Alzheimer’s risk written in genes

Researchers believe damage that contributes to Alzheimer’s begins 50 years before the disease strikes.

New research from the US has uncovered evidence that damage to the brain that could contribute to the development of Alzheimer’s disease begins developing from a young age in people who carry an unfortunate combination of genes. 

It is known that genes play a strong role in the development of Alzheimer’s disease, but so far, according to a study published in the May edition of the Journal of Neuroscience, “few gene variants have been identified that reliably contribute to that risk”.

One of the few that have been identified is a common variant of the CLU gene, carried by 88 per cent of Caucasians, which “begins to damage your brain a full 50 years before people normally get Alzheimer’s”, according to a news release from the University of California, Los Angeles (UCLA).

The research team, led by Professor Paul Thompson, scanned the brains of 398 healthy adults ranging from 20 to 30 years of age, using a new type of magnetic resonance imaging (MRI) scan that maps the brain’s connections, also known as ‘white matter’.

They compared those carrying a C-allele variant of the CLU gene with those who had a different variant, the CLU T-allele, and found that there was already degeneration occurring in the white matter of those 20-somethings with the risk gene.

“For example, Alzheimer’s has traditionally been considered a disease marked by neuronal cell loss and widespread grey-matter atrophy,” Professor Thompson said. “But degeneration of myelin in white-matter fibre pathways is more and more being considered a key disease component and another possible pathway to the disease, and this discovery supports that.”

Professor Thompson drew four main conclusions from the research.

“This risk gene damages your brain a full 50 years before people normally get Alzheimer’s. The damage can be seen on an MRI scan, but there are no symptoms yet.

“[Secondly], it’s now known what this mysterious gene does — namely, make your brain wiring vulnerable to attack by impairing the wiring before any senile plaques or tangles develop.

“Finally, knowing the role of this gene is useful in predicting a person’s risk of the disease and in seeing if you can step in and protect the brain in the 50-year time window you have before the disease begins to develop.”

“We know that many lifestyle factors, such as regular exercise and a healthful diet, may reduce the risk of cognitive decline, particularly in those genetically at risk for Alzheimer’s, so this reminds us how important that is.”

The professor said the brain could compensate for the changes observed in the study’s young participants and that other factors, such as the normal neuron death that is associated with age, would most likely to contribute to the development of Alzheimer’s disease.

“So it’s unlikely we are seeing the earliest possible signs of Alzheimer’s-associated brain changes in these young people,” he said.

“It’s more likely the reduced fibre integrity represents an early developmental vulnerability that may reduce brain resilience to later Alzheimer’s disease pathology. In other words, its mechanism of action may not be part of the classic Alzheimer’s pathways that lead to abnormal amyloid plaque and neurofibrillary tangle accumulation in the brain.”

Tags: alzheimers-disease, dementia, research,

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