The neurodegenerative Alzheimer’s disease is the most common form of dementia, which usually occurs in people over the age of 65. About 24 million people worldwide suffer from this disease, which is named after the physician Alois Alzheimer. He first described the disease in 1906.
Alzheimer’s: What happens in the brain?
In Alzheimer’s patients, nerve cells in the brain gradually die, causing the brain to shrink by up to 20 percent. At the same time, the cerebral ventricles expand and the convoluted furrows on the brain surface deepen. This decomposition process begins in the olfactory brain (rhinencephalon) and then spreads to brain regions in charge of memory. In the final stage, the entire brain surface is affected.
Cell death often first affects the deeper lying brain structure or the nucleus basalis. Its nerve cells produce the nerve messenger acetylcholine. If there is a lack of acetylcholine due to cell death, information processing is disturbed so that short-term memory disorders occur.
It is now known that two different types of protein deposits can be found in the affected brain regions, which are responsible for cell death. However, it is not clear why these protein deposits are formed.
In some blood vessels and between nerve cells, insoluble plaques of the protein beta-amyloid are formed, whose function is unknown. In healthy people, the brain breaks down this protein, but not in Alzheimer’s patients. Instead, the protein is deposited in the brain, where it inhibits the supply of oxygen and energy, causing the nerve cells to die.
In addition, the so-called tau fibrils are formed in the brain of affected people. These are insoluble fibres from the tau protein which disturb the transport and stabilisation processes in the brain cells.
Alzheimer’s: What are the risk factors?
The main risk factor for the disease is age. At least one in five people between the ages of 80 and 90 are affected. Among the over-90s it is even more than a third. In contrast, only two percent of 65-year-olds are affected.
Experts assume that age alone does not cause Alzheimer’s disease, but that other risk factors are added before the disease breaks out. These include:
- High blood pressure
- Diabetes
- Increased cholesterol level
- Vascular calcifications (arteriosclerosis)
- Elevated homocysteine level in the blood
- Genetic causes
Another risk factor is oxidative stress. This causes aggressive oxygen compounds, which in turn play an important role in the formation of protein deposits in the brain.
It is also thought that chronic inflammation in the body could increase the risk of Alzheimer’s, as it promotes the formation of protein deposits. However, brain infections caused by viruses or head injuries are also suspected of triggering the disease.
Alzheimer’s: symptoms and stages
Alzheimer’s disease is divided into the three following stages:
- Early stage: The first signs of Alzheimer’s disease are small gaps in short-term memory. For example, people with Alzheimer’s disease cannot remember what was said in the last conversation or they misplace things and cannot find them again. They can also have problems finding their way around and finding words. All these things can frighten affected people and make them react with resistance, depression, withdrawal or aggression.
- Middle stage: This is the stage when memory problems increase. In addition to short-term memory, long-term memory is also disturbed, which means that familiar faces, for example, are less easily recognised. Spatial and temporal orientation also deteriorates and those affected need more and more help in everyday life. Many patients also experience a pronounced urge to move and strong restlessness. Some even develop delusional beliefs or fears.
- Late stage: Patients in the late stages of the disease are completely in need of care. Speech is very limited and problems with breathing, chewing and swallowing increase. In addition, the limbs stiffen, making patients bedridden. They also lose control of the bladder and bowel. Family members or other people close to them are no longer recognised. As the immune system is weakened, infections are also common.
Diagnosis of Alzheimer’s disease
To date, there are no specific laboratory tests or individual tests that can be used to make a clear diagnosis of Alzheimer’s disease. If Alzheimer’s disease is suspected, a detailed discussion is usually first held with the patient’s family doctor, who then refers the patient to a neurologist.
In order to rule out other diseases, the doctor will first routinely examine the patient and conduct a detailed medical history interview. If other causes could be excluded, various tests (watch test, mini-mental status test, DemTect) can be used to determine whether dementia is present. However, these tests cannot differentiate between other forms of dementia, such as vascular dementia. Therefore, imaging procedures such as magnetic resonance imaging (MRI) and computer tomography (CT) are used. These can be used to check whether there has been a loss of brain matter, which confirms the suspicion of dementia.
CSF diagnostics also provide relatively reliable results. A sample is taken from the cerebrospinal fluid in the lumbar spine and then examined in the laboratory. If the amyloid and tau proteins in the cerebrospinal fluid are found to be altered, it is very likely that Alzheimer’s disease is present.
What is the difference between dementia and Alzheimer’s?
In common parlance, the terms Alzheimer’s and dementia are used synonymously. However, there are more than 50 different forms of dementia. What all forms of dementia have in common is that there is a permanent or progressive impairment of brain function. A distinction is made between primary and secondary dementia. While primary dementia, like Alzheimer’s disease, has its origin in the brain, secondary dementia is caused by another disease (e.g. alcohol addiction).
Alzheimer’s: treatment and therapy
There is no cure for Alzheimer’s disease. That is why the therapy aims to help the person with Alzheimer’s so that they can cope with their everyday life for as long as possible. To improve the quality of life, drugs and non-drug therapies are used.
