The Grim Diagnosis of Alzheimer's Disease

"Neurodegeneration is a general term that we use when cells and their connections don't work properly, which means there isn't proper communication between brain cells."

"This affects basic physiological functions such as memory and the ability to store and receive information which is what happens when someone has Alzheimer's."

Dr.Jack Jhamandas, professor, University of Alberta

 

"Memories are stored in our synaptic connections and to retrieve them our brain has to release the correct chemical to allow communication to happen."

"When someone has Alzheimer's, sometimes this works and sometimes it doesn't."

"The initiating event happens early on, maybe even decades before someone shows up to the doctor's office with symptoms."

"That's where the problem is; we don't know what the real underlying initiating events are or when they start, which makes it difficult to devise treatments. In a sense, you're trying to work backwards; you don't know who the affected individuals will be because it could be ten to 20 years before they start to show symptoms."

Dr.Jane Rylett, professor, scientist, Western University. Scientific director, CIHR Institute of Aging

Alzheimer's Society of Canada

First described in 1906, Alzheimer's disease after a century of research and billions spent on that research, the complex brain disease is still little understood, and a long way off from a cure. As a neurodegenerative disease impacting memory, thinking and behaviour, a cruelly merciless undermining of personality and personhood, and the body's slow descent into full malfunction in lockstep with that of the brain and all associated functions, the disease continues its fearful inroads in the elderly population worldwide.

Science is of the opinion that three main events lead to Alzheiner's; that the first of which is the amyloid protein which builds up to form toxic plaques in the brain; added to that is neurofibrillary tangles (abnormal accumulations of the tau proteins in the brain), and finally, inflammation in brain cells and the role this plays in accommodating toxins entering the brain. When these three main malfunctions occur complementarily, cells no longer function, they die off, leading the brain to shrink.

What causes these proteins to build and the brain to become inflamed however, remains a mystery to science. Approximately five percent of Alzheimer's cases can be traced to genetic predisposition, but science puzzles over what might catalyze the events leading to Alzheimer's in the aggregate 95 percent of Alzheimer's cases.

A range of brain disorders are known generally as dementia, the impact of which is memory loss, diminished thinking and affected behaviour. The most common form of dementia is recognized as Alzheimer's disease which accounts for roughly 80 percent of all dementia cases, while many other form -- including vascular dementia, the result of small strokes in the brain, and Lewy body dementia which frequently has an effect on mobility -- are also part of the dementia family of diseases.

 

When Alzheimer's is at work destroying brain and body function, amyloid protein plaques become deposited in the cortex and hippocampus areas of the brain, both important for learning, and memory. With the progression of the disease, amyloid plaques and tau proteins start their destructive increase in other parts of the brain, impacting areas responsible for language and behaviour, among others. In early stages of Alzheimer's, many people remain capable of retrieving memories, but that capacity shrinks as the disease carries on and connections break down, resulting in memories fading from recall.

 

Countless attempts have taken place focusing on two major areas of drug research; first drugs that bind to and destroy amyloid plaques or prevent plaques from forming. The second route targets the tau protein responsible for forming tangles. According to Doctors Rylett and Jhamandas, nothing thus far has borne positive results and they speculate that this may possibly result from the fact that over time as the disease progresses the brain undergoes years of change before it is even clear that Alzheimer's is in the picture.

Leading to the hypothesis that the brain could possibly be, at that juncture, too critically damaged for a drug to reverse or prevent impairments. With Alzheimer's, frustratingly, there is no cure, but there are drugs that help to reduce symptoms in the short term. The drugs represent two broad categories; acetylcholinesterase inhibitors and memantine; the former to boost levels of the chemical messenger acetylcholine which has a vital role in memory retention and exists in abnormally low levels in those with Alzheimer's.

 

Glutamate is regulated by memantine, a treatment used in later stages of the disease; the glutamate an important chemical messenger that becomes impaired with Alzheimer's. Research indicates that exercise, a healthy diet and social interactions are associated with better brain health and thus those whose lifestyle includes those elements stand at lower risk of developing Alzheimer's. 

 

Research has been focusing on the development of a biomarker which, according to Dr.Rylett, could potentially take the form of a blood test or imagining test.

"The idea is these biomarkers would be predictive of who is at highest risk of developing Alzheimer's or other dementias at some point in their lives."

"If we knew that first, then we could start looking at other drug and lifestyle choices that could impact the course of trajectory of the disease."

National Institute on Aging