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Headlines Published on 28 October 2005

Title Adding another dimension to ‘brainfood’

European researchers, publishing in a leading scientific journal, show a biological link between cholesterol and Alzheimer’s disease. Authors of the paper acknowledge the EU’s contribution to their work through the Lipidiet project, which investigated the role of lipids in neurodegeneration.

Figure showing the recent findings by the Lipidiet EU project published in Nature Cell Biology. © Lipidiet
Figure showing the recent findings by the Lipidiet EU project published in Nature Cell Biology.
© Lipidiet
Alzheimer’s, or the ‘memory disease’, as it is sometimes called, is a fatal condition affecting higher brain function. Around one-third of the EU population develops it during their lifetime. It generally affects the elderly but early onset is known. Its prevalence in older people has led to the misconception that “losing your mind” is just part of ageing. Scientists are keen to dispel this, showing that Alzheimer’s is a disease and not a process of normal ageing. On average, it progresses from the first clinically apparent symptoms to death in about nine years. But this can vary.

The disease starts with minor memory problems and ends with patients completely forgetting even friends and family and becoming dependent on full-time care. Until now, the only treatments have been for the symptoms. More active treatments and possibly a cure will take the burden of Alzheimer’s off healthcare systems and families who have to watch this tragic degradation of the mind.

While the cause of Alzheimer’s is still not fully understood, science is well on the way to providing some answers. It is already known that, in most cases, the disease is not inherited but may depend on environmental and genetic factors – in around 5% of cases, it is inherited through mutations in three different genes. These cases have revealed much about the disease, according to the Lipidiet project team.

Lipidiet – which stands for ‘Role of Lipids in Neurodegeneration and their Preventive Potential in Diet’ – was funded by the EU’s Fifth Framework Programme (FP5). The project’s coordinator, Tobias Hartmann of Heidelberg University, Germany, is the senior author of a recent publication in Nature Cell Biology which shows that regulation of cholesterol and another fat called ‘sphingomyelin’ (SM) involves a protein – called amyloid precursor protein (APP) – which is found in the brain, but also other organs like the heart, kidneys and lungs.

Lipidiet sought to better understand the basic cellular principles at work in the disease. The seven partners in the project cover an array of specialties, including molecular biology, neurobiology, lipid metabolism, physiology and medicine, and behavioural sciences, as well as a private firm specialising in health-targeted food.

What’s cholesterol got to do with it?
APP contains a small region – the amyloid beta domain. This domain is cut off from APP by certain enzymes, known as secretases. Accumulation of amyloid beta forms, over time, a hard plaque in the human brain which is difficult to break down. Everyone produces this but the quantity and its effects are not all the same. This is an area that has traditionally stumped scientists. But using mouse models to firm up the relationship between this accumulation and the onset of Alzheimer’s, the European team is now closer to understanding the sequence of events.

The team’s newly-published findings show that amyloid beta, while toxic and disease causing when over produced, has a normal and non-toxic function. And this normal function is to regulate cellular lipid levels. Their function results in regulatory cycles in which the amyloid beta reduces cholesterol synthesis and sphingomyelin levels, the team writes in a recent statement.

The very same lipids control the activity of the enzyme which produces amyloid beta, resulting in altered amyloid-beta levels, leading to the troubling plaque. Altering these regulatory cycles – with drugs, genetics, or even diet – changes amyloid-beta production and thus the risk for Alzheimer’s, say the researchers.

“Knowledge of the natural amyloid-beta peptide function allows us to re-evaluate therapeutic and preventive approaches to Alzheimer’s disease and to generate more effective and safer novel therapies,” notes the team. What’s more it explains the link between Alzheimer's and cholesterol, and how statins (cholesterol-lowering drugs) work to prevent it.

How does this relate to food and the Lipidiet project? Well, Lipids are an insoluble fat found in the blood and organs, including the brain. We eat foods with varying fat content and types. A strong case had already been presented for the use of lipid- and cholesterol-lowering drugs to either prevent or slow down Alzheimer’s. But non-drug approaches are equally promising.

A ‘designer diet’ that can delay the onset of Alzheimer's had earlier been devised by Lipidiet, according to a CORDIS News story. The consortium is testing it in clinical trials to validate its effectiveness and provide a more convincing case for diet’s potential to prevent, delay or slow down Alzheimer’s disease.

Source:  EU project and Nature Cell Biology

Research Contacts page

More information:

  • Nutrition and diet must be given priority (CORDIS News 30 November 2004)
  • Lipidiet press statement (see ‘recent update’)

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