The Devastating and Increasing Prevalence of Alzheimer’s
According to the World Health Organization, there are an estimated 5.2 million people in the U.S. with Alzheimer’s disease and 20 million worldwide. The prevalence of Alzheimer’s disease doubles every five years after the age of 65 and reaches nearly 50% after age 85. Increased life expectancy in the U.S. and other developed countries has fueled an unprecedented growth in the elderly population that is leading to dramatic increases in the incidence of Alzheimer’s disease. By 2050, the number of people in the U.S. aged 65 and older is projected to increase by 283%.
Cannabinoids have the potential to treat, slow or prevent the progression of Alzheimer’s and should be thoroughly and immediately researched.
Cannabinoids and the Nervous System
It has been a while since the therapeutic benefits of cannabinoids have been discovered. However, with advances in medical science and technology, and with increased knowledge about how cannabinoids work with our CB1 and CB2 receptors, a number of therapeutic applications have been discovered either through natural cannabinoids or synthetic chemicals that have a high affinity for cannabinoid receptors.
Looking at the nervous system, for instance, it has been determined that the great number of CB1 receptors in the brain correlate with the role of cannabinoids in the treatment of incurable diseases. Of all the neurodegenerative diseases, Alzheimer’s is the most common form of dementia. It is characterized by impairment in memory and cognition.
Alzheimer’s patients battle with many pathological conditions that might be targeted by the cannabinoids.
What Effects Do Cannabinoids Have on Abnormal Proteins in Alzheimer’s Disease?
In Alzheimer’s disease, a number of abnormal proteins accumulate in the brain cells. These proteins are known as beta-amyloid proteins. Tau proteins in dead nerve cells (proteins that have been chemically altered) are also characteristic of Alzheimer’s disease. Research has shown that synthetic cannabinoids provide a strong protective action for neurons against amyloid beta proteins. This results in an improvement of cognitive functions and memory.
Additionally, studies have shown that some cannabinoids, including cannabidiol (CBD) and WIN55, 212-2, are capable of inhibiting the chemical changes to tau proteins. These changes are mainly due to excessive phosphorylation.
Cannabinoids Serve as Anti-Inflammatories and Modulators of Nerve Signals
Inflammation of the neurons is another characteristic of Alzheimer’s disease. This is due to the abundance of microglia cells which causes toxicity and damage to nerve cells. Studies have shown that a combination of tetrahydrocannabinol (THC) and cannabidiol (CBD) can inhibit the action of microglial cells, thus preventing inflammation. THC can also inhibit the degradation of acetylcholine, thus facilitating effective transmission of nerve signals.
The Clinical Effects of Cannabinoids
Some clinical trials are available to check the efficacy of cannabinoids on Alzheimer’s. Research has shown that THC and its derivatives may cause a significant reduction of the magnitude of behavioral changes and night-time agitation alongside alleviation of weak appetite that is linked to the disease.
A synthetic cannabinoid, known as Nabilone, plays an effective role in patients who do not respond positively to antipsychotic medications. All in all, there are very few side effects of cannabis in the treatment of Alzheimer’s, such as tiredness or euphoria, which do not require that you stop treatment.
It is obvious that cannabinoids can protect and repair neurons and dramatically ease the symptoms of Alzheimer’s. And while the research thus far is encouraging, we need to continue to study and develop cannabinoids in order to fully understand their potential to prevent and minimize the devastation of diseases like Alzheimer’s.
We must educate patients and generate awareness about cannabinoids. There is a huge population of people suffering from degenerative diseases and a world of people who do not know that cannabinoids could help protect them from such a fate. Why would we not do everything in our power to get this life-altering information into the hands of people immediately?
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Ahmad R., Goffin K., Van den Stock J., De Winter F. L., Cleeren E., Bormans G., et al. (2013). In vivo type 1 cannabinoid receptor availability in Alzheimer’s disease. Eur. Neuropsychopharmacol. 24 242–250 10.1016/j.euroneuro.2013.10.002 [PubMed] [Cross Ref]
Akiyama H., Barger S., Barnum S., Bradt B., Bauer J., Cole G. M., et al. (2000). Inflammation and Alzheimer’s disease. Neurobiol. Aging 21 383–42110.1016/S0197-4580(00)00124-X [PMC free article] [PubMed] [Cross Ref]
Ankarcrona M., Mangialasche F., Winblad B. (2010). Rethinking Alzheimer’s disease therapy: are mitochondria the key? J. Alzheimers Dis. 20(Suppl. 2) S579–S59010.3233/JAD-2010-100327 [PubMed] [Cross Ref]
Aso E., Juvés S., Maldonado R., Ferrer I. (2013). CB2 cannabinoid receptor agonist ameliorates Alzheimer-like phenotype in AβPP/PS1 mice. J. Alzheimers Dis. 35 847–85810.3233/JAD-130137 [PubMed] [Cross Ref]
Aso E., Palomer E., Juvés S., Maldonado R., Muñoz F. J., Ferrer I. (2012). CB1 agonist ACEA protects neurons and reduces the cognitive impairment of AβPP/PS1 mice. J. Alzheimers Dis. 30 439–459 10.3233/JAD-2012-111862 [PubMed] [Cross Ref]
Athanasiou A., Clarke A. B., Turner A. E., Kumaran N. M., Vakilpour S., Smith P. A., et al. (2007). Cannabinoid receptor agonists are mitochondrial inhibitors: a unified hypothesis of how cannabinoids modulate mitochondrial function and induce cell death. Biochem. Biophys. Res. Commun. 364 131–13710.1016/j.bbrc.2007.09.107 [PubMed] [Cross Ref]
Bachmeier C., Beaulieu-Abdelahad D., Mullan M., Paris D. (2013). Role of the cannabinoid system in the transit of beta-amyloid across the blood–brain barrier. Mol. Cell. Neurosci. 56 255–26210.1016/j.mcn.2013.06.004 [PubMed] [Cross Ref]
Bénard G., Massa F., Puente N., Lourenço J., Bellocchio L., Soria-Gómez E., et al. (2012). Mitochondrial CB1 receptors regulate neuronal energy metabolism. Nat. Neurosci. 15 558–56410.1038/nn.3053 [PubMed] [Cross Ref]
Benito C., Núñez E., Tolón R. M., Carrier E. J., Rábano A., Hillard C. J., et al. (2003). Cannabinoid CB2 receptors and fatty acid amide hydrolase are selectively overexpressed in neuritic plaque-associated glia in Alzheimer’s disease brains. J. Neurosci. 23 11136–11141 [PubMed]
Benito C., Tolón R. M., Castillo A. I., Ruiz-Valdepeñas L., Martïnez-Orgado J. A., Fernández-Sánchez F. J., et al. (2012). β-Amyloid exacerbates inflammation in astrocytes lacking fatty acid amide hydrolase through a mechanism involving PPAR-α, PPAR-γ and TRPV1, but not CB1 or CB2 receptors. Br. J. Pharmacol. 166 1474–148910.1111/j.1476-5381.2012.01889.x [PMC free article] [PubMed] [Cross Ref]