Alzheimer’s Education & Treatment
Originally described by Alois Alzheimer in 1907, Alzheimer’s disease (AD) has emerged as the most common type of dementia in the elderly today. Although the definitive diagnosis of AD requires histologic confirmation, in the absence of a readily discernible cause, the clinician may establish the diagnosis antemortem, with a fair degree of certainty, based on the clinical findings of a gradually progressive cognitive decline that results in the loss of memory, language skills, and a progressive decline in the ability to do activities of daily living, and executive function.
As the aging population continues to grow at a vigorous pace, it becomes increasingly important to recognize the clinical spectrum of AD because of the possible benefit of medical intervention. In recent years, research studies have made major advances in our understanding of the histopathogenesis, genetic risk factors, and treatment options for this devastating neurodegenerative disease.
AD is a progressive dementia with memory loss as the major clinical manifestation. Although short-term memory impairment is often the manifesting symptom, remote memory loss also appears to be affected over time. Another important feature of AD is the disturbance of language. The language difficulties evolve into a communication breakdown as the patient struggles with a markedly limited vocabulary, word finding problems, and defects in verbal comprehension.
Other cortical signs and symptoms such as apraxia, acalculia, and visuospatial dysfunction may become apparent over the course of the disease. With the development of apraxia, patients lose the ability to carry out such simple tasks as combing their hair or using the shower. Acalculia may become evident when the patient is no longer able to maintain a checkbook or household accounts. Visuospatial abnormalities can also be seen as patients become disoriented with their body position in space and frequently may become lost.
Behavioral problems emerge throughout the various stages of the disease. Mood disturbances such as depression, anxiety, or apathy may be present early on in AD, whereas delusions, hallucinations, and psychosis can be prominent in later stages. In advanced stages of AD, patients may exhibit tremor and gait disturbance, , urinary incontinence, and myoclonus. Seizures can also be seen in some patients with late-stage disease. Patients with end-stage AD may end up in a vegetative state when all cognitive activity ceases
Scientists are still trying to fully understand the cause or causes of Alzheimer’s disease; however, plaques and tangles and the risk factors that affect a person’s likelihood of developing the disease should be understood.
Plaques and Tangles
Alzheimer’s disease is characterized by a build-up of proteins in the brain. Though this cannot be measured in a living person, extensive autopsy studies have revealed this phenomenon. The build-up manifests in two ways:
- Plaques – deposits of the protein beta-amyloid that accumulate in the spaces between nerve cells
- Tangles – deposits of the protein tau that accumulate inside of nerve cells
Scientists are still studying how plaques and tangles are related to Alzheimer’s disease. One theory is that they block the nerve cells’ ability to communicate with each other, making it difficult for the cells to survive.
Autopsies have shown that most people develop some plaques and tangles as they age, but people with Alzheimer’s develop far more than those who do not develop the disease. Scientists still don’t know why some people develop so many compared to others. However, several risk factors for Alzheimer’s disease have been uncovered.
Advancing age is the number one risk factor for developing Alzheimer’s disease. One out of eight people over the age of 65 has Alzheimer’s disease, and almost one out of every two people over the age of 85 has Alzheimer’s. The probability of being diagnosed with Alzheimer’s nearly doubles every five years after age 65.
People who have a parent or sibling that developed Alzheimer’s disease are two to three times more likely to develop the disease than those with no family history of Alzheimer’s. If more than one close relative has been affected, the risk increases even more.
Scientists have identified two kinds of genes that are associated with this familial risk factor. The first is thought to be a “risk gene,” ApoE 4, which increases the likelihood of developing Alzheimer’s, but does not guarantee it. In addition to ApoE 4, scientists think there could be up to a dozen more risk genes yet to be discovered.
The second kind of gene is a “deterministic gene” and is much rarer than risk genes. Deterministic genes are only found in a few hundred extended families around the world. If a deterministic gene is inherited, the person will undoubtedly develop Alzheimer’s, probably at a much earlier age.
Although age and family history are out of our control, scientists have also identified several lifestyle factors that can influence a person’s risk of developing Alzheimer’s disease. A connection has been found between serious head injury and future development of Alzheimer’s, so those who practice safety measures such as wearing helmets and seat belts and not engaging in activities where there is a high risk of falling are at an advantage.
Scientific research is also providing valuable information about how drug and non-drug approaches to treatment can improve day-to-day functioning and maximize quality of life. Drug treatments currently available are used to manage the cognitive symptoms of Alzheimer’s, such as changes in thinking, memory and perception. Several prescription drugs are currently approved by the U.S. Food and Drug Administration (FDA) to treat people who have been diagnosed with Alzheimer’s disease (AD). Treating the symptoms of AD can provide patients with comfort, dignity, and independence for a longer period of time and can encourage and assist their caregivers as well.
It is important to understand that none of these medications stops the disease itself.
Treatment for Mild to Moderate AD
Medications called cholinesterase inhibitors are prescribed for mild to moderate AD. These drugs may help delay or prevent symptoms from becoming worse for a limited time and may help control some behavioral symptoms. The medications include: Razadyne® (galantamine, formerly known as Reminyl® and now available as a generic drug), Exelon® (rivastigmine), and Aricept® (donepezil).
Scientists do not yet fully understand how cholinesterase inhibitors work to treat AD, but research indicates that they prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking. As AD progresses, the brain produces less and less acetylcholine; therefore, cholinesterase inhibitors may eventually lose their effect.
No published study directly compares these drugs. Because they work in a similar way, switching from one of these drugs to another probably will not produce significantly different results. However, an AD patient may respond better to one drug than another.
Treatment for Moderate to Severe AD
A medication known as Namenda® (memantine), an N-methyl D-aspartate (NMDA) antagonist, is prescribed to treat moderate to severe AD. This drug’s main effect is to delay progression of some of the symptoms of moderate to severe AD. It may allow patients to maintain certain daily functions a little longer than they would without the medication. For example, Namenda® may help a patient in the later stages of AD maintain his or her ability to use the bathroom independently for several more months, a benefit for both patients and caregivers.
Namenda® is believed to work by regulating glutamate, an important brain chemical. When produced in excessive amounts, glutamate may lead to brain cell death. Because NMDA antagonists work very differently from cholinesterase inhibitors, the two types of drugs can be prescribed in combination.
The FDA has also approved Aricept® for the treatment of moderate to severe AD.