Book

I am excited to announce the publication of my book ‘Tangled Up – The science and history of Alzheimer’s disease’.

You can purchase the book directly by clicking the below links:

Alternatively search for the title of the book on your country specific Amazon website.

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You can also read of a sample of the content here

Book figures (high-resolution, coloured versions):

Mrs Auguste Deter – taken ~1907
Dr. Alois Alzheimer – taken ~1910-1911
Hippocampus – For illustration purposes the hippocampus is coloured green. In real life, the hippocampus has the same colour as the rest of the brain. The picture on the left shows that hippocampus in the brain with parts of the brain removed to illustrate how deep the hippocampus is located in the brain. The pictures on the right show on top the hippocampus when removed from the brain and below as a comparison a picture of a seahorse. It illustrates why anatomists named the hippocampus as such, as it has resemblance to a seahorse, whose latin name is ‘hippocampus’.
Amyloid Precursor Protein pathways – On the left, the normal cutting of the protein is shown, which can be recycled by the body. On the right, the ‘abnormal’ cutting of hte protein is shown, leading to beta-amyloid fibrils and plaques, which, together with tau seem to cause Alzheimer’s disease.
Tau protein – In the top left corner, an illustration of how tau helps stabilise the microtubule. The remaining figure illustrates that the phophorylation of tau leads to the disintegration of the microtubule. It further shows the aggregation of hyperphosphorylated tau into fibrils and tangles, which together with amyloid fibrils and plaques seem to be the cause for Alzheimer’s disease.
Alzheimer’s disease progression – The graph shows a hypothetical progression of Alzheimer’s disease. We can see the x-axis (the horizontal line) shows the progression of the disease from healthy/‘presymptomatic’ all the way to Alzheimer’s disease. With the term presymptomatic we mean people who have the initial changes associated with Alzheimer’s disease in their brain but have not yet developed symptoms, hence they are referred to as presymptomatic (pre from the Latin preposition ‘prae’ = ‘before’). The y-axis (the vertical line) shows us how the level of disease changes, with lower values showing ‘healthy’ levels and higher levels showing ‘unhealthy’ levels. The exact threshold where healthy changes to unhealthy for these variables is still a matter for debate and, for now, we just have to accept that at some point the factors change from healthy to unhealthy. Finally, the dashed lines show potential transition points from Healthy/‘Presymptomatic’ to Mild Cognitive Impairment to Alzheimer’s disease. The dashed lines are merely to give an indication when someone is likely to receive a diagnosis of Mild Cognitive Impairment or Alzheimer’s disease. But again, this might differ between individuals, as some might report their symptoms earlier or later, and similarly, doctors might diagnose someone earlier or later.
Genetics in Alzheimer’s disease – This graph illustrates the most common genes involved in Alzheimer’s disease. However, htere is a big difference between the red cluster and the other cluster of genes. The red clusters are all causing familial Alzheimer’s disease. This means that if we have such a gene we will definitely develop Alzheimer’s disease, in essence these genes (PSEN1, PSEN 2, APP) cause Alzheimer’s disease. The good news is that these genes are exceedingly rare in the population, which we can see on the x-axis. Indeed, less than 1% of people with Alzheimer’s disease will have these familial Alzheimer’s disease genes. The other three genes (APOe4:e4, APOe3:e4, TREM2) are ‘only’ risk genes for Alzheimer’s disease. This means that if we have such genes, we have an increased risk for Alzheimer’s disease but it does not mean that we will develop definitely Alzheimer’s disease. It is important to understand this difference, since we can modulate our risk genese by medication or lifestyle choices we make. We can see that the risk genes are more common than the familial Alzheimer genes, but are still fairly rare in the population. In essence, it is highly unlikely that our genes will cause us to develop Alzheimer’s disease.