Alzheimer’s Disease Treatment

All currently available treatments for Alzheimer’s disease slow the cognitive decline, and or improve cognitive function and or relieve the symptoms associated with Alzheimer’s disease. Unfortunately at this point there is no treatment that will cure Alzheimer’s disease and no way to stop the progression of the disease.

Alzheimer’s Disease Treatment with Drugs

Treatment for improving cognitive function in Alzheimer’s Disease – the Acetylcholinesterase inhibitors

Neurons (nerve cells) communicate with one another by releasing a chemical (neurotransmitter) from one neuron onto another. The second neuron detects this neurotransmitter and information is thus shared between them. After a few brief moments, the neurotransmitter is either broken apart by an enzyme, taken back up into the first neuron, or simply floats away by diffusion. At this point the signaling between nerve cells is finished—until, of course, the first cell releases another batch of neurotransmitter. When this signaling system operates across millions of neurons and billions of communication sites (synapses), the brain is able to perform all of the functions that we take for granted like thinking, moving, and forming memories.

The primary Alzheimer’s disease treatments are drugs that attempt to improve memory and cognitive capacity. Since the main type of brain cell that is destroyed in Alzheimer’s disease is one that communicates using acetylcholine as a neurotransmitter, the main drugs used to treat patients with Alzheimer’s disease work on acetylcholine nerve cells.

Donepezil (Aricept), tacrine (Cognex), rivastigmine (Exelon) and galantamine (Razadyne, Reminyl) are drugs that increase neurotransmission at neurons that use acetylcholine as a neurotransmitter. Aricept, Cognex and Exelon are acetylcholinesterase inhibitors that act in the central nervous system (CNS; essentially brain and spinal cord). Cognex is rarely prescribed because of its potentially serious side effects, specifically liver damage.

Acetylcholinesterase inhibitors are drugs that prevent the breakdown of acetylcholine by enzymes. As you probably guessed, those enzymes carry the name acetylcholinesterases. By increasing the amount of acetylcholine available for neurotransmission between cells, communication is improved even when some of the acetylcholine-containing neurons have died. This approach does not work when too many nerve cells have died, but it can make matters better for a certain period of time. This is why acetylcholinesterase inhibitors delay cognitive decline in patients with Alzheimer’s disease for a period of time, but then no longer help.

Galantamine (Razadyne) works to improve acetylcholine neurotransmission, too, although the exact mechanism is unclear. It probably acts as an acetylcholinesterase inhibitor, though it may also have other ways to improve acetylcholine nerve cell function.

The most common side effects of acetylcholinesterase inhibitors are nausea, vomiting, decreased appetite and diarrhea. Cognex as particular effects on the liver, which is why it is no longer commonly used as an Alzheimer’s disease treatment.

Neuroprotection treatment for in Alzheimer’s Disease – the Glutamate receptors antagonists

When a chemical neurotransmitter is released on a neuron, the nerve cell that receives it becomes activated. The activation is stimulated by the chemical, it causes ions like sodium and calcium to rush into the cell. Eventually a small electrical current called an action potential is evoked and this is what leads that second neuron to eventually release its own chemical neurotransmitter on the next nerve cell down the line (or a muscle).

Unfortunately, this activation can be overdone—if a cell is overly stimulated, it causes a number of harmful processes within the cell. High amounts of calcium in the cell can be toxic, for example. If the stimulation is sustained, the cell will eventually die from what is called an excitotoxic insult.

One of the ways in which acetylcholine cells are thought to die in Alzheimer’s disease is through excitotoxic insult (though this is likely to only be one part in a very complex disease process). One Alzheimer’s disease drug that attempts to prevent this damage is called memantine (Namenda, Axura). One way that memantine works is to block overstimulation of vulnerable neurons.

The chemical neurotransmitter that activates the vulnerable acetylcholine nerve cells is glutamate. Glutamate is the most abundant stimulating neurotransmitter in the brain. Memantine is intended to block glutamate from overly stimulating the neurons that tend to die in Alzheimer’s disease. Protecting these neurons may help preserve memory and cognitive function; however it is not clear if memantine ultimately prevents cell death. It certainly does not stop the progression of the disease.

Side effects of memantine include headache, confusion, dizziness and constipation.

Alzheimer’s Disease Dietary interventions – Medical diets and supplements

Another feature of Alzheimer’s disease is that the brain cells of affected individuals do not take up glucose from the blood like they should, especially in elderly patients. Glucose, which is a sugar, is the primary food for brain cells. When there is not enough glucose in the blood, the brain can run on ketones if it has to (in everyone, not just Alzheimer’s disease patients).

