Alzheimer’s disease (AD) is also a progressive, neurodegenerative disorder of unknown etiology. However, beyond that, all similarity to Amyotrophic lateral sclerosis (ALS)/Lou Gehrig’s disease, stops. AD is characterized by a progressive deterioration of memory and overall cognitive functioning. Other symptoms of AD include aggressive behavior and agitation, depression, appetite loss, and occasionally, in advanced cases, difficulty walking. The disease is estimated to affect about 5 million Americans. In 2006 the worldwide prevalence was 26.6 million. By 2050, prevalence is expected to quadruple, by which time one in eighty-five persons worldwide will be living with the disease (Brookmeyer et al. 2007). Alzheimer’s usually begins after age sixty, though some younger people may very rarely have early-onset Alzheimer’s. The risk of developing Alzheimer’s goes up with age. Around 5 percent of men and women ages sixty-five to seventy-four have Alzheimer’s, and nearly half of those age eighty-five and older may have the disease, though Alzheimer’s is not a normal part of aging.
There are a number of physiological and anatomical changes that occur in the brains of AD patients. Nerve cells die in parts of the brain that are vital to memory and other functions, and connections (synapses) between nerve cells are broken. This disruption in synaptic connections within the brain lead to impaired thinking and memory problems. Alzheimer’s starts with mild memory problems and can end with severe brain damage. How fast the disease works and the course the disease takes vary from person to person. Average Alzheimer’s patients live from eight to ten years after they are diagnosed, though they can live as long as twenty years. Biopsies of the brains of AD patients show numerous amyloid plaques- hardened protein deposits that are thought to directly cause most of the central nervous system dysfunction seen in AD.
Sometimes the term dementia is used to describe the symptoms caused by these changes in brain function. Some symptoms may include asking the same questions repeatedly; becoming lost in familiar places; being unable to follow directions; getting disoriented about time, people, and places; and neglecting personal safety, hygiene, and nutrition. There is no set schedule or rate at which people with dementia develop symptoms. While dementia is certainly part of AD, there are also many other conditions, reversible and permanent, that can cause dementia.
There are currently no Food and Drug Administration (FDA)- approved treatments or medications available that actually modify the disease course of AD. There are only a few drugs (Aricept [donepezil] and Namenda [memantine]) that have been FDA-approved to treat symptoms of the disease, but these drugs do not actually improve the long-term prognosis. None of these drugs halt the formation of plaques in the brains of AD patients.
There is now ample evidence in the medical literature to indicate that cannabis may provide not only symptomatic relief to patients afflicted with AD, but it also actually limits the formation of new plaques in the brain. Thus, it appears that cannabis may actually slow down the progression of the disease. In a study done at Scripps Research Institute in California, researchers reported that delta 9-THC, both in the test tube and in computer models, inhibited the enzyme responsible for the aggregation of amyloid plaque, which is the primary marker for AD, in a manner considerably superior to the FDA-approved AD drugs such as donepezil and tacrine (Cognex) (Eubanks et al. 2006).
This study identified a mechanism whereby cannabinoids can directly impact AD pathology. The researchers concluded that cannabinoids, including delta 9-THC, may provide an improved therapeutic treatment for AD that simultaneously treats both the symptoms and the progression of the disease. Other studies, both in vitro and in vivo, have shown that cannabidiol (CBD) and the synthetic cannabinoid WIN-55,212-2 can help prevent brain cell death that results from exposure to the amyloid plaques and can also improve memory (Iuvone et al. 2004; Marchalant et al. 2008; Marchalant, Rosi, and Wenk 2007).
Other recent studies have shown that injecting the synthetic cannabinoid WIN 55,212-2 directly into the brain significantly decreased neurotoxicity and helped prevent cognitive impairment in rats injected with amyloid-beta peptide (a protein that induces AD in rats) (Ferraro et al. 2001; Ramirez et al. 2005). The cannabinoid appeared to reduce the neuroinflammation associated with AD. Pervious preclinical studies have demonstrated that cannabinoids can prevent cell death by antioxidation (Hampson et al. 1998). In addition to potentially modifying the progression of AD, recent clinical trials also indicate that cannabinoid therapy reduces agitation and improves appetite and weight gain in patients with AD.
Daily administration of 2.5mg of synthetic THC over a two week period reduced nocturnal motor activity and agitation in AD patients in a open-label pilot study (Walther et al. 2006). Improved weight gain and mood state were also noted among AD patients administered cannabinoids in a separate study previously published (Volicer et al. 1997). Thus, far, at least two chemicals in cannabis, THC and CBD, have been shown to be effective against AD-related pathology. Additional studies using cannabis to treat AD are clearly warranted, as we face a looming global epidemic of Alzheimer’s disease as the population ages. Any advances in therapeutic and preventative strategies that lead to even small delays in Alzheimer’s onset and progression can significantly reduce the global burden of the disease (Brookmeyer et al. 2007).
When cannabinoid receptors in the central nervous system are activated, this triggers signaling pathways in the brain that are lined to neuronal repair and cell maintenance, and the release of other compounds that further activate neuroprotective responses. Additionally, it is clear that our own internal marijuana, the endocannabinoids, are released in response to pathogenic events, thus representing a potential compensatory repair mechanism. Enhancing this “on demand’ action of endocannabinoids is an important strategy the body uses to help prevent further brain injury as well as promote healing. The neuroprotective activities of both externally administered cannabinoids (i.e. transdermal patches, lotions, salves, etc.) and the internal endocannabinoids (sublingual, suppositories, edibles, oils, etc.) are novel processes that can be effectively exploited to help promote and protect the nervous system in the face of disease or physical and chemical trauma.