Neuroprotection and CBD. Can cannabidiol help with Alzheimer’s disease?

by in About CBD 18 February 2019

The beneficial effects of cannabidiol (CBD) have been described in treatment methods for a wide range of mental disorders, including anxiety, psychosis and depression. Do we know the exact mechanism of this action? As in the case of antidepressants or atypical antipsychotics, studies indicate that CBD administered at a single high dose or in supplementation induces brain plastic changes [1]. For example, CBD eases the decline in hippocampal neurogenesis and density of spinal dendrites induced by chronic stress and prevents the activation of microglia and the reduction of the number of GABA neurons in the pharmacological model of schizophrenia [1]. It has been proven that CBD modulates the pathways of cell fate regulation (such as autophagy) or other neuronal survival pathways in neurodegenerative experimental models, suggesting a potential benefit of CBD treatment for psychiatric or cognitive symptoms associated with neurodegeneration [1].


What are neurodegenerative diseases?

The most well-known neurodegenerative diseases, i.e. those that lead to damage to nerve cells, and hence to the impairment of brain cognitive functions, include:

– Alzheimer’s disease

– Parkinson’s disease

– Huntington’s chorea (a genetically conditioned disease)

– amyotrophic lateral sclerosis (ALS)

– multiple sclerosis

– Alexander’s disease


People suffering from neurodegenerative diseases lose a large number of nerve cells over time which leads mainly to motor damage (as in the case of Parkinson’s disease) or cognitive functions associated, inter alia, with memory leading to its disappearance (as in the case of Alzheimer’s disease). Unfortunately, nowadays these diseases are incurable. Neuron protection against degradation through CBD supplementation may, however, slow down the process of their development.


The brain changes all the time

Although it was once thought that our brain does not create new nerve cells, we now know that it is malleable, that is, changes during one’s life, creating new networks and neuronal pathways. The concept of neuroplasticity also includes biochemical and pharmacological adaptations (intracellular pathways, receptors, synaptic proteins), changes in neural networks (changes in communication, dendritic remodeling and), as well as generation of new neurons (neurogenesis even in adults) [2]. These neuroplastic modifications may also be adaptive or maladaptive. The mechanisms responsible for these changes may allow us to understand the pathophysiology of mental illness and find new treatments [3]. Mental disorders may result from significant neuroplastic changes, and thus erroneous brain plasticity [4]. Understanding the mechanisms of action of antipsychotics is complicated but, above all, complex.


Let’s look at the CBD activity

Most importantly, cannabidiol does not have psychoactive properties, so it does not cause any  psychotomimetic or anxiety effects and does not become addictive after repeated use [5]. In addition, the CBD has a broad spectrum of other possible therapeutic activities that include anxiolytic, antipsychotic, antidepressant and neuroprotective effects in a wide range of psychiatric and neurodegenerative disorders [5,6]. Although the majority of these putative therapeutic properties were initially described in animal models, clinical studies have confirmed the beneficial effects of CBD in anxiety, schizophrenia, epilepsy and multiple sclerosis [7,8,9]. Neuroimaging clearly showed that CBD affects areas of the brain involved in the neurobiology of mental disorders [1].


CBD affects neuroplastics

The scientific work reads:

‘A single dose of CBD, administered orally in healthy volunteers, has been shown to alter resting activity in the limbic and paralimic regions of the brain [10]. CBD reduced the activity of the left almond-hippocampal body, hypothalamus and posterior rim, increasing the activity of the left parahippocampal gyrus compared to placebo. In healthy volunteers treated with CBD, a decrease in amygdala and anterior and posterior rim activity as well as a disorder in the cerebrospinal myeloma of the anterior amygdala was observed [11, 12]. Furhter’s imaging studies have also shown that CBD changes activity in other areas of the brain associated with neuropsychiatric disorders, such as medial and left cortex and temporal and prefrontal pivots’ [13, 14]. (Borgwardt et al., 2008, Bhattacharyya et al., 2010, Table Table11).


How do we benefit?

In simpler language this means that potentially CBD, through its influence on neuroplastics and neuroprotection, can help treating anxiety, epilepsy, multiple sclerosis and schizophrenia. These diseases, through their very complex aetiology and the mechanism of formation, are difficult to treat. Antipsychotic, antiepileptic or antidepressant drugs have many side effects, are often addictive or have a narrow therapeutic index. Research shows that CBD is safe even at high doses causing at most drowsiness and fatigue. Cannabidiol can become an excellent alternative in neuroplastic disorders and its supplementation will then be a great prevention of these diseases.


