There is a new way to combat Alzheimer’s disease and other forms of dementia. By combining Sildenafil, the active ingredient of Viagra, with the acetylcholinesterase inhibitor, Aricept, scientists have discovered that this new medication is more effective than either of its individual components when tested in mice studies. What makes this medication so promising is that it could potentially be used to treat a range of neurological disorders, from Alzheimer’s disease and other types of dementia to Parkinson’s disease and multiple sclerosis. We will explore the possible reasons why this medication is so effective and whether or not you should consider trying it for yourself.
Exercise
It is well known that exercise can greatly boost your mental health. In particular, several studies have shown that exercise can delay the onset of Alzheimer’s disease and improve the quality of patients’ lives while suffering from the disease. In one study, scientists evaluated the effects of physical activity on dementia risk and found that people who were physically active had a lower risk of developing dementia, compared to those who were inactive.
Similarly, a study published in the Journal of the American Medical Association (JAMA) found that being physically active can reduce your risk of developing Alzheimer’s disease by 52%. The research also revealed that older adults who were physically active had fewer Alzheimer’s-related brain changes than those who were inactive. Based on these findings, it would seem that exercise could offer some protection against Alzheimer’s disease.
Anti-inflammatory Agents
Alzheimer’s disease is a neurodegenerative disorder that is characterized by the buildup of plaques in the brain. These plaques are composed of toxic proteins that cause inflammation and damage to nerve cells and synapses. Several studies suggest that this neuroinflammation plays a critical role in the pathogenesis of the disease. One theory is that as the disease progresses, the brain becomes less capable of maintaining a proper anti-inflammatory response, leaving the body open to a variety of other conditions, including infections, cancer, and heart disease.
In light of this, many researchers have turned to exploring the use of anti-inflammatory agents as a possible treatment for Alzheimer’s disease. One class of these agents is the non-steroidal anti-inflammatory drugs (NSAIDs). These drugs inhibit the activity of the enzymatic protein, cyclooxygenase-2 (COX-2), which is responsible for producing prostaglandins, inflammatory molecules that play a critical role in the body’s immune system.
One of the more popular NSAIDs, Celebrex, has proven effective in treating Alzheimer’s disease in several studies. Its use has been linked to a decreased risk of progression of the disease and reduced agitation in patients. Alzheimer’s disease is a progressive disease and, as a result, most patients will experience some degree of cognitive impairment. For this reason, NSAIDs could provide some significant benefits to these individuals.
Boosting Neurogenesis
Another theory regarding the neural basis of Alzheimer’s disease involves the role of neurogenesis, or the generation of new neurons. Many researchers believe that as the disease progresses, the generation of new nerve cells slows, resulting in cognitive impairment. According to this theory, treatments that speed up neurogenesis could be effective in alleviating Alzheimer’s disease symptoms.
One way of stimulating neurogenesis is through the use of antidepressants. Several studies have shown that selective serotonin reuptake inhibitors (SSRIs) can increase the survival of new nerve cells in the brains of mice and rats. Another factor that could play a role in the generation of new nerve cells is the stress hormone, cortisol. Interestingly, the drug Dexamethasone, which is commonly used to treat inflammation, has also been shown to increase the number of new cells in the brain, raising the possibility that its anti-inflammatory properties could contribute to its neuroprotective effects.
Protecting Nerve Cells
Some studies suggest that one way in which the body protects itself from Alzheimer’s disease is through the production of antibodies. These antibodies bind to toxic proteins that are found in brain plaques, preventing harmful compounds from interacting with and damaging nerve cells. The immune system produces these antibodies as a result of continuous exposure to these proteins. This could explain why Alzheimer’s disease is so prevalent in older adults – they have had more time to develop antibodies against these proteins and can, therefore, better protect their nerve cells from damage.
One of the proteins that the body’s immune system produces antibodies against is β-Amyloid. In studies, mice lacking the gene that encodes for β-Amyloid develop less neuroinflammation and exhibit improved memory and learning. Therefore, if your body does not produce β-Amyloid, it may be possible to reduce your risk of Alzheimer’s disease. A potential treatment for Alzheimer’s disease that functions by preventing β-Amyloid production is Aβ vaccination.
Treating Angiogenesis, or the Growth of Blood Vessels
Another theory regarding the cause of Alzheimer’s disease focuses on the role of blood vessels, or angiogenesis. In this theory, as the disease progresses, the brain becomes deprived of oxygen and nutrients, resulting in chronic low-level inflammation. This, in turn, could lead to the formation of blood vessels in an attempt to reestablish normal brain function. Scientists have dubbed this type of blood vessel formation ‘arteriogenesis’.
Researchers have also suggested that certain medications could increase the likelihood of developing Alzheimer’s disease by inducing arteriogenesis. One example is the anti-angiogenic medication Avastin, which has been shown to cause a significant increase in the incidence of Alzheimer’s disease in mice. Similarly, the use of Valsartan, an antagonist of angiotensin II, has also been shown to promote the development of Alzheimer’s disease in mice. Interestingly, some NSAIDs have been shown to inhibit angiotensin II, suggesting that this drug class could be used to treat or prevent Alzheimer’s disease by boosting blood vessels and oxygen supply to the brain.
Oxidative Stress
Alzheimer’s disease is associated with significant oxidative stress, or an imbalance between the production of free radicals, or molecules that contain oxygen, and antioxidants, which neutralize these molecules. Several studies have shown that increased oxidative stress is linked to the onset of the disease. What makes this stress so dangerous is that free radicals can harm nearly every aspect of a cell, including its DNA, proteins, and organelles. The body requires a delicate balance between these species to maintain health. When this balance is disturbed, it can lead to cell damage and death.
One way in which the body attempts to keep this balance is through the production of antioxidant enzymes, including superoxide dismutase and glutathione peroxidase. Research suggests that up to 90% of Alzheimer’s disease cases could be prevented by increasing the levels of these enzymes in the human body. One reason why trials with this medication met with such success is because of its potent anti-inflammatory and neuroprotective properties. It is possible that this combination of effects prevents the body from experiencing the type of chronic low-level inflammation that leads to Alzheimer’s disease. As a result, there may be less of a chance for these toxic proteins to induce damage in the first place.
Protecting Neurotransmission
Alzheimer’s disease is characterized by the decline in cognitive function, including memory loss and the impairment of executive function. Several theories propose that this decline is caused by neurodegeneration or the death of nerve cells. However, some scientists believe that this loss of function could be due to damage to the system that transmits nerve impulses from one region of the brain to another. This system is called the ‘neurotransmission’ and, as a result, medications that could protect it could be helpful in preserving memory and cognition in patients with Alzheimer’s disease. One such medication is gabapentin, which has been shown to prevent the destruction of neurons and synapses and reverse age-related memory impairment in mice. Another example is the benzodiazepine, clonazepam, which has been shown to increase the number of neurons and synapses in the brains of mice with Alzheimer’s disease.
Improving Mitochondrial Function
Many signs of aging are associated with an impairment of mitochondrial function. One theory is that because of the damage that free radicals can inflict on mitochondria, the body gradually loses its ability to produce sufficient amounts of ATP, or energy, to allow cells to function properly. As a result, it becomes more and more difficult for the body to maintain a healthy metabolism as it gets older.