The Disease

Alzheimer’s disease is an progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. In most people (~95%), symptoms first appear in their mid-60s, however, there is autosomal dominant genetic form of the disease in which the symptoms onset earlier in life.  Regardless of the cause, two unique findings in the brain are associated with the disease: 1) amyloid plaques deposition between the brain cells and 2) the deposition of protein fibers within the brain cells called neurofibrillary tangles, both of which lead to a loss of connections between brain cells.  Amyloid plaques consist of normal protein fragments that are normally eliminated from the brain but in AD, these proteins accumulate and form hard, insoluble plaques.   Neurofibrillary tangles are made up of microtubules that are normally found in the brain and function to transport materials within the nerve cells so they can function normally.  However, in AD, the protein that makes up these fibers (tau) is abnormal and causes the tubules to collapse, resulting in abnormal nerve cell function.  These pathologically findings cause inflammation and oxidative stress in the brain all of which causes and promotes neurodegeneration.  In general, as the symptoms of AD deteriorate, the plaques and tangles become more pronounced and the neuroinflammation and oxidative stress increase.  Alzheimer’s has been thought to be continually progressive and irreversible, however, recent studies suggest that this may not be completely true.


In the laboratory CBD protects brain cells, prevents nerve degeneration, decreases plaques, is anti-inflammatory, decreases oxidative stress, and improves cell life.  Each of these effects would be beneficial in AD.  In addition, CBD decreases the production of amyloid plaques.  In animal models of AD, CBD has the same effects and, as it has these effects, the memories and thinking process of the animals improve.  CBD even improves the memories and thinking processes of animals with advanced AD. Very little human research using CBD to treat AD has been done.  However, in a small 4-week study of 10 human patients with advanced AD, CBD improved their symptoms.

Laboratory Studies

CBD has been found in-vitro:  to be neuroprotective, to prevent hippocampal and cortical neurodegeneration, to reduce tau hyperphosphorylation, to lower amyloid b levels, to be anti-inflammatory, and to act as an antioxidant. 1-5 In addition, CBD protects against Ab mediated neurotoxicity and microglial- activated neurotoxicity and improves cell viability.6-8 CBD decreases the oxidative stress in neuroinflammation.9  GPR3 is a modulator of beta-arrestin 2 (BA2) and its stimulation by agonists results in over production of BA2 while its stimulation by inverse agonists results in lowering of BA2.10 Beta-arrestin 2 (BA2) is produced by stimulation of GPR3 receptors and results in the production of amyloid in human brain cultures.10

Live Animal Studies

CBD reduces inflammation by reducing NO and interleukin-1b (IL-1b) release.11 IL-1b is involved in neurodegeneration and the over-production of NO, which causes tau hyperphosphorylation.  In addition, CBD is an inverse agonist for GPR3 which when stimulated inversely should result in decreased production of amyloid in brain tissue and subsequently a decrease in the number of plaques.12 Eradiation of GPR3 results in the loss of plaques and the restoration of memory in a mice model of AD.13 In both mice and rat models of AD, CBD was able to reverse the pathological changes found in AD. 4,7,12-20 CBD has been found restore memory and other cognitive defects in animals that have the disease—even in animals with advanced disease.4,7,13,14,17,19,20 Finally, CBD has been shown to prevent the development of AD.21

Human Studies

GPR3 expression is elevated in the sporadic Alzheimer’s disease brain, is highly expressed in areas of the normal human brain implicated in Alzheimer’s disease and this upregulation correlates with the progression of the disease 13,22.  Over a 4-week period involving 10 patients, CBD decreased the amount and severity of delusions, agitation/aggression, irritability, and apathy of patients with AD and improved the amount of sleep in these patients.  In addition, it decreased the amount and severity of caregiver distress. No adverse reactions were noted during the treatment time.23

Bottom Line

CBD significantly reverses the neural pathology in animal models of Alzheimer’s Disease and improves the memory and thinking of the animals.  Whether this will translate to humans is not yet scientifically proven.  However, a small, non-controlled study indicates promise.  At this time, the FDA does not recommend CBD for the treatment of Alzheimer’s Disease



