Alzheimer’s Disease – Explained!

Alzheimer’s Disease (named after Alois Alzheimer, who first described the disease in a lecture in 1906) is the most common dementia. But what is dementia? ‘Dementia’ is used to describe a collection of symptoms including difficulty with problem solving, thinking and language, but is most often associated with memory loss. There are many different types of dementia, but as Alzheimer’s Disease accounts for 50-60% of all cases of dementia, it is arguably the biggest problem and commands the most attention (and research funding!)

Alzheimer’s Disease is a growing problem because of our aging population. The symptoms of Alzheimer’s Disease tend to start to develop after 65 years of age – and we didn’t used to live that long! With better medical care and individuals living way past their 80th birthdays, the number of people that are old enough to develop Alzheimer’s disease is growing. It’s an awful and distressing condition for both those suffering from it, as well as for those caring for their afflicted family members or friends.

Most people have heard of Alzheimer’s Disease, and most people know it causes memory loss. But what actually causes Alzheimer’s Disease? What is it??

In the Brain

In Alzheimer’s Disease, cells in the part of the brain called the ‘Hippocampus’ begin to die. The Hippocampus is so called because the person who identified it thought it looked like a sea horse (in Greek, ‘hippo’ = horse, ‘kampus’ = sea monster). They were wrong, but the name stuck. The hippocampus is responsible for forming our memories, so damage to this area explains the memory loss in Alzheimer’s disease. As the disease progresses, cell death spreads to other parts of the brain, and can affect other functions such as problem solving and language.


So why do the cells die?

There appears to be an accumulation of two different proteins within the Alzheimer’s Disease brain. These are ‘Beta-Amyloid,’ which clumps together to form ‘plaques,’ and ‘Tau’ that forms ‘tangles.’ However, the association between these and Alzheimer’s disease is not completely clear. Many people develop plaques and tangles in old age, but have no memory problems. On the other hand, some individuals with very severe Alzheimer’s Disease may not have very severe plaques and tangles. Nevertheless, the presence of a lot of Beta-Amyloid and Tau in brain cells interferes with how cells normally function and communicate with each other. If brain cells can no longer communicate with each other, memories can no longer be formed and the cells will die. Attempts are therefore being made to reduce Beta-Amyloid plaques and Tau tangles as a part of Alzheimer’s Disease research.


So there are plaques and tangles in the Alzheimer’s Disease brain, and brain cells die, but why?

I described in a previous post what genes are and why they are important to research ( Genes act like templates for cells to make proteins, and these proteins can also control the function of other proteins. Therefore changes in genes may underlie the differences we see in Beta-Amyloid and Tau proteins.

Alzheimer’s Disease is not caused by a change in a single gene. It seems as though changes in several different genes all contribute to the increased risk of developing Alzheimer’s Disease, but by no means does carrying changes in these genes mean that you will definitely develop Alzheimer’s Disease.

However, the genes that have so far been associated with Alzheimer’s Disease are:

–          APP (‘Amyloid precursor protein’) – helps brain cells communicate with each other. Changes in APP therefore mean that brain cells can less effectively communicate.


–          Presenelins 1 & 2 – breaks down proteins in cells that are no longer needed, including Beta-Amyloid. If Beta-Amyloid is not effectively disposed of, it may form plaques


–          APOE (‘Apolipoprotein E’) – transports fats around cells, and also helps break down Beta-Amyloid. Some versions of APOE are less efficient at breaking down Beta-Amyloid.


So if the cause of Alzheimer’s Disease is not entirely due to our genes, then our environment and lifestyles are also likely to play a role. However, bear in mind that like genes, environmental and lifestyle factors have only been associated with increasing the risk of developing Alzheimer’s Disease, and are not in themselves a cause.

Obesity in mid-life increases the risk of developing Alzheimer’s Disease, as does sleep deprivation, although they don’t seem to affect the levels of beta-amyloid or tau found in brain cells. On the other hand, physical exercise may reduce the levels of tau in the brain and therefore reduces the risk of Alzheimer’s Disease. And good news for coffee drinkers! – regular caffeine intake might reduce the risk of developing Alzheimer’s Disease and delay when symptoms may develop.

However, it is difficult to prove whether environmental and lifestyle factors actually make a difference to the development of Alzheimer’s Disease, as these often rely on questionnaires or surveys, then a correlation between their answers and development of disease. Many studies have also only been carried out in rats or mice so far, and might not prove to be as important in humans. Therefore all of these things that are commonly reported in the media as ‘causing’ or ‘curing’ Alzheimer’s Disease (and/or cancer, usually!) should be taken with a pinch of salt.

But there is hope!

There have not been any recent major breakthroughs in developing a treatment for Alzheimer’s Disease, but this reflects the complexity of the problem, not the quality of the work or effort being put in to finding a cure. There are also several options available for slowing the progression of the disease, so it is definitely worth raising any concerns you may have either about yourself or a loved one with a GP. Below are some links to some fantastic charities and associations that can provide more information on Alzheimer’s Disease and dementia, or that you can donate to should you want to help fund the research effort (I am nodding enthusiastically!)

The Biocheminist


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3 responses to “Alzheimer’s Disease – Explained!”

  1. Roger says :

    Very interesting and easy to read article. I have heard that it can only be confirmed that someone had Alzheimer’s Disease after there has been a post mortem examination. Is this true? A diagnosis while alive can only be a high possibility?

    • thebiocheminist says :

      It is true that Alzheimer’s Disease can only be diagnosed with 100% certainty following a post-mortem, as this has typically been the only way to see if plaques and tangles are present. To an extent, the diagnosis of Alzheimer’s Disease is still reliant on ruling out everything else first.
      However, Alzheimer’s Disease can now be diagnosed with a very high level of confidence by using several different diagnostic tests – in particular, there has been fantastic progress in brain imaging techniques such as MRI (magnetic resonance imaging). This is a non-invasive way of scanning the structure of the brain, and as well as being able to rule out any other problems (such as stroke or tumour) that might be causing dementia, it can also pick up small changes in the size of different parts of the brain, such as the Hippocampus. As cells in the Hippocampus (and later in the Cortex) die in Alzheimer’s Disease, the Hippocampus shrinks, and this has been shown to be a good marker for the development and progression of Alzheimer’s Disease. It is currently being used as an ‘outcome measure’ in clinical trials for Alzheimer’s Disease treatments.
      Some hospitals around the world have also been working on developing a chemical tracer that attaches to the Beta-Amyloid plaques, and ‘lights up’ under a particular type of brain imaging scan (PET, or ‘positron emmission tomography’). The development of ways to measure, predict, track and diagnose Alzheimer’s Disease is a huge field of research, as these measures will tell us whether new drugs and treatments are working in clinical trials.

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