Where did Alzheimer's get its namesake?

I recently attended a talk that opened with a biography of the man who discovered the pathological condition of dementia and diagnosed the disease that bears his name, Alois Alzheimer.

Alzheimer was a German psychiatrist, and began his residency in 1888 at the Hospital for the Mentally Ill and Epileptics in Frankfurt, Germany. He became interested in research on the cortex of the human brain, and continued his education in psychiatry and neuropathology. In 1903, under the tutelage of Emil Kraepelin, Alzheimer created a new laboratory for brain research at the Munich medical school.

Having published many papers on conditions and diseases of the brain, Alzheimer gave a remarkable lecture in 1906 that made him famous, in which he described an 'unusual disease of the cerebral cortex', the first form of dementia, in his patient Auguste Deter.


The first Alzheimer’s patient

Auguste Deter, died 9 April 1906

Auguste, a woman in her fifties, demonstrated symptoms not unlike the prevailing markers of dementia: reduced comprehension and memory loss, disorientation, delusions and hallucinations. She died at 55 years-old, and due to her age, she was given a “presenile dementia” diagnosis. However, the post-mortem showed various abnormalities of the brain, including thinner than normal and senile plaque in the cerebral cortex, previously only encountered in elderly people. Alzheimer was able to identify the neurofibrillary tangles in the brain, which had never previously been described.

It was Emil Kraepelin’s suggestion that the newly discovered disease be given the name “Alzheimer’s disease”, after its founder.

Today, the methods for diagnosing Alzheimer's disease is still typically based on the same investigative methods used in 1906. This is remarkable compared with the development of investigative methods for other diseases, and it speaks volumes about the quality of Alzheimer's discovery.

Potential Precursor to Alzheimer's

As people age, they may experience a waning in their cognitive abilities, including memory and thinking skills. However, if the changes are greater than the cognitive changes associated with normal aging, then there may be more at play.

Mild Cognitive Impairment or (MCI) is a descriptive syndrome rather than a specific condition or disease where an individual experiences mild but measurable changes in memory, language, thinking or judgement noticeable to the person affected and to family and friends.  

Typically, changes in cognition are not significant enough to interfere with daily life =, but do increase the risk of developing Alzheimer's or another dementia.  For the majority of people who have MCI, memory is the cognitive ability most affected.

However, not everyone diagnosed with MCI goes on to develop Alzheimer’s, rather some people remain stable and others may even show an improvement in cognitive abilities over time.

Approximately 15 to 20 per cent of people age 65 or older have MCI.
— Alzheimer's Association

Mild cognitive impairment is a categorized as a clinical diagnosis. A medical professional determines the presence or absence of MCI by evaluating a person’s cognitive and behavioural changes, and using professional judgement about the possible causes and severity of the symptoms. 

People diagnosed with MCI have different patterns of symptoms with many possible underlying causes, often leading to many unanswered questions. It is important to seek out information, education and support in order to help live with this condition effectively.

Whether MCI, dementia or Alzheimer's, try to focus on and nurturing current abilities without worrying about what might happen in the future.

Blood Test Breakthrough

Until now, the only way to measure plaques in the brain, a hallmark of Alzheimer's disease, has been through expensive and invasive testing methods that are generally only available in a research setting.

However, Doctor Koichi Tanaka has developed a minimally invasive, cost-effective blood test measuring for a specific peptide to detect if a person is at the earliest stages of Alzheimer's disease. 

The test has shown to have a greater than 90 per cent accuracy at predicting people at risk of Alzheimer’s, raising hopes of earlier and more precise interventions in the treatment of the devastating condition.

It was developed as part of a 30 year journey and its success proven by Australian scientists at the Florey Institute and Japanese researchers at the National Centre for Geriatrics and Gerontology (NCGG).

To assess the accuracy of the approach, researchers compared samples indicating plaques taken at NCGG against patient samples with plaques from the Australian Imaging, Biomarker and Lifestyle Study.

This test will help detect if people are on the pathway to Alzheimer’s or if they are symptomatic, it can suggest that there are other causes - it may even suggest how quickly someone could deteriorate.