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  2. Hamelink C, etal. (2005) Comparison of cannabidiol, antioxidants, and diuretics in reversing binge ethanol-induced neurotoxicity. J Pharmacol Exp Ther 314:780–788, 2005.
  3. Esposito G, etal. (2006a). The marijuana component cannabidiol inhibits b-amyloid-induced tau protein hyperphosphorylation through Wnt/b-catenin pathway rescue in PC12 cells. J Mol Med 2006, 84:253–258
  4. Marin-Moreno A, etal. Prolonged oral cannabinoid administration prevents neuroinflammation, lowers b-amyloid levels and improves cognitive performance in Tg APP 2576 mice. J Neuroinflam 9(8) 1-15, 2012.
  5. Mukhopadhyay P, etal.(2011) Cannabidiol protects against hepatic ischemia/reperfusion injury by attenuating inflammatory signaling and response, oxidative/nitrative stress, and cell death. Free Radic Biol Med 2011, 50:1368–1381.
  6. Janefjord E, etal. (2014). Cannabinoid effects on b amyloid fibril and aggregate formation, neuronal and microglial-activated neurotoxicity in-vitro. Cell Mol Neurobiol 34:31–42, 2014.
  7. Marin-Moreno A, etal. Cannabidiol and other cannibinoids reduce microglial activation in-vivo and in-vitro: Relevance to Alzheimer’s Disease. Mol Pharm 79: 964-973, 2011
  8. Harvey B, etal. (2012). Contrasting protective effects of cannabinoids against oxidative stress andamyloid-b evoked neurotoxicity invitro. Neurotoxicology 33:138–146, 2012.
  9. Vallée A, et al. Effects of cannabidiol interactions with Wnt/β-catenin pathway and PPARγ on oxidative stress and neuroinflammation in Alzheimer’s disease. Acta Biochim Biophys Sin (Shanghai). 2017 Oct 1;49(10):853-866.
  10. Thathiah A, etal. β-arrestin 2 regulates Aβ generation and γ-secretase activity in Alzheimer’s disease. Nat Med. 2013 Jan;19(1):43-9.
  11. Esposito G, etal. (2007). Cannabidiol in-vivo blunts b-amyloid induced neuroinflammation by suppressingIL-1b and iNOS expression. Br J Pharmacol 2007 151:1272–1279.
  12. Aso E., et al. Cannabis-based medicine reduces multiple pathological processes in AβPP/PS1 mice. J Laun AS, etal. GPR3, GPR6, and GPR12 as novel molecular targets: their biological functions and interaction with cannabidiol. Acta Pharmacol Sin. 2018 Jun 25.  Alzheimers Dis.2015;43(3):977-91.
  13. Huang Y, etal. Loss of GPR3 reduces the amyloid plaque burden and improves memory in Alzheimer’s disease mouse models. Sci Transl Med. 2015 Oct 14;7(309):309ra164.
  14. Aso E., et al. Cannabinoid Receptor 2 Participates in Amyloid-β Processing in a Mouse Model of Alzheimer’s Disease but Plays a Minor Role in the Therapeutic Properties of a Cannabis-Based Medicine. J Alzheimers Dis. 2016;51(2):489-500.
  15. Casarejos MJ, et al. Natural cannabinoids improve dopamine neurotransmission and tau and amyloid pathology in a mouse model of tauopathy. J Alzheimers Dis. 2013;35(3):525-39.
  16. Esposito G, etal. (2011). Cannabidiol reduces Ab-induced neuroinflammation and promotes hippocampal neurogenesis through PPARg PLoSONE 2011, 6:e28668.
  17. Hughes B and Herron C. Cannabidiol Reverses Deficits in Hippocampal LTP in a Model of Alzheimer’s Disease. Neurochem Res. 2018 Mar 24.
  18. Scuderi C, et al. Cannabidiol promotes amyloid precursor protein ubiquitination and reduction of beta amyloid expression in SHSY5YAPP+ cells through PPARγ involvement. Phytother Res. 2014 Jul;28(7):1007-13.
  19. Cheng D, et al. Chronic cannabidiol treatment improves social and object recognition in double transgenic APPswe/PS1∆E9 mice. Psychopharmacology (Berl). 2014b Aug;231(15):3009-17.
  20. Aso E, et al. Delineating the Efficacy of a Cannabis-Based Medicine at Advanced Stages of Dementia in a Murine Model. J Alzheimers Dis. 2016 Oct 4;54(3):903-912.
  21. Cheng D, et al. Long-term cannabidiol treatment prevents the development of social recognition memory deficits in Alzheimer’s disease transgenic mice. J Alzheimers Dis. 2014;42(4):1383-96
  22. Thathiah A, etal. The orphan G protein-coupled receptor 3 modulates amyloid-beta peptide generation in neurons. 2009 Feb 13;323(5916):946-51.
  23. Shelef AJ, et al. Safety and Efficacy of Medical Cannabis Oil for Behavioral and Psychological Symptoms of Dementia: An-Open Label, Add-On, Pilot Study. Alzheimers Dis. 2016;51(1):15-19.


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