Using CBD Oil for Alzheimer’s Disease

Getting started with using CBD oil for Alzheimer’s disease is simple.

You need to find a product that contains a full spectrum of terpenes, cannabinoids, and other phytochemicals from your local dispensary or online shop.

The usual dose of CBD for assisting in this condition can vary significantly; however, most people will start anecdotally somewhere around the 300 mg per day mark.

Depending on how this affects each person individually, the dose can either be increased or decreased.

Top Three Best CBD Oils For Alzheimer’s Disease

• Royal CBD Oil
• Gold Bee CBD Oil
• CBDistillery CBD Oil

Will I Notice Benefits Right Away?

The main benefits of CBD oil for Alzheimer’s disease is the theoretical possibility of slowing the progression of the disease.

For this reason, the benefits won’t be as clear as they will be for other conditions such as pain or inflammation.

When it comes to Alzheimer’s disease, CBD oil should be taken every day, along with a balanced diet and regular exercise to get the best effects out of it. Take any medications as prescribed, and be sure to follow up regularly with your doctor, especially before you begin a CBD regimen to avoid interactions and/or if you have liver health issues.

The idea is that the CBD oil might make Alzheimer’s progression slower, helping to increase patients’ quality of life in the long-term. Of course, further clinical research will be needed to demonstrate any true or characteristic benefit.

What is Alzheimer’s Disease?

Alzheimer’s dementia is a chronic degenerative condition affecting the brain.

It results from a gradual breakdown of the grey matter in the brain, resulting in a number of psychological, behavioral, and cognitive changes.

Grey matter makes up the outer portion of the brain and is responsible for most of what we experience as thought. It’s where we make decisions, form memories, and solve problems.

The symptoms of Alzheimer’s Disease (dementia) come on gradually in 4 stages:

The Possible Causes of Alzheimer’s Disease

Despite how common Alzheimer’s disease is, we still lack a thorough understanding of what exactly causes the condition. But, of course, there are a few prevailing theories that are gaining more evidence.

1. Amyloid-beta Plaques

Amyloid-beta is a sticky substance produced in the brain as a byproduct of normal neuron activity.

Normally, the glial cells – a group of special cells in the brain that act as the garbage disposal crew, among other things – come out at night to clear out these plaques, preventing them from building up and causing damage to the neurons.

Unfortunately, as we age, our cleanup crew doesn’t work as efficiently as it used to, allowing this amyloid-beta to build up and form thick plaques on the nerve cells and blood vessels. It is also likely that the fluids in the brain do not flush out as well as they used to also because of this plaque build-up.

Eventually, this causes the nerve cell to die off and blood flow to worsen.

As more of these cells continue to die, we start to see an increase in neuroinflammation, tau protein tangles, and the symptoms of Alzheimer’s disease progress.

Interestingly, a strong genetic link was found between the ApoE4 enzyme — an enzyme responsible for helping glial cells clear out amyloid-beta — and the risk of developing Alzheimer’s disease [20]. More recently discovered, ApoE4 is also linked to increased tau protein tangles, which are more strongly correlated to worse clinical symptoms than amyloid-beta plaques [21]. However, amyloid-beta plaques still probably play an important role in starting the disease process.

This makes preventing amyloid-beta a primary treatment aim for doctors trying to treat or prevent the condition.

2. Tau Protein Tangles

The most probable cause of Alzheimer’s disease is a buildup of another substance in the brain, known as tau proteins [3].

These tau proteins accumulate and become neurofibrillary tangles, which are toxic for neurons. However, this mechanism is poorly understood and is actually associated with a lot of other conditions. Any condition involving issues with these proteins are referred to as tauopathies.

Proteins are the main building blocks of life – much of what we’re made of can be distilled down to a protein. These tau proteins are just one type of protein that makes up our body. When they start to break down, they form unorganized “tangles”.

They’re essentially “knots in the nerve cells”, building up inside and hurting their ability to function normally.

There are a few experimental medications currently being tested that target these tau tangles, but some of the newest, most promising candidates are coming from the natural world in plant-based chemicals.

3. Poor Blood Flow to the Brain

As we age, blood flow to the brain may begin to decline.

Blood brings nutrients and oxygen to the cells. It’s also responsible for clearing out the garbage and toxic byproducts.

Think about it as living in a city.

Our houses are the cells, and the roads represent blood flow.

In order to get the water and food we need, we must build a road that connects our house to the rest of the city. We also need these roads for the garbage trucks to come and pick up the garbage we left out the night before.

If for any reason the road becomes blocked, we won’t have any access to food, and our garbage begins to pile up outside the house.