The so-called cholinesterase inhibitors such as rivastigmine or donepezil are supposed to block an enzyme in the brain that breaks down the messenger substance acetylcholine. However, the lack of acetylcholine can only be compensated for in the early to middle stages of the disease. This makes it easier for the person concerned to carry out everyday activities and to maintain mental performance for longer.
Some experts in Alzheimer’s research assume that people with Alzheimer’s have an excess of the messenger substance glutamate in their brain cells. This could contribute to the death of brain cells. This is why people with moderate to severe Alzheimer’s disease often receive the active substance memantine, which, like cholinesterase inhibitors, can delay the deterioration of mental abilities.
In some cases, doctors prescribe neuroleptics like haloperidol or risperidone to relieve various symptoms of the disease, such as anxiety, fear, aggressiveness or passivity. However, these drugs have serious side effects. Among other things, they can increase the risk of a stroke, so close monitoring is needed.
Many people affected suffer from depression and related symptoms too. To relieve these symptoms, patients often receive antidepressants like paroxetine, sertraline, or citalopram.
Alzheimer’s disease: non-drug treatment
In order for Alzheimer’s patients to be able to lead their own lives for a certain period of time, various therapies are useful. These include, among others:
- Cognitive training
- Reality Orientation Training
- Behavioural Therapy
- Autobiographical work
- Ergotherapy
- Physiotherapy
- Art and music therapy
Alzheimer’s: course of the disease and prognosis
On average, Alzheimer’s dementia leads to death after about eight to ten years. Some people develop the disease much more quickly and others get it more slowly. Generally speaking, the later a person falls ill, the shorter the course of the disease.
Studies on the neuroprotective effects of cannabis
Alzheimer’s dementia is thought to be associated with oxidative stress, inflammation of nervous tissue (neuroinflammation) and excitotoxicity. The latter describes the harmfulness of neurotransmitters such as glutamate, which contribute to the death of nerve cells. Especially in recent years, the neuroprotective (cell-protective) properties of cannabinoids have attracted a lot of interest.
Changes in the endocannabinoid system have been observed in the brains of Alzheimer’s patients (1). This could indicate that the endocannabinoid system either contributes to the development of the disease or is altered by it. For example, cannabinoids from the cannabis plant could reduce oxidative stress and protect nerve cells from the harmful effects of beta-amyloid. Cannabinoids could therefore offer a multi-faceted approach to the treatment of Alzheimer’s disease.
The main focus of research has been on the non-psychoactive cannabinoid cannabidiol (CBD). For example, researchers investigated the effect of CBD on cultured cells of rats in a study (2). After exposing the cells to beta-amyloid, the researchers observed a marked reduction in cell survival. Treating cells with CBD before exposure to beta-amyloid also significantly increased cell survival.
What is particularly interesting is that Italian researchers even believe that CBD might be able to promote neurogenesis, the growth of new nerve tissue (3). Using the rat model, they were able to show that CBD interacts with the peroxisome-proliferator-activated receptors (PPARγ), which are located in the cell nucleus. Through blocking PPARγ, CBD could significantly reduce the effect on neuronal damage. In addition, the researchers observed that CBD stimulates the neurogenesis of the hippocampus due to the interaction with PPARγ. These results show that the receptor probably seems to play an important role in mediating CBD actions.
Studies have also been done with the psychoactive component of the cannabis plant. The aim of one study was to assess the potential therapeutic qualities of tetrahydrocannabinol (THC) in slowing down or stopping Alzheimer’s dementia (4). In cell trials, the researchers found that THC could lower amyloid levels at low doses.
Alzheimer’s disease and medical cannabis: more research is needed
Research into the effects of cannabis on Alzheimer’s dementia is still in its infancy, but the interest is great. Interesting studies have already started. For example, at the University of Notre Dame in Western Australia, where 50 people with Alzheimer’s disease or mild dementia are participating. They are investigating the effect of a cannabis-based drug from MGC Pharmaceuticals, which was developed specifically for the treatment of Alzheimer’s dementia.
So far, existing studies have shown that the endocannabinoid system is believed to play an important role in neurodegenerative diseases. However, the complex relationships are still unclear. Studies have also shown that cannabinoids might be able to have a positive effect on Alzheimer’s disease. Unfortunately, there are as yet no confirmed results that show the combination of cannabinoids and their dosage.
(1) Campbell VA, Gowran A. Alzheimer’s disease; taking the edge off with cannabinoids?. Br J Pharmacol. 2007;152(5):655-662. doi:10.1038/sj.bjp.0707446
(2) Iuvone T, Esposito G, Esposito R, Santamaria R, Di Rosa M, Izzo AA. Neuroprotective effect of cannabidiol, a non-psychoactive component from Cannabis sativa, on beta-amyloid-induced toxicity in PC12 cells. J Neurochem. 2004;89(1):134-141. doi:10.1111/j.1471-4159.2003.02327.x
(3) Esposito G, Scuderi C, Valenza M, et al. Cannabidiol reduces Aβ-induced neuroinflammation and promotes hippocampal neurogenesis through PPARγ involvement. PLoS One. 2011;6(12):e28668. doi:10.1371/journal.pone.0028668
(4) Cao C, Li Y, Liu H, et al. The potential therapeutic effects of THC on Alzheimer’s disease. J Alzheimers Dis. 2014;42(3):973-984. doi:10.3233/JAD-140093