To learn more about this potentially revolutionary discovery, read the study published in Nature in its entirety.

Showing Vulnerability to Build Awareness

January 8th was the official launch of the Alzheimer Society of Canada's January Alzheimer Awareness campaign, I live with dementia. This is especially exciting because I have the honour of being featured in it!

This amazing feat all started when I reached out to the Alzheimer Society of Canada to become a media spokesperson in June 2017. The Communications Director of the Society, Roseanne Meandro, has worked with me since to help me get my story out there.

In September, Ramp Communications contacted me to do a photoshoot for the campaign. It just so happened that the photoshoot landed on my birthday, so I felt very special. David Tam, the Creative Director from Pear Tree Photography managed to get the shot used for the campaign right off the bat.

I continued to work with David Brouitt, the Creative Director of Ramp Ad, to refine my story, which was set to be featured as part of the campaign.

For the remainder of 2017, the campaign was under embargo, so we couldn't talk about it publicly. 

But now the word is out there and I am so thrilled to get a chance to share! My hope is, and has been since I decided to become a public advocate for this cause, that by allowing myself to be vulnerable, it will resonate with people.   

I want to personally thank all of the people who made this campaign possible, and  I encourage you to start a discussion about dementia using the #ilivewithdementia

Read my story. 

APOE gene gateway to halting the disease's progression

An increasing number of studies demonstrate that the APOE gene, responsible for encoding a protein called apolipoprotein E, dramatically raises the risk of Alzheimer's, partly by encouraging amyloid beta to collect into damaging plaques, a key component of the disease.

There are three types of the APOE gene, called alleles: APOE2, E3 and E4. Everyone has two copies of the gene and the combination determines your APOE "genotype". There are six APOE genotypes: E2/E2, E2/E3, E2/E4, E3/E3, E3/E4, and E4/E4. 

The E4 variant of the gene is "the most prevalent genetic risk factor" for Alzheimer's, with over half of people with the condition having this gene expressed. Studies also show that people who have both copies of the gene have a 12-fold higher risk of developing Alzheimer's disease.

A study led by Dr. David Holtzman, head of the Department of Neurology at the Washington University School of Medicine in St. Louis, MO, Research was conducted to understand the role of APOE in the formation of Alzheimer's disease. 

A Ph.D. student named Tien-Phat Huynh, Dr. Holtzman and colleagues, targeted the APOE protein using a kind of DNA-based molecule created by co-author Tracy Cole, PhD, and others at Ionis Pharmaceuticals. The molecule – known as an antisense oligonucleotide – interferes with the instructions for building the APOE protein. The findings are now published in the journal Neuron.

The researchers injected the compound into the fluid surrounding the brains of newborn mice. For comparison, they gave other newborn mice either saltwater or a placebo “oligo” that does not interfere with the APOE instructions.

Levels of APOE protein dropped by about half in mice given the APOE compound as compared with those that received the placebo oligo or saltwater. 

Dr. Holtzman said about his findings, "If you wanted to target APOE to affect the amyloid process, the best thing would be to start before the plaques form."

Gene and drug therapy are in the works, but more work is needed before the compound could be evaluated in people.

To learn more about these programs and other APOE-related drug discovery programs, investigate the  Alzheimer's Drug Discovery Foundation research portfolio with a filter for "APOE4."


Most under-recognized public health threat

According to a report published by Statistics Canada in 2014, Dementia is the 8th leading cause of death in Canada. It is the only cause of death among the top 10 without a way to prevent it, cure it or even slow its progression.

Too often Alzheimer's is treated as a issue that only impacts people that are aging, but I can attest to the fact that that is simply incorrect. This disease has far reaching impacts and the burden will continue to deepen.  

According to the Alzheimer Society of Canada, as of 2016, the combined health-care system and out-of-pocket caregiver costs are estimated at $10.4 billion per year. By 2031, this figure is expected to increase by 60 per cent, to $16.6 billion.