If this happens for too long, we will eventually die of starvation or from an infection from the rotting garbage.

It’s similar to the brain. If blood flow is bottlenecked for too long, the neurons will die of toxic overload and lack of nutrients or oxygen.

This is related to the pathological processes taking place with Alzheimer’s disease. The same amyloid-beta plaques that are neurotoxic also bind to blood vessels in the brain and reduce the ability of the blood vessel to exchange materials and clear things out. It also weakens the blood vessel wall and increases the risk of stroke. The risk of developing amyloid plaques on blood vessels is higher in people with more ApoE4 genetic inheritance.

Therefore improving blood flow to the brain is one of the primary goals of hospitals when treating the condition.

4. Glial Cell Dysfunction

Remember the garbage disposal cells we talked about earlier?

These are the glial cells.

They’re the most abundant cell type in the brain and for good reason.

They’re tasked with keeping the functional part of the brain, the neurons, working at their best – and they do that by fighting pathogens, removing dead neurons, keeping the neurons in place, bringing in oxygen and nutrients, and more!

As soon as the glial cells stop doing their job, the neurons will start to degrade, causing all kinds of issues with cognition. This includes Alzheimer’s disease or other forms of dementia.

The Apo enzymes are supposed to help glial cells and astrocytes to envelop and degrade amyloid-beta proteins before they become plaques. ApoE4 is the least efficient in carrying amyloid-beta to glial cells, thereby increasing the risk of developing Alzheimer’s dementia.

Anything that improves the health and function of the glial cells is theoretically likely going to go a long way in offsetting the processes behind Alzheimer’s disease.

5. Oxidative Damage

We all need oxygen to survive, but did you know it’s also the main reason we age?

Oxidative damage refers to a special type of chemical reaction known as “oxidation”.

Fitting name right?

Oxidation happens when molecules steal electrons from other molecules. When this happens, the molecules that had their electrons stolen start to degrade and fall apart. If enough molecules are affected on a cell, the cell may die.

When these molecules make up the outside of our nerve cells, this becomes a major problem.

Oxidative damage occurs whenever toxic compounds like amyloid-beta, lactic acid, heavy metals, or other free radical compounds are allowed to build up outside the cell.

Over time, oxidative damage may be a risk factor for Alzheimer’s disease.

Antioxidant support is a common method of protecting the brain, as well as every other organ in the human body. This is one of the strengths offered to us from the natural world, as some plants tend to be very high in antioxidant compounds.

Common Treatments for Alzheimer’s Disease

While no medication can stop Alzheimer’s disease, there are a few commonly used to slow down its progression. These can help the patient live more comfortably and prolong their independence.

Cholinesterase inhibitors (galantamine, rivastigmine, and donepezil) seem to prevent the breakdown of acetylcholine and work best for mild to moderate cases. These can provide some relief of symptoms and help control behavior.

N-methyl D-aspartate (NMDA) antagonists like memantine help those with moderate to severe Alzheimer’s disease maintain daily functions a little longer.

Since CBD can interact with certain medications, it’s important you talk to your doctor before combining it with over-the-counter or prescription drugs.

Summing it All Up: CBD and Alzheimer’s Disease

CBD oils may potentially offer an excellent array of benefits for the progression of Alzheimer’s disease, as suggested by early but exciting research.

The indicated effects of the oil are mainly preventative in nature, helping to slow the progression of the disease and improve the overall quality of life.

If you want to avoid the psychoactive effects, we recommend choosing a product that has less than 0.03% THC content.

But if you don’t mind the psychoactivity and live in a country or state where THC oils are legal, we highly recommend going with a product containing closer to a 1:1 ratio of CBD to THC for maximum benefits.

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References Cited In This Article