Research and scientific publications on the basis of which the article was written:

  1.        Plastic and Neuroprotective Mechanisms Involved in the Therapeutic Effects of Cannabidiol in Psychiatric Disorders. Alline C. Campos, Manoela V. Fogaça, Franciele F. Scarante, Sâmia R. L. Joca, Amanda J. Sales, Felipe V. Gomes, Andreza B. Sonego, Naielly S. Rodrigues, Ismael Galve-Roperh, andFrancisco S. Guimarães.
  2.        Adult neuroplasticity: more than 40 years of research. Fuchs E, Flügge G. Neural Plast. 2014; 2014():541870.
  3.        The dynamic brain: neuroplasticity and mental health. Kays JL, Hurley RA, Taber KH. J Neuropsychiatry Clin Neurosci. 2012 Spring; 24(2):118-24.
  4.        ICD and DSM: neuroplasticity and staging are still missing. Pallanti S. CNS Spectr. 2016 Aug; 21(4):276-8.
  5.        From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology. Ligresti A, De Petrocellis L, Di Marzo V. Physiol Rev. 2016 Oct; 96(4):1593-659.
  6.        Cannabidiol, neuroprotection and neuropsychiatric disorders. Campos AC, Fogaça MV, Sonego AB, Guimarães FS. Pharmacol Res. 2016 Oct; 112():119-127.
  7.        Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naïve social phobia patients. Bergamaschi MM, Queiroz RH, Chagas MH, de Oliveira DC, De Martinis BS, Kapczinski F, Quevedo J, Roesler R, Schröder N, Nardi AE, Martín-Santos R, Hallak JE, Zuardi AW, Crippa JA. Neuropsychopharmacology. 2011 May; 36(6):1219-26.
  8.        Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Leweke FM, Piomelli D, Pahlisch F, Muhl D, Gerth CW, Hoyer C, Klosterkötter J, Hellmich M, Koethe D. Transl Psychiatry. 2012 Mar 20; 2():e94.
  9.        From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology. Ligresti A, De Petrocellis L, Di Marzo V. Physiol Rev. 2016 Oct; 96(4):1593-659.
  10.     Effects of cannabidiol (CBD) on regional cerebral blood flow. Crippa JA, Zuardi AW, Garrido GE, Wichert-Ana L, Guarnieri R, Ferrari L, Azevedo-Marques PM, Hallak JE, McGuire PK, Filho Busatto G. Neuropsychopharmacology. 2004 Feb; 29(2):417-26.
  11. Distinct effects of {delta}9-tetrahydrocannabinol and cannabidiol on neural activation during emotional processing. Fusar-Poli P, Crippa JA, Bhattacharyya S, Borgwardt SJ, Allen P, Martin-Santos R, Seal M, Surguladze SA, O’Carrol C, Atakan Z, Zuardi AW, McGuire PK. Arch Gen Psychiatry. 2009 Jan; 66(1):95-105.
  12.     Modulation of effective connectivity during emotional processing by Delta 9-tetrahydrocannabinol and cannabidiol. Fusar-Poli P, Allen P, Bhattacharyya S, Crippa JA, Mechelli A, Borgwardt S, Martin-Santos R, Seal ML, O’Carrol C, Atakan Z, Zuardi AW, McGuire P. Int J Neuropsychopharmacol. 2010 May; 13(4):421-32.
  13. Neural basis of Delta-9-tetrahydrocannabinol and cannabidiol: effects during response inhibition. Borgwardt SJ, Allen P, Bhattacharyya S, Fusar-Poli P, Crippa JA, Seal ML, Fraccaro V, Atakan Z, Martin-Santos R, O’Carroll C, Rubia K, McGuire PK. Biol Psychiatry. 2008 Dec 1; 64(11):966-73.
  14. Opposite effects of delta-9-tetrahydrocannabinol and cannabidiol on human brain function and psychopathology. Bhattacharyya S, Morrison PD, Fusar-Poli P, Martin-Santos R, Borgwardt S, Winton-Brown T, Nosarti C, O’ Carroll CM, Seal M, Allen P, Mehta MA, Stone JM, Tunstall N, Giampietro V, Kapur S, Murray RM, Zuardi AW, Crippa JA, Atakan Z, McGuire PK. Neuropsychopharmacology. 2010 Feb; 35(3):764-74.


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