reported feeling less high after using cannabis and this was corroborated by significant reduction at post-treatment on the CEQ Euphoria subscale. As such, CBD may be a valuable adjunct to psychological treatments for cannabis dependence. Furthermore, subjective ratings of preferred level of cannabis intoxication were negatively associated with increased subicular region growth.” It further concluded that “these results speak to the potential for CBD treatment to restore hippocampal pathology in a range of clinical populations (e.g., schizophrenia, Alzheimer’s disease, and major depressive disorder).” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5908414/)

A 2012 study that reviewed the use of CBD in psychiatric disorders found that “CBD has been recently tested against the consequences of chronic unpredictable stress, which includes anhedonia and anxiety-like behaviour. Chronic treatment with CBD was able to prevent these behavioural changes, an effect that depends on hippocampal neurogenesis, similar to antidepressant drugs. This observation further strengthens the notion that this natural cannabinoid should be considered as a potential approach for the treatment of mood disorders. CBD is a safe compound with a wide range of therapeutic applications, including the treatment of psychiatric disorders. These findings make this drug an attractive candidate for future clinical use.” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481531/)


Studies have shown thus far that CBD is a safe and natural neuroprotectant. It can be used for a variety of medical conditions including ones that we normally wouldn’t associate with needing neuroprotection such as diabetes. But it also works on those that we do associate with neurology such as Alzheimer’s disease, Parkinson’s disease, schizophrenia, depression and more.

With the pharmaceutical industry consistently creating new drugs, patenting the formula, and selling them at astronomical prices, CBD provides a less expensive and readily available alternative to these synthetic medications.