1. Iuvone, T., Esposito, G., Esposito, R., Santamaria, R., Di Rosa, M., & Izzo, A. A. (2004). Neuroprotective effect of cannabidiol, a non‐psychoactive component from Cannabis sativa, on β‐amyloid‐induced toxicity in PC12 cells. Journal of neurochemistry, 89(1), 134-141.
2. Koo, E. H., Lansbury, P. T., & Kelly, J. W. (1999). Amyloid diseases: abnormal protein aggregation in neurodegeneration. Proceedings of the National Academy of Sciences, 96(18), 9989-9990.
3. Lee, V. M., Balin, B. J., Otvos, L., & Trojanowski, J. Q. (1991). A68: a major subunit of paired helical filaments and derivatized forms of normal Tau. Science, 251(4994), 675-678.
4. Hampson AJ, Grimaldi M, Axelrod J, Wink D. Cannabidiol and ()Delta-9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl Acad Sci USA. 1998;95(14):8268-73.
5. Aazza, S., Lyoussi, B., & Miguel, M. G. (2011). Antioxidant and antiacetylcholinesterase activities of some commercial essential oils and their major compounds. Molecules, 16(9), 7672-7690.
6. Öztürk, M. (2012). Anticholinesterase and antioxidant activities of Savoury (Satureja thymbra L.) with identified major terpenes of the essential oil. Food chemistry, 134(1), 48-54.
7. Hampson, A. J., Grimaldi, M., Lolic, M., Wink, D., Rosenthal, R., & Axelrod, J. (2000). Neuroprotective Antioxidants from Marijuana a. Annals of the New York Academy of Sciences, 899(1), 274-282.
8. Bicas, J. L., Neri-Numa, I. A., Ruiz, A. L. T. G., De Carvalho, J. E., & Pastore, G. M. (2011). Evaluation of the antioxidant and antiproliferative potential of bioflavors. Food and Chemical Toxicology, 49(7), 1610-1615.
9. Perry, N. S., Bollen, C., Perry, E. K., & Ballard, C. (2003). Salvia for dementia therapy: review of pharmacological activity and pilot tolerability clinical trial. Pharmacology biochemistry and behavior, 75(3), 651-659.
10. Carta, G., Nava, F., & Gessa, G. L. (1998). Inhibition of hippocampal acetylcholine release after acute and repeated Δ 9-tetrahydrocannabinol in rats. Brain research, 809(1), 1-4. Chicago
11. Gessa, G. L., Mascia, M. S., Casu, M. A., & Carta, G. (1997). Inhibition of hippocampal acetylcholine release by cannabinoids: reversal by SR 141716A. European journal of pharmacology, 327(1), R1-R2.
12. Juergens, U. R., Stöber, M., Schmidt-Schilling, L., Kleuver, T., & Vetter, H. (1998). Antiinflammatory effects of euclyptol (1.8-cineole) in bronchial asthma: inhibition of arachidonic acid metabolism in human blood monocytes ex vivo. European journal of medical research, 3(9), 407-412.
13. Lin, W. Y., Kuo, Y. H., Chang, Y. L., Teng, C. M., Wang, E. C., Ishikawa, T., & Chen, I. S. (2003). Anti-platelet aggregation and chemical constituents from the rhizome of Gynura japonica. Planta medica, 69(08), 757-764.
14. Li, Y. H., Sun, X. P., Zhang, Y. Q., & Wang, N. S. (2008). The antithrombotic effect of borneol related to its anticoagulant property. The American Journal of Chinese Medicine, 36(04), 719-727.
15. Garrido, G. E., Wichert-Ana, L., Guarnieri, R., Ferrari, L., … & McGuire, P. K. (2004). Effects of cannabidiol (CBD) on regional cerebral blood flow. Neuropsychopharmacology, 29(2), 417.
16. Calcul, L., Zhang, B., Jinwal, U. K., Dickey, C. A., & Baker, B. J. (2012). Natural products as a rich source of tau-targeting drugs for Alzheimer’s disease. Future medicinal chemistry, 4(13), 1751-1761.
17. Frisoni, G. B., Testa, C., Zorzan, A., Sabattoli, F., Beltramello, A., Soininen, H., & Laakso, M. P. (2002). Detection of grey matter loss in mild Alzheimer’s disease with voxel based morphometry. Journal of Neurology, Neurosurgery & Psychiatry, 73(6), 657-664.
18. Zhang, X. (2004). Cholinergic activity and amyloid precursor protein processing in aging and Alzheimer’s disease. Current Drug Targets-CNS & Neurological Disorders, 3(2), 137-152.
19. Stages of Alzheimer’s. (n.d.). Retrieved November 12, 2019, from https://www.alz.org/alzheimers-dementia/stages.
20. Strittmatter, W. J. , Saunders AM, Schmechel D., et. al. (1993). Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease. Proceedings of the National Academy of Sciences Mar 1993, 90 (5) 1977-1981; DOI: 10.1073/pnas.90.5.1977
21. Shi, Y. et al. (2017). ApoE markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy. Nature http://dx.doi.org.proxygw.wrlc.org/10.1038/nature24016 
22. Watt, G., & Karl, T. (2017). In vivo Evidence for Therapeutic Properties of Cannabidiol (CBD) for Alzheimer’s Disease. Frontiers in pharmacology, 8, 20. doi:10.3389/fphar.2017.00020