Therefore, one recently approved treatment for Alzheimer’s disease is a dietary intervention increases ketone levels in the blood. Ketones are better able to make it into brain cells and provide energy when glucose uptake is lacking. Thus the brain cells at least have some food/energy source with which to function.¹

Caprylidene (Axona) is a medical food available only by prescription that creates ketone bodies. Axona was approved by the FDA in 2009 for the treatment of moderate to severe Alzheimer’s disease. Axona is rather well tolerated but it can cause flatulence, bloating, diarrhea, dizziness and headache.

Another dietary intervention used to treat Alzheimer’s disease is vitamin E. One large study showed that supplementation with high doses of vitamin E was able to delay the clinical progression of the disease (not necessarily the loss of nerve cells in the brain). Vitamin E was able to keep cognitive test scores from falling as fast as they would without treatment and delayed nursing home placement for patients of Alzheimer’s disease.² However this effect of vitamin E is controversial³ and may actually make matters worse.⁴

Vitamin E is a rather potent antioxidant. One of the ways that cells can die (including the cells in the basal forebrain affected by Alzheimer’s disease) is through oxidative damage. Harmful oxygen species and free radicals can poke holes in the side of cells, destroying them. An antioxidant like vitamin E could potentially neutralize those reactive oxygen species before they can cause cell damage.

While vitamin E is available without a prescription, it should be used with care in high doses. Vitamin E is a fat-soluble vitamin, which means that the portion of the vitamin is not used by the body or excreted is stored in fat cells in the body. This is in contrast to a water soluble vitamin like vitamin C, which is filtered out by the kidney and urinated quite effectively. As a fat soluble vitamin, vitamin E can accumulate in the body and cause problems. Therefore, high dose vitamin E treatment should be supervised by a physician.

Future Alzheimer’s disease medications that are actively being researched include anti-inflammatory drugs, antioxidants, neurotrophic and growth factors. The goal is to either protect neurons from dying, help patients perform better cognitively, or both. Eventually scientists hope to develop a vaccine against some of the proteins that cause Alzheimer’s disease. However, the disease needs to be much better understood to determine if this would be helpful.

It is important to recognize that current Alzheimer’s disease treatments do not prevent nerve cells from eventually dying; they simply improve memory and thinking ability for a period of time. At best, they tend to slow the cognitive decline that is seen in Alzheimer’s disease. Patients can expect to get only six months to a year of slowed cognitive decline by taking currently available current medicines.

Brain Exercsing is an Alzheimer’s disease treatment

One promising Alzheimer’s disease treatment is not related to drugs at all. Several lines of evidence indicate that patients are helped by performing mentally challenging tasks. People that routinely solve crossword puzzles, brainteasers, and memory games delay onset of Alzheimer’s disease and delay the loss of cognitive abilities. In addition to keeping the brain “fit,” keeping the body physically fit is another important way to improve cognitive function/delay cognitive decline.⁵ The research in these areas is in its relative infancy, but the initial data is quite encouraging.

Treatment of psychiatric and behavioral issues that occur in Alzheimer's Disease

In addition to treatments for the cognitive symptoms of Alzheimer’s disease, there are a number of behavioral issues that arise as part of the disease process. Patients and caregivers of patients with Alzheimer’s disease report that patients experience:

• Anxiety

• Depression

• Hallucinations and/or delusions

• Physical or verbal outbursts

• Restlessness

These behavioral issues are part of the disease process, but are treated with some of the same psychiatric medicines that would be used in patients without Alzheimer’s disease. The major difference is that certain psychoactive medications are not appropriate for use in the elderly and especially elderly patients with dementia. While it is important to treat these behavioral symptoms when possible (both for patients and caregivers), choosing a medication needs to be done thoughtfully and carefully.

The safest medications to treat anxiety, depression, and irritability are selective serotonin reuptake inhibitors (SSRIs) and the newer antidepressants. Examples include fluoxetine (Prozac), paroxetine (Paxil) and sertraline (Zoloft). Tricyclic antidepressants are tolerated less well by elderly patients and patients with Alzheimer’s disease. Tricyclic antidepressants also interact with a number of other medications.

Hallucinations are sensations of visions, sounds, odors or physical feelings that are not really there. Hearing voices in one’s mind that cannot be silenced is an example of a hallucination. Delusions are firmly held beliefs that something virtually impossible or highly unlikely is true or happening. A belief that the government has implanted a listening device in a patient’s dental filling would be a delusion. Hallucinations and delusions are psychotic symptoms and are seen in a number of mental illnesses. These symptoms are particularly troubling for caregivers since they lead to combativeness and resistance on the part of the patient.

