No easy fix for Alzheimer’s disease
If pharmaceuticals can’t save you, maybe you can save yourself by changing your lifestyle. Norman Swan explains how.
Hopes of a cure for Alzheimer’s disease being on the horizon took a blow when drug giant Pfizer announced in January that, after two decades and millions of dollars spent, it was pulling the plug on Alzheimer’s research.
Pfizer’s research had focused on trying to clear away brain deposits of a protein called amyloid beta. Some researchers think those deposits might have been the wrong target. Others think trials failed because treatments started too late, and because people who were selected for treatment might not all have been suffering from Alzheimer’s disease.
The latest strategy is to try to select people who show diagnostic markers of an earlier stage of Alzheimer’s disease.
It is known as the Alzheimer’s prodrome. At this stage people experience some memory problems but still fall within the norms of cognitive function. There are, however, clinically detectable changes: samples of cerebrospinal fluid show raised levels of amyloid beta and MRI scans show shrinkage of the hippocampus, the structure crucial for forming memories.
One great hope – for vitamin fans and researchers alike – is that dietary supplements could prevent the worsening of Alzheimer’s disease. So far antioxidants, in particular vitamin E, have been disappointing but there has been hope for a supplement called Fortasyn Connect.
Designed to boost brain function, it contains a cocktail of omega 3 fatty acids, minerals and vitamins (specifically DHA, EPA, uridine monophosphate, choline, vitamins B12, B6, C, E, and folic acid, phospholipids and selenium). The concentrations of these nutrients in the blood and brains of patients with Alzheimer’s disease are lower than normal.
The same factors that protect against heart disease protect vessels in the brain.
Animal studies show the cocktail improves communication between brain cells, blood flow, regeneration of cells in the hippocampus, and cognitive function.
This hopeful tonic, now marketed by Dutch company Nutricia as ‘Souvenaid’, had been previously tested in three clinical trials on people with mild to moderate Alzheimer’s disease. The trials, lasting three to six months, suggested a helpful effect only in people with mild Alzheimer’s.
So a consortium of researchers in Europe and the US, including academics and people from pharmaceutical companies, decided to test patients at the earlier, prodromal stage of the disease – having mild memory problems but detectable brain changes and elevated levels of amyloid beta in their cerebrospinal fluid.
Recruited from memory clinics across Finland, Germany, the Netherlands and Sweden, 311 people aged 55 to 85 completed the study. Half got Souvenaid as a strawberry or vanilla-flavoured daily drink; half just got a flavoured drink.
There was, however, less shrinkage of the hippocampus in the supplemented group, along with a slight but significant positive effect suggested by a secondary measure of how well the patients were functioning, a Clinical Dementia Rating based on structured interviews.
Which may or may not mean something. The trouble with the study was that the overall rate of cognitive decline was slower than expected in both groups. That suggests there needed to be more people in the study, and that it might have needed to go on longer. So it is still an open question whether this cocktail has an effect. Even if it does, it is unlikely to be dramatic.
Is there any clear evidence of something that can forestall Alzheimer’s disease?
A modest bit of good news is that the same factors that protect against heart disease – healthy food, keeping your weight down, exercise, lowering high blood pressure, avoiding diabetes and not smoking – protect against blood-vessel disease in the brain, which it is thought contributes to Alzheimer’s disease. This is supported by statistics from Europe that indicate dementia rates are falling with heart disease and stroke incidence.
One of the strongest protective factors, though, is education. A 2014 study published in Lancet Neurology found the more education a person received early in life, the later they developed dementia, or not at all. That fits with the ‘cognitive reserve’ theory – the more educated you are, the denser your neural networks, so you have more brain capacity to start with.
While the evidence isn’t clear, you certainly can’t do any harm by learning a language or a musical instrument in mid-life, in the hope it will exercise your brain enough to keep dementia at bay at least for a little longer.