Originally published in The Ottawa Citizen February 14, 2005

Watching someone we love lose their sense of self has become an all-too-common occurrence in Canada and, indeed, in many parts of the world. Even as adults, our childhood image of our parents is firmly imprinted into our minds. The piece-by-piece loss of this image is painful to witness and frightening to the afflicted.

Although we associate dementia (the loss of intellectual capacity, gradual loss of memory, mood swings, changes in behaviour and inability to perform daily tasks) with the aged, Alzheimer’s disease, the most common form of dementia, occurs throughout adulthood.

How many Canadians suffer from Alzheimer’s? How do you recognize it? What have we learned about this disease? What treatments are available and what progress can we expect in the future?

The most common form of Alzheimer’s disease is Sporadic, involving 90 to 95 per cent of all cases. There is a rare genetically inherited form called Familial Autosomal Dominant that accounts for the remaining five to 10 per cent. Two-thirds of the 280,000 Canadians afflicted are women. One in four Canadians has a family member with the disease. Within the next 25 years, as baby boomers age, the number afflicted will increase to 750,000.

Today, $5.5 billion a year is spent providing nursing-home care, medications and community support services for people with dementia. Annual per person costs proportionally increase with disease severity: $9,541 for those with mild disease to $36,794 for those with severe disease.

We know the disease causes gradual unrelenting brain injury and damage. The brain is organized into different zones, each responsible for a specific function. For example, short-term memory loss, loss of vocabulary skill, and the inability to recognize familiar faces is associated with damage to the temporal lobe and hippocampus.

Despite these changes, people still appreciate, respond to and experience a full range of emotional responses.

Brain tissue becomes damaged because too much beta amyloid protein is secreted into the region. The carrier molecules that usually transport the protein away from the area are overwhelmed. As a result, plaques form and destroy the brain cells (neurons). In addition, twisting choking stringy material within living neurons (neurofibrillary tangles) destroy more of them.

Patients and their family and friends have difficulty pinpointing when the symptoms began because of the slow, progressive nature of the illness. Indeed, many of the treatments available work best in those with mild to moderate disease. An early diagnosis is essential to try to limit the speed of disease progression and improve quality of life.

Although there is no cure for Alzheimer’s disease, there are three cholinesterase inhibitor medications, donepezil (Aricept), rivastigmine (Exelon) and galantamine hydrobromide (Reminyl), available for people with mild to moderate disease that can help improve or slow the decline of cognitive tasks such as memory, language and orientation (knowing the date, time, and who you are). They can stabilize the person’s ability to cope with the responsibilities of daily life.

Notable in Alzheimer’s disease, many of the neurons that are destroyed produce acetylcholine, a neurotransmitter linked to learning and memory. When a neuron activates, it will communicate with the adjacent neuron by sending acetylcholine to it. The acetylcholine in turn will activate the next cell to keep the message going.

These cholinesterase inhibitor medications increase the amount of acetylcholine in the brain by blocking cholinesterase, the enzyme that breaks down acetylcholine, leading to an improvement of some symptoms.

Recently, mamantine (Ebixa), a different class of medication, was approved for use for people with moderate to severe disease.

Cessation of therapy results in symptom relapse after a few weeks. It requires about three months of therapy to see peak improvements. Over the next nine to 12 months, there is a slow return to the original starting point. Thereafter, the decline is slowed compared to those who do not take the medication.

New research is promising. A new drug called Alzhemed, currently in clinical trials, appears to prevent the formation of amyloid plaques and encourages the mopping-up of the beta amyloid before it reaches threatening levels.

Recently, an antibody vaccine against beta amyloid was injected into the brains of mice, and reduced plaque formation.

Although there is no known means to prevent Alzheimer’s disease, there are lifestyle measures that can reduce the rate of onset of the disease: exercise (walking has been shown to delay cognitive decline), smoking cessation, controlling high blood pressure and elevated cholesterol levels, moderate alcohol intake, and healthy eating habits.

Advances will continue as researchers gain more insight into the mechanism of the disease. This is happening now and offers hope to those suffering with this disease and to their families.

The Alzheimer Society of Canada website, www.alzheimer.ca, contains a plethora of information about the disease.