Understanding Alzheimer's disease: Dr. Sandra Black
Published: January 21, 2014
In honour of Alzheimer’s Awareness month, Erin Vollick sat down with Sandra Black to discover more about the science behind this devastating disease - and potential ways to combat the disease decades before symptoms appear.
Dr. Black holds the Brill Chair in Neurology in the University of Toronto’s Faculty of Medicine, and is cross-appointed to the Institute of Biomaterials & Biomedical Engineering. She is the executive director of the Toronto Dementia Research Alliance and director of the Brain Sciences Research at the Sunnybrook Research Institute.
What are the differences between Alzheimer’s disease and dementia?
Dementia refers to a state of mental decline, defined by loss of critical abilities such as memory and attention, expressing thoughts in words, planning ahead, organizing and making decisions. To be called dementia, the decline has to be severe enough that the person is no longer able to function completely independently in usual activities of daily living.
There are actually about 80 causes of dementia. One of those is Alzheimer’s disease, which is a key, common contributing factor to dementia but is often combined with stroke and diseases of the small vessels, especially in older people. In fact Alzheimer’s in conjunction with vascular disease of the brain is actually the most common underpinning of dementia in our society.
When was the first case of Alzheimer’s disease detected?
In 1906, [Aloysius] Alois Alzheimer reported a new disease, later named after him, which he called “presenile dementia”; he found “plaques” and “tangles” in the brain in the autopsy of a woman whose memory loss and other symptoms began at age 49. Interestingly, around the turn of the twentieth century, the average life expectancy was 47 years of age.
In the 1960s and 70s, when the electron microscope was invented, researchers noticed that the plaques and tangles seen in the older onset Alzheimer patients had exactly the same microstructure as pre-senile cases, so they realized the “senile” and “pre-senile” cases were the same disease, pathologically speaking.
What are the projections for the number of patients expected to suffer from Alzheimers in the future, and its implications for health care?
A study published in The New England Journal of Medicine suggests we are unprepared for the coming surge in the cost and cases of dementia. Worldwide, 38 million people suffer from dementia right now, with the number predicted to more than triple in a generation. By 2040, 9.1 million people in the US and 1.1 million in Canada are expected to have dementia. Dementia care is currently estimated to be $15 billion in Canada and $215 billion in the US. So the economic and social costs are significant.
We know the devastating effects of Alzheimer’s, but what actually causes disease?
There are two classical autopsy findings patients with Alzheimer’s, but we still don’t know what causes this to happen in common variety Alzheimer’s. The first is the amyloid plaque, a sticky deposit of amyloid protein found in between cells in the brain. Amyloid is toxic not only to brain cells but also to brain blood vessels.
The second hallmark of Alzheimer’s disease is the tau protein, which deposits in the microtubular system of the neurons, preventing transport of nutrients and other molecules between the nerve cell body along the axons to the nerve terminations, where nerve cells connect with each other (called synapses). The cells gradually die.
Furthermore, researchers have found a very strong correlation between Alzheimer pathology and silent stroke disease and degree of mental decline. High blood pressure is a key risk factor for brain damage as it can lead to blood vessel injury and stroke as well as speed up Alzheimer’s disease.
How is your lab tackling the study and treatment of Alzheimer’s?
In addition to active involvement in clinical treatment trials, we have been pursuing longitudinal studies in patients with Alzheimer’s and other dementias for some years, using standardized brain imaging and other assessments and developing pipelines to quantify brain tissue loss, small vessel disease burden and stroke lesions. Recently, we have begun to collaborate more actively with memory programs in other U of T academic healthcare centres through a collaborative network, the Toronto Dementia Research Alliance, which I direct, and across Ontario through the Ontario Brain Institute Neurodegeneration project, which is just getting underway. The goal is to gain new insight into mechanisms and genetics and use advanced brain imaging and clinical measures across the different dementias, to predict patterns and rates of decline, and to bring treatments more rapidly to our patients.
Being able to see that a person has amyloid plaques in their brain even before symptoms start opens up new possibilities for preventing decline. For example, we are participating in an international study whereby individuals over 65, who may be at risk for developing Alzheimer’s disease possibly because of family history, will be offered an amyloid PET scan. If they show evidence of amyloid in their brain, they will be invited to participate in a treatment trial with a antibody against amyloid being provided by Eli Lilly, called Solanezumab.
This is very novel as the individuals will still be completely normal and could be as much as 10 years before the onset of the dementia symptoms. The hope is to delay or prevent that onset.
Is Alzheimer’s preventable? What can we do to minimize the risk of developing Alzheimer’s?
We’ve known for about 20 years now about the link between Alzheimer’s and blood vessel disease. The biggest lesson from many observational studies is: take care of your body and you take care of your brain.
Eat heart healthy. Look after your hypertension.
Exercise! Even 30 minutes of aerobic exercise three times a week could improve your brain’s health.
Another really important factor that is emerging is sleep. Poor or insufficient sleep is becoming recognized to also be a risk factor for dementia and we may have a partial explanation. The brain has its own lymphatic system that helps to circulate the cerebrospinal fluid between cells and flushes out the toxins within. This system starts to slow down with aging. But here’s a key finding: most of this flushing happens during sleep!
Erin Vollick is a writer with the University of Toronto's Institute of Biomaterials & Biomedical Engineering.