In an earlier post I talked about the passing of Bill C-233An Act respecting a national strategy for Alzheimer’s disease and other dementias, making Canada the 30th Country with a National Dementia Strategy.

This is a step in the right direction, but what are we doing to help the people with dementia and their families right now? 

I want to find a way to unify us, caregivers and sufferers alike, so we can share our experiences in order to influence policy. 

Dementia is still not being seen as the epidemic that it is. The percentage of the Canadian Institutes of Health Research’s budget invested in dementia research is only 5%

A commitment to more public funding for dementia research is the best place to start.

Find out how Canada compares to these and other G7 nations in funding Alzheimer’s research.

Link Between Brain and Behaviour

There is a direct link between our brain and how we behave. This is because the brain acts as the control centre for the actions and reactions to stimuli in the environment. For a person living with Alzheimer's, the link is disrupted and the brain's messages are no longer relayed. 

It is important to know alterations in a person's behaviour can be an indication of specific physical changes to certain areas of the brain. 

The main areas of concern in Alzheimer disease:

Limbic system controls memory and emotion; it links the lobes of the brain, enabling them to connect behaviour with memories. It also controls emotion and daily function such as sleeping and eating. The Limbic system is affected early on in Alzheimer disease. 

A common example of what can happen when the limbic system is involved is that the person may not be able to find an object having forgotten where it was put. He/she may immediately assume it has been stolen. The person may become very emotional and may blame others for taking it. To diffuse the situation, do not argue, but rather suggest a plan of how to retrieve the missing object.

Temporal Lobes contains the major memory centre of the brain called the hippocampus, also part of the Limbic System, where verbal and visual memory are processed.

Verbal memories are words. Memories related to what we read, say or hear, whereas visual memory is what we use to recognize objects, faces and places, to guide us around our environments.

The Temporal Lobes also control new learning and short-term memory. We know the Temporal Lobes are affected when the individual begins to experience lapses in short-term memory. That is to say, something that happened five minutes ago is quickly forgotten. There is no ability to retain memories of the recent past and therefore the person lives in the present moment. What is seen now is reality.

For example, if you have been for a visit and left, the person that is beyond the early stage of the disease will have no memory of your visit to them. You were never there, because you are not there now. The person will no longer be able to connect time and place to the present reality.

The person may lose vocabulary skills and have difficulty understanding what words mean. He/she may go out to a familiar place and then not know how he/she got there or how to get home again.

Damage to the temporal occipital part on both sides of the brain may also cause Agnosia, that is not recognizing familiar faces, objects or places.

For the person with Alzheimer disease, losing the connection to familiar faces must be terrifying. And for caregivers, this can be one of the most heart breaking symptoms of the disease; the moment when their loved one no longer knows who they are.

A useful tip is to have photos of special people prominently displayed with their names clearly shown. This can be used to help the person reminisce about special times with people who are important to them.

The condition also applies to objects. The person may no longer recognize a familiar object or its purpose. For example, not understanding what a hair brush is for.

Part of the Alzheimer Journey is about discovering how the progressive degeneration of brain cells will impact an individual's behaviour, mood and emotions.

When supporting a person with dementia who is behaving out of character, try and look beyond the behaviour itself to discover the root cause. Sometimes behavioural changes can be a result of frustration, a sense of being out of control, or a feeling of not being listened to or understood.

Personality changes could be the earliest sign of Alzheimer's, so here are 10 early symptoms of dementia to be aware of.

Cutting edge research

I was so excited when I heard that the Medical Arts Health Research Group facility in Penticton, BC is conducting a study to evaluate the efficacy of a new medication (Aducanumab) on early Alzheimer's disease. 

This study is project is part of a global study called Biogen Engage Study and is looking to determine whether Aducanumab, can slow progression of early Alzheimer’s disease, as well as investigate whether it’s safe to use in patients.

The hallmark of Alzheimer’s disease is the development of plaques (sticky deposits, sometimes called clumps) and tangles of certain types of proteins in the brains. These plaques are made up of a protein called beta-amyloid, which is thought to be a major cause of brain cell death which contributes to the progression of Alzheimer’s disease.