There are several reasonably safe treatments for hallucinations and delusions. Haloperidol (Haldol) is one of the older treatments and can still be effective; however newer antipsychotic medications like olanzapine (Zyprexa), quetiapine (Seroquel), risperidone (Risperdal) may be better for treating Alzheimer’s disease patients.

Anxiety, “sundowning,” restlessness, and disruptive behavior can be difficult to endure and difficult to treat. The traditional anxiety medications need to be used extremely carefully in patients with Alzheimer’s disease. The standard anti-anxiety (anxiolytic) drugs are benzodiazepines and include drugs like lorazepam (Ativan) and diazepam (Valium). While Ativan may be safe in certain cases (others may not be), all benzodiazepines need to be used with caution in the elderly and in the treatment of Alzheimer’s disease-related behavioral symptoms. Most behavioral issues are addressed with antidepressants and antipsychotics (neuroleptics).

Some of the behavioral symptoms of Alzheimer’s disease can be anticipated or avoided. Patients with Alzheimer’s disease often become confused and irritable when they are moved away from a setting that they recognize. For example, if a patient has a medical issue and needs to be temporarily hospitalized, the change in environment can be extremely stressful. Facing the challenges of a world that is increasingly confusing and unpredictable for the patient can be exhausting and lead to extreme frustration. While it may seem like it would be nice to have a patient get out of the house for a visit or a trip, in moderate to severe dementia, this could be a potent trigger of stress and disruptive behavior.

While variety and mental stimulation is probably helpful early in Alzheimer’s disease, it is can be counterproductive when the disease has progressed to later stages. When Alzheimer’s disease has progressed, it is better to stick to comfortable routines, familiar faces, and light topics of conversation. Avoiding conflict is the best approach. Since patients with Alzheimer’s disease often have limited capacity to direct attention, when provocative topics come up, remaining upbeat and changing topics as quickly as possible can prevent an escalation of the problem.

Patients with Alzheimer’s disease become increasingly suspicious and distrustful as the disease progresses. Paranoid behavior and/or feelings of vulnerability are very common. It is essential to provide a secure, protected environment for patients struggling with these feelings and to constantly reassure the patient about these security measures. Firearms and other objects that could be used as a weapon should not be kept in the living environment—the potential for a catastrophic event is too great.

An important part of Alzheimer’s disease treatment is for caregivers to seek support and aid from others as much as possible. The disease process is emotionally and physically draining for all involved. Without support, the patient will not receive adequate treatment and the caregivers will become victims of the process. Alzheimer’s disease is an intensely difficult disease, one that impacts many lives. However there are others that share this experience and burden. Identifying and making use of available resources is incredibly important to the overall treatment of Alzheimer’s disease.

Alzheimer’s Disease in Conclusion

Alzheimer’s disease is a neurological disease associated with memory loss, behavioral changes, and a loss in cognitive ability. The disease is progressive, meaning that it gets worse over time. In Alzheimer’s disease, nerve cells in particular areas of the brain die, including the basal forebrain. There are also abnormal things that appear in brain tissue that can be seen under a microscope, specifically amyloid plaques and neurofibrillary tangles.

Alzheimers disease cannot be stopped. It can be slowed. Sometimes the effects on behavior and thinking can be reversed, at least for a while.

The value in treatimg Alzheimer's disease is that it allows the person and their loved ones to share more quality time together, and for the sufferer of Alzheimer's disease live a longer fruitful life, enjoying as much of it as is possible.

Alzheimer's Disease Treatment Reference List

(1) Henderson S, Vogel J, Barr L, Garvin F, Jones J, Costantini L. Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer's disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutrition & Metabolism 2009;6:31.

(2) Sano M, Ernesto C, Thomas RG et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study. N Engl J Med 1997;336:1216-1222.

(3) Petersen RC, Thomas RG, Grundman M et al. Vitamin E and donepezil for the treatment of mild cognitive impairment. N Engl J Med 2005;352:2379-2388.

(4) Lloret A, Badia MC, Mora NJ, Pallardo FV, Alonso MD, Vina J. Vitamin E paradox in Alzheimer's disease: it does not prevent loss of cognition and may even be detrimental. J Alzheimers Dis 2009;17:143-149.

(5) Heyn P, Abreu BC, Ottenbacher KJ. The effects of exercise training on elderly persons with cognitive impairment and dementia: a meta-analysis. Arch Phys Med Rehabil 2004;85:1694-1704.

ABOUT THE AUTHOR: Michael T. Spako is an M.D. who chose to pursue a medical writing career instead of a doctors practice. I am pleased to have him as the principal writer for this cradle cap treatment site, and look forward to his further contributions. Donald Urquhart, Psychologist, Editor.

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