When it comes to Alzheimer’s disease and its hereditary nature, it is a vast and complex subject. There are direct disease-causing hereditary genes that usually give rise to forms of the disease with an early onset, or, for example, Down’s syndrome, which is a chromosomal abnormality that arises during foetal development and leads to early-onset Alzheimer’s in 100% of cases, as the amyloid gene is present on chromosome 13 but in six copies (two more than usual).

There are also disease-associated genes – so-called polygenic causes of disease – where many genes interact, but none of the genes alone causes the disease. This is usually the case when there is a family cluster of, for example, Parkinson’s disease or Alzheimer’s, sometimes spanning several generations, but usually with the onset of the disease at an advanced age. This is what is meant by ‘risk genes’ – that is, you have a higher risk of developing a disease, but as the genes do not cause the disease on their own, it is not predictable. This is likely to be the case with Alzheimer’s disease in the instances of your mother and grandmother.

There is a statistical link between a higher risk of being diagnosed with Alzheimer’s disease and having previously been diagnosed with Parkinson’s disease. This link is also complicated, as it can be difficult to distinguish Lewy body dementia (DLB) from Parkinson’s disease (PD). DLB often has an Alzheimer’s component, and it is not uncommon for diagnoses of DLB and Alzheimer’s to be made simultaneously, or for Alzheimer’s disease to progress to DLB or vice versa; however, this requires that the respective disease processes – which are different – can be identified.

In the case of Alzheimer’s disease, for example, tau/phosphotau and alpha/beta amyloid, as well as neurofilaments in cerebrospinal fluid samples, increase as the disease progresses, and symptoms of DLB can be detected in various tests and examinations.

It is therefore difficult to state with certainty whether there is an increased risk of Alzheimer’s disease in people with Parkinson’s disease in the absence of other complicating factors./Håkan Widner