Many researchers think that developing drugs to target beta-amyloid could help to slow or halt the progress of the disease, when taken early.

The ENGAGE and EMERGE studies is trying to determine how safe and effective an investigational anti-plaque medication is in slowing the progression of early Alzheimer’s disease.

They are looking for 2,700 participants from around the world to take part.

If you are worried about memory loss, review the top 10 warning signs of Alzheimer disease.

What causes Alzheimer's Disease?

There are a number of theories as to what causes changes in how the brain works and which of these changes leads to or causes Alzheimer's disease. Scientists do know that it is breakdown in a part of the brain's processes interferes with its ability to function effectively.  

Two abnormal structures that are accepted as indicators of Alzheimer's disease are:

  • Amyloid plaques- dense protein deposits that form outside and around nerve cells in the brain. Whether they are a cause or a by-product of Alzheimer's disease is not yet known. Are thought to cause damage to nearby nerve cells.
  • Neurofibrillary tangles - inside the affected nerve cells are twisted strands of fibrils called tangles. These tangles appear to destroy the cells internal structure. 

As cells are damaged by Alzheimer's disease, the functions controlled by the affected parts of the brain, such as memory, language, problem solving skills, become impaired or lost all together. The nerve cells stop working, lose their ability to communicate with other nerve cells and the die. As the nerve cells die, the brain shrinks is size and weight.

Over time this disease affects different areas of the brain. Alzheimer's affects each person individually because of the person's personality, personal history and life experiences. As the disease unfolds however, it follows a specific pattern for most people.

Learn more about Alzheimer's and how it affects the brain.


With Dementia, A Cup Of Tea Is Not So Easy

My family is of British heritage so having a cup of tea in my house growing up was customary. Unfortunately, I am not sure if I tasked my mum with conducting this tradition today, she would remember all the steps required to complete it.

That is because a seemingly menial task, like making a cup of tea, is actual a complicated series of activities undertaken by the brain to turn a simple idea into a completed action. Different parts of the brain have to work together to control thinking, learning and remembering. 

The brain has 100 billion nerve cells (neurons). Each nerve cell connects with many others to form communication networks. The networks are responsible for the way the brain's messages are relayed and form the basis of memories, thoughts and feelings.

For someone suffering from dementia, amyloid plaques and neurofibrillary tangles deprive the neurons of oxygen, rendering them unable to communicate, and eventually leading to the death of the nerve cell. As the nerves cells die, the brain shrink resulting in simple tasks in daily life like brushing one's teeth becoming too convoluted. 

A simple example from daily life that shows how functions controlled by different parts of the brain work together is the task of making a cup of tea.

First you have a thought, I feel like having a cup of tea. Now a whole series of activities have to happen in different parts of the brain before you can enjoy that cup of tea.

The brain has to:

  1. switch on your motor to make you get up and go to the kitchen;
  2. remember where the tea bags are stored;
  3. recognize what container looks like and understand that the label has a connection to the contents;
  4. recall and understand entire sequence of actions for making tea
    (i.e., grab a cup, locate a teaspoon, put the tea bag in the cup); 
  5. connect the visual image of the tap with the activity of running water;
  6. know the right amount of water has to be measured;
  7. know how to turn on the kettle;
  8. exercise patience while the kettle to boils;
  9. recognize when the procedure has finished; 
  10. know that the boiling water has to be poured over the tea bag and left to steep.
  11. know to remove tea bag from the cup; 
  12. remind you to put in milk and sugar if that is your preference; 
  13. tell you to raise the cup up to your mouth in order to drink; and
  14. tell the part that controls the reflex action of swallowing to function correctly.

And now you have your cup of tea to enjoy! Not as menial of a task after all.

Alzheimer's Disease affects not only the individual's ability to initiate and follow a process like this, but also the ability to recognize that a process like this if required.

So next time you go to make your morning pick-me-up, remember how lucky you are to have the mental capacity to be able to complete

To learn more about how dementia affects the brain, take